LncRNA name Synonyms geneid ensg_name refseq_id position cancer type ICD-0-3 ICD-0-3 methods sample regulated function description pubmed id year title TP73-AS1 TP73-AS1, KIAA0495, PDAM 57212 ENSG00000227372 NR_033708 GRCh38_1:3735601-3747336 breast cancer C50 NA qPCR, Luciferase reporter assay, Western blot breast cancer tissues, cell lines (Hs578Bst, BT474, MDA-MB-231, T47D, MCF-7, and MDA-MB-453) up-regulated TP73-AS1 was specifically upregulated in BC tissues and BC cell lines and was correlated to a poorer prognosis in patients with BC. TP73-AS1 could regulate miR-200a through direct targeting. Moreover, TP73-AS1 might compete with TFAM for miR-200a binding thus to promote TFAM expression.TP73-AS1 promoted BC cell proliferation through acting as a competing endogenous RNA (ceRNA) by sponging miR-200a. High TP73-AS1 expression in BC was related with poorer clinicopathological parameters and shorter overall survival. 28639399 2017 TP73-AS1 promotes breast cancer cell proliferation through miR-200a-mediated TFAM inhibition. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA microarray, qPCR etc. breast cancer tissues, cell line (SKBR-3) down-regulated Expression of the lncRNA GAS5 was decreased in SKBR-3/Tr cells and in breast cancer tissue from trastuzumab-treated patients. Inhibition of GAS5 promoted SKBR-3 cell proliferation, and GAS5 knockdown partially reversed lapatinib-induced inhibition of SKBR-3/Tr cell proliferation. GAS5 suppresses cancer proliferation by acting as a molecular sponge for miR-21, leading to the de-repression of phosphatase and tensin homologs (PTEN), the endogenous target of miR-21. Moreover, mTOR activation associated with reduced GAS5 expression was required to suppress PTEN. 27034004 2016 Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP TRAIL-resistant hepatocellular carcinoma cell lines (HepG2R and Bel-7402R) up-regulated CASC2, a well-established tumor suppressive long non-coding RNA, could serve as a Sponge of miR-24 and miR-221, thus modulating TRAIL-induced tumor cell apoptosis TRAIL resistance of hepatocellular carcinoma. Taken together, we demonstrated a CASC2/miR-24/miR-221 axis, which can affect the TRAIL resistance of hepatocellular carcinoma through regulating caspase 3/8; through acting as a Sponge of miR-24 and miR-221, CASC2 may contribute to improving hepatocellular carcinoma TRAIL resistance, and finally promoting the treatment efficiency of TRAIL-based therapies. 29476051 2018 CASC2/miR-24/miR-221 modulates the TRAIL resistance of hepatocellular carcinoma cell through caspase-8/caspase-3. PRNCR1 PRNCR1, CARLo-3, PCAT8 101867536 ENSG00000282961 NR_109833 GRCh38_8:127079874-127092600 glioblastoma multiforme NA M9440/3 qPCR etc. GBM tissues, serum down-regulated Firstly, RT-qPCR was performed to verify the 10 lncRNAs using 90 GBM tissues from patients showing response to TMZ and 90 from patients showing no response. Among these, four lncRNAs (MALAT1, LOC100506474, MEG3 and PRNCR1) were found significantly dysregulated in responding tissues compared with non-responding tissues. 28187000 2017 MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 glioma NA M9380/3 qPCR, Luciferase reporter assay, Western blot glioma tissues, cell lines (U257 and U87) down-regulated CASC2 is downregulated in gliomas, resulting in increased miR-193a-5p level and a decrease in mTOR expression, which further induces protective autophagy, leading to TMZ resistance. Inhibition of autophagy helps to increase the efficacy of TMZ. 29136760 2017 Upregulation of CASC2 sensitized glioma to temozolomide cytotoxicity through autophagy inhibition by sponging miR-193a-5p and regulating mTOR expression. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioblastoma multiforme NA M9440/3 qRT-PCR, in vitro knockdown, RNAi GBM cell lines (U87, T98G and LN-18, U251) up-regulated Importantly, our nanocomplex is able to target CSCs that are considered to be the prime culprits in therapeutic resistance and recurrence of GBM. Attenuation of MALAT1 by RNA interference significantly lowered the growth, motility and stemness of GBM cells. In addition, silencing of MALAT1 clearly improved the sensitivity of GBM cells to chemotherapeutic agents including the current first-line therapy of GBM [temozolomide (TMZ)]. In animal models of GBM, tumor involution with a modest but statistically significant survival benefit was achieved with concurrent treatment of TMZ and nanocomplex-mediated silencing of MALAT1.Expressions of both OCT4 and NANOG, transcription factors known to maintain pluripotency and self-renewal of embryonic stem cells, were significantly reduced (34.2% and 20.2%, respectively) after scL-siMAL treatment. 29202181 2018 Targeted nanocomplex carrying siRNA against MALAT1 sensitizes glioblastoma to temozolomide. RP11-838N2.4 NA NA NA NA GRCh38_18:3466250-3478978 glioblastoma NA M9440/3 qPCR, Western blot, RIP etc. glioblastoma tissues, cell lines (U87, U251) down-regulated We found that the level of the lncRNA RP11-838N2.4 was lower in TMZ-resistant GBM cells (U87TR, U251TR) compared to the parental, non-resistant GBM cells (U87, U251).In GBM patients, the decreased level of lncRNA RP11-838N2.4 correlated with higher risk of GBM relapse, as well as shorter postoperative survival times.Moreover, lncRNA RP11-838N2.4 acts as an endogenous sponge, suppressing the function of miR-10a through conserved sequences and increasing the expression of EphA8 that enhanced the rate of cell apoptosis, thereby intensified sensitivity of GBM cells to TMZ 27270310 2016 Long noncoding RNA RP11-838N2.4 enhances the cytotoxic effects of temozolomide by inhibiting the functions of miR-10a in glioblastoma cell lines linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 breast cancer C50 NA qPCR, Western blot, RIP etc. cell line MCF-7 up-regulated linc-RoR functions as an onco-lncRNA to promote estrogen-independent growth of ER+ breast cancer. Under estrogen deprivation, linc-RoR causes the upregulation of phosphorylated MAPK/ERK pathway which in turn activates ER signaling. Knockout of linc-RoR abrogates estrogen deprivation-induced ERK activation as well as ER phosphorylation, whereas re-expression of linc-RoR restores all above phenotypes. Moreover, we show that the ERK-specific phosphatase Dual Specificity Phosphatase 7 (DUSP7), also known as MKP-X, is involved in linc-RoR KOinduced repression of MAPK/ERK signaling. Interestingly, linc-RoR KO increases the protein stability of DUSP7, resulting in repression of ERK phosphorylation. Clinical data analysis reveal that DUSP7 expression is lower in ER+ breast cancer samples than that in ER- breast cancer. Moreover, downregulation of DUSP7 expression is associated with poor patient survival. 29041978 2017 Linc-RoR promotes MAPK/ERK signaling and confers estrogen-independent growth of breast cancer UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 cholangiocarcinoma NA M810/3 qPCR, Western blot etc. CCA tissues up-regulated For the part of functional assays, knockdown of UCA1 could attenuate CCA cell growth both in vitro and in vivo. Besides, UCA1 facilitates apoptosis via Bcl-2/caspase-3 pathway. In addition, UCA1 regulates migration and invasion potential of CCA cells by affecting EMT. Furthermore, AKT/GSK-3B axis was activated to upregulate CCND1 expression due to overexpression of UCA1 in CCA. To summary, UCA1 might be a potentially useful prognostic biomarker and therapeutic target for CCA. 29221199 2017 Long non-coding RNA UCA1 indicates an unfavorable prognosis and promotes tumorigenesis via regulating AKT/GSK-3B signaling pathway in cholangiocarcinoma HOXA13 HOXA13, HOX1, HOX1J NA ENSG00000106031 NA GRCh38_7:27193503-27200106 hepatocellular carcinoma C22.0 M8170/3 qPCR, microarray hepatocellular carcinoma tissues up-regulated patients with HOXA13-positive HCC had worse overall survival than those with HOXA13-negative HCC. HOXA13 and HOTTIP were expressed in the same neoplastic hepatocyte populations.Stable overexpression of HOXA13 in liver cancer cell lines resulted in increased colony formation on soft agar and migration potential as well as reduced sensitivity to sorafenib in vitro. 29035381 2017 High expression of HOXA13 correlates with poorly differentiated hepatocellular carcinomas and modulates sorafenib response in in vitro models. PEG10 PEG10, EDR, HB-1, MEF3L, Mar2, Mart2, RGAG3, RTL2, SIRH1 NA ENSG00000242265 NA GRCh38_7:94656325-94669695 diffuse large B-cell lymphoma NA M9680/3 qPCR, RNAi etc. DLBCL tissues, cell lines (OCI-LY-3, OCI-LY-7, OCI-LY-10 etc.) up-regulated We first found that the expression of PEG10 was upregulated in DLBCL tumorous tissues and that cell lines compared with the normal. Moreover, we illustrated that PEG10 was significantly correlated with B symptoms, IPI score, CHOP-like treatment and rituximab. 25864113 2015 Upregulation of long noncoding RNA PEG10 associates with poor prognosis in diffuse large B cell lymphoma with facilitating tumorigenicity. lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 102800311 NA NA NA prostate cancer C61.9 NA qPCR, Western blot cell lines (DU145 and LNCaP) down-regulated lincRNA-p21 silencing in DU145 and LNCaP cells induced up-regulation of PKM2 and activation of glycolysis, which could be reversed by PKM2 knockdown or rapamycin treatment.the proliferation and tumorigenesis of lincRNA-p21-silenced prostate cancer cells were significantly inhibited after knocking down PKM2. 3-bromopyruvate (3-Brpa) or rapamycin treatment largely decreased the tumour burden. PKM2 expression was inversely correlated with the lincRNA-p21 level and the survival of prostate cancer patients. 28994148 2017 LincRNA-p21 suppresses development of human prostate cancer through inhibition of PKM2. lncRNA-LET NPTN-IT1, lncRNA-LET 101241892 ENSG00000281183 NR_103844 GRCh38_15:73567012-73569294 non small cell lung cancer C34 M8046/3 qPCR, Western blot NSCLC tissues, cell lines (A549, 95D, NCI-H292, and NCI-H1975, HBE) down-regulated Decreased lncRNA-LET expression was strongly associated with advanced tumor stages and poorer overall survival of NSCLC patients.overexpression of lncRNA-LET in NSCLC H292 cells significantly suppressed cell proliferation, migration and invasion, and promoted cell cycle arrest and apoptosis.lncRNA-LET overexpression significantly reduced the expression of Notch1 intracellular Domain (NICD1) in H292 cells while knockdown of lncRNA-LET increased NICD1 expression in H1975 cells. 29416684 2017 Downregulation of long non-coding RNA LET predicts poor prognosis and increases Notch signaling in non-small cell lung cancer. lncAGER AGER-1 NA ENSG00000204305 NA GRCh38_6:32180968-32184324 lung cancer C34 NA qRT-PCR, western blotting, Luciferase reporter assay lung cancer tissues, lung cancer cell lines (PC9, L78, A549, GLC-82, SBC-5, 95D, NCI-H460, NCI-H292 and NCI- H1395) down-regulated LncAGER expression was moderately correlated with AGER expression underlying a mechanism that lncAGER upregulates AGER by competitively binding to miRNA-185. LncAGER was significantly down-regulated in 76.4% of lung cancer tissues compared to adjacent normal tissues due to promoter hypermethylation. Over-expression of the lncRNA resulted in significant decreases in proliferation rate, migration ability,colony formation efficiency of lung cancer cells and tumor growth in nude mice. 29068471 2017 Long non-coding RNA AGER-1 functionally upregulates the innate immunity gene AGER and approximates its anti-tumor effect in lung cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, RNAi, Luciferase reporter assay cell lines (KURAMOCHI, A2780p, A2780_CR5) differential expression Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. 28420874 2017 Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer LINC00857 LINC00857 439990 ENSG00000237523 NR_038464 GRCh38_10:80207710-80219657 bladder cancer C67 NA qPCR etc. cell lines (UM‐UC‐3 (ATCC: CRL‐1749) and T24 (ATCC: HTB‐4)) differential expression Furthermore, LINC00857 knockdown sensitized UM-UC-3 and T24 bladder cancer cells to cisplatin, via the negative regulation of the LMAN1 gene. Our data indicate that LINC00857 plays an important role in the regulation of response to platinum-based chemotherapy. 29856124 2018 LINC00857 expression predicts and mediates the response to platinum-based chemotherapy in muscle-invasive bladder cancer ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 lung adenocarcinoma C34 M8140/3 qPCR, Western blot etc. LAD tissues, cell line A549/Taxol up-regulated Our results showed that ANRIL functioning as a potential oncogene was up-regulated in LAD, and promoted the acquisition of chemo-resistance in paclitaxel partly through the mitochondrial pathway by modulating the expression of apoptosis-related protein cleaved-PARP and Bcl-2. 28402932 2017 The long noncoding RNA ANRIL acts as an oncogene and contributes to paclitaxel resistance of lung adenocarcinoma A549 cells NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 ovarian cancer C56.9 NA qPCR, luciferase reporter assay, Western blot etc. cell lines (SKOV3, HeyA-8) up-regulated NEAT1 was upregulated, and miR-194 was downregulated in PTX-resistant ovarian cancer tissues and cells.Functionally, NEAT1 knockdown enhanced cell sensitivity to PTX via promoting PTX-induced apoptosis in vitro. NEAT1 was identifed as a molecular sponge of miR-194 to upregulate ZEB1 expression. Mechanistically, NEAT1-knockdown-induced PTX sensitivity was mediated by miR-194/ZEB1 axis.Moreover, NEAT1 knockdown improved PTX sensitivity of ovarian cancer in vivo. 29180871 2017 lncrna NEAT1 contributes to paclitaxel resistance of ovarian cancer cells by regulating ZeB1 expression via mir-194 PCAT7 PCAT7, PCAN-R2 101928099 ENSG00000231806 NR_121566 GRCh38_9:94555054-94603990 non small cell lung cancer C34 M8046/3 qPCR, Luciferase reporter assay, Western blot NSCLC tissues, cell lines (SUNE-1, CNE-1, HNE-1, CNE-2, C666-1 and HONE-1) up-regulated Overexpression of PCAT7 resulted in the promotion of tumor cell proliferation,inhibition of cells apoptosis, facilitation of cells metastasis, and formation of EMT phenotype, while PCAT7 expression deletion remarkably prohibited cell proliferation, accelerated their apoptosis, weakened metastasis, and reversed EMT to MET.PCAT7 participates in tumor progression in NSCLC by inhibiting miR-134-5p.higher PCAT7 expression implied a worse survival rate in NPC patients. 29275424 2017 Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC). MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 colorectal cancer C19.9 NA RT-qPCR, Western blot, in vitro knockdown CRC cell lines (HT29, SW480) up-regulated lncRNA MALAT1 was significantly upregulated in the oxymatrine resistant cells (P<0.01), while knockdown of MALAT1 partially reversed the EMT phenotype in HT29 resistant cells.Furthermore, oxymatrine treatment suppressed the migration and invasion ability of CRC cells, however, this effect was significantly reversed by overexpression of MALAT1. Finally, we investigated the clinical role of MALAT1 and found that high lncRNA MALAT1 expression level is associated with poor prognosis in CRC patients receiving oxymatrine treatment(P<0.01). 29328404 2018 Chronic oxymatrine treatment induces resistance and epithelial mesenchymal transition through targeting the long non-coding RNA MALAT1 in colorectal cancer CASC11 CASC11, CARLo-7, LINC00990, TCONS_00014535 100270680 ENSG00000249375 NR_117101 GRCh38_8:127730194-127733967 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated The results showed that the expression levels of lncRNA ENST00000438347, ENST00000518376, ENST00000502804, and NR_073454 were significantly higher in HCC specimens than those in corresponding adjacent non-tumorous tissues. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. ENST00000460497 RPL9P20, RPL9_7_879 NA NA NA GRCh38_8:17150203-17150909 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. ENST00000502804 CXCL1P1, CXCL1P, GRO1P, GROP, MGSAP, SCYB1P NA ENSG00000250339 NA GRCh38_4:73944011-73944324 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated The results showed that the expression levels of lncRNA ENST00000438347, ENST00000518376, ENST00000502804, and NR_073455 were significantly higher in HCC specimens than those in corresponding adjacent non-tumorous tissues. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. LOC389641 RP11-1149O23.3, LOC389641 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. NEST00000480069 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. NR_073453 LINC00601 101101772 ENSG00000235180 NR_073453 GRCh38_10:126413869-126421879 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. NR_073453 LINC00601 101101772 ENSG00000235180 NR_073453 GRCh38_10:126413869-126421879 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated The results showed that the expression levels of lncRNA ENST00000438347, ENST00000518376, ENST00000502804, and NR_073456 were significantly higher in HCC specimens than those in corresponding adjacent non-tumorous tissues. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 gastric cancer C16 NA Microarray, qRT-PCR, RIP GC tissues, normal gastric tissues, Gastric cancer cell lines (SNU-484, SNU-520, SNU-620, SNU-638, SNU-668, AGS, NCI-N87, SNU-1, SNU-5, KATO) up-regulated Upregulated PANDAR in GC patients was positively correlated with increased tumour size, advanced TNM classification and a poor survival rate in GC patients. As a target, the CDKN1A gene was successfully downregulated by PANDAR. PANDAR controlled the transcription of the CDKN1A gene by competitively binding with p53 protein. In combination with a p53 activator (nutlin3), the knockout of PANDAR by CRISPR/Cas9 technology synergistically inhibited GC tumour growth in vivo.upregulated HOTAIR inhibits the expression of p53 by enhancing the p53 promoter histone H3 lysine 27 trimethylation (H3K27me3), and the overexpression of PANDAR increases the stability of the p53 protein in response to DNA damage. 29416011 2018 Long noncoding RNA PANDAR blocks CDKN1A gene transcription by competitive interaction with p53 protein in gastric cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 cervical cancer C53 NA qPCR, Western blot etc. cell lines (SiHa and HeLa) down-regulated Real-time PCR and Western blotting were used to measure the gene and protein expression, respectively, of microRNA (miRNA) miR-142-3p, long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript-1 (MALAT1), and high-mobility group AT-hook 2 (HMGA2). We found that metformin could suppress cervical cancer migration and invasion. During the process of tumor metastasis, miR-142-3p was significantly upregulated, whereas lncRNA MATAL1 and HMGA2 were suppressed by metformin. The binding site that allow the direct interaction between miR-142-3p and MALAT1 were located in the 3' untranslated region (3' UTR) of lncRNA MATAL1 and HMGA2 at base pairs (bp) 4452-5255, while that between miR-142-3p and HMGA2 was located at bp 1562-2521 of HMGA2. 29704494 2018 Metformin, a first-line drug for type 2 diabetes mellitus, disrupts the MALAT1/miR-142-3p sponge to decrease invasion and migration in cervical cancer cells. SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 387066 ENSG00000203875 NR_003038 GRCh38_6:85660950-85678736 chronic myeloid leukemia NA M9863/3 qPCR, Western blot etc. cell line (K562) up-regulated SNHG5 and ABCC2 expressions were up-regulated in the isolated peripheral blood cells of the CML patients when compared with healthy controls, and SNHG5 expression levels was positively correlated with ABCC2 in CML patients.In vitro studies showed that the expressions of SNHG5 and ABCC2 were up-regulated in imatinib resistant cells (K562-R) when compared to K562 cells. Overexpression of SNHG5 suppressed the expression of miR-205-5p and the expression of SNHG5 was negatively correlated with the miR-205-5p expression in CML patients. In addition, ABCC2 was predicted as a downstream target of miR-205-5p, and overexpression of miR-205-5p suppressed the expression of ABCC2 in K562-R cells.overexpression of SNHG5 in K562 cells increased imatinib resistance and knock-down of SNHG5 reduced the imatinib resistance in K562-R cells. Further experiments showed that SNHG5 promotes imatinib resistance through regulating ABCC2. Taken together, SNHG5 promotes imatinib resistance in CML via acting as a competing endogenous RNA against miR-205-5p. 28861326 2017 LncRNA SNHG5 regulates imatinib resistance in chronic myeloid leukemia via acting as a CeRNA against MiR-205-5p. CCDC26 CCDC26, RAM 137196 ENSG00000229140 NR_130917 GRCh38_8:128634199-129683679 gastrointestinal stromal tumor C16 M8936/0 qRT-PCR, Western blot, in vitro knockdown GIST cell lines (GIST-882 and GIST-T1) differential expression We found that human GIST-882 cells with lower CCDC26 expression were less sensitive to imatinib compared with GIST-T1 cells with higher CCDC26 expression. CCDC26 expression decreased in a time-dependent manner in the presence of imatinib. Moreover, small interfering RNA (siRNA) knockdown of CCDC26 increased GIST cell sensitivity to imatinib. The RNA pull-down experiment showed that CCDC26 can interact with c-KIT and that CCDC26 knockdown can upregulate c-KIT expression. We also found that inhibiting c-KIT induced resistance to imatinib. 29423012 2018 CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT. SUMO1P3 NA NA ENSG00000235082 NA GRCh38_1:160317403-160317706 breast cancer C50 NA qPCR, Luciferase reporter assay breast cancer tissues, cell lines (MCF-10A, MCF7, MDA-MB-231, MDA-MB-468, and SKBR-3) up-regulated high levels of SUMO1P3 expression associated significantly with tumor progression and poor survival of breast cancer patients.knockdown of SUMO1P3 suppressed proliferation, migration, and invasion of breast cancer cells. SUMO1P3 binds to miR-320a,which has been identified as a tumor suppressor in various cancers, including breast cancer. the tumor-promoting effects of SUMO1P3 in breast cancer are partly mediated by negative regulation of miR-320a. 29312511 2017 The long non-coding RNA SUMO1P3 facilitates breast cancer progression by negatively regulating miR-320a. lncTCF7 WSPAR, LncTCF7, TCONS_00009511, NR_033449 6932 ENSG00000081059 NA GRCh38_5:134114711-134151865 glioma NA M9380/3 qPCR, in vitro knockdown glioma tissues up-regulated lncTCF7 was significantly associated with WHO grade and tumour size.patients with high lncTCF7 expression levels exhibited markedly worse overall survival prognoses. knockdown of lncTCF7 significantly inhibited glioma cell migration, proliferation and tumorigenicity in vitro and in vivo. hypoxia induced lncTCF7 expression in an autocrine manner through IL-6 in glioma. 29234033 2017 lncTCF7 is a negative prognostic factor, and knockdown of lncTCF7 inhibits migration, proliferation and tumorigenicity in glioma. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 prostate cancer C61.9 NA RNA-seq, qPCR, ChIP etc. prostate cancer tissues, cell lines (LnCaP, PC3) up-regulated Among putatively ERa-regulated intergenic long non-coding RNAs (lncRNAs), we identified nuclear enriched abundant transcript 1 (NEAT1) as the most significantly overexpressed lncRNA in prostate cancer. Prostate cancer cells expressing high levels of NEAT1 were recalcitrant to androgen or AR antagonists. NEAT1 drives oncogenic growth by altering the epigenetic landscape of target gene promoters to favour transcription. 25415230 2014 The oestrogen receptor alpha-regulated lncRNA NEAT1 is a critical modulator of prostate cancer. AB209630 NA NA NA NA GRCh38_9:69248696-69251364 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, Western blot pancreatic ductal adenocarcinoma tissues, cell lines (Panc-1 and BXPC-3) down-regulated increased expression of lncRNA AB209630 could suppress cell proliferation and cell colony formation ability in gemcitabine resistance cells of PDAC. upregulation of lncRNA AB209630 suppressed the PI3K/AKT signaling pathway in gemcitabine resistance cells.lncRNA AB209630 expression was dramatically downregulated in PDAC tissues compared to adjacent normal tissues. Lower PDAC expression predicted a poor prognosis in PDAC patients. lncRNA AB209630 expression associated 184 with poor overall survival time. 29526843 2018 LncRNA AB209630 inhibits gemcitabine resistance cell proliferation by regulating PI3K/AKT signaling in pancreatic ductal adenocarcinoma. FOXD2-AS1 NA 84793 ENSG00000237424 NR_026878 GRCh38_1:47432133-47434641 bladder cancer C67 NA qPCR, Western blot, Luciferase reporter assay etc. cell line (T24) up-regulated LncRNA FOXD2-AS1 was high-expressed in gemcitabine-resistant bladder cancer cells. In vitro experiments, FOXD2-AS1 knockdown suppressed the 50% inhibitive concentration (IC50) of gemcitabine, drug-resistance related genes (MDR1, MRP2, LRP1) expression,invasion and ABCC3 protein expression in gemcitabine-resistant bladder cancer cells (T24/GEM, 5637/GEM). In vivo of xenograft assay, FOXD2-AS1 knockdown inhibited the tumor growth of bladder cancer cells.Bioinformatics program and validation experiments confirmed that FOXD2-AS1 positively regulated ABCC3 protein through targeting miR-143,acting as a competing endogenous RNA (ceRNA).In summary,the vital roles of FOXD2-AS1/miR-143/ABCC3 axis in gemcitabine resistance of bladder cancer cells, providing a novel therapeutic strategy for bladder cancer. We found that lncRNA FOXD2-AS1 sponged miR-143 to indirectly target ABCC3 protein ex- pression, consisting the FOXD2-AS1/miR-143/ABCC3 axis. 29674277 2018 Long noncoding RNA FOXD2-AS1 accelerates the gemcitabine-resistance of bladder cancer by sponging miR-143. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, in vitro knockdown, RNAi cell lines (PC9, RPC9) up-regulated HOTAIR silencing resulted in the upregulation of B cell lymphoma 2-associated X protein (Bax), Caspase-3 and transforming growth factor a (TGF-a) and downregulation of EGFR and B cell lymphoma 2 (Bcl-2) levels. HOTAIR normally prevents the activation of Bax/Caspase-3 while inducing TGF-a/EGFR signaling. 29467862 2017 Lentivirus-mediated silencing of HOTAIR lncRNA restores gefitinib sensitivity by activating Bax/Caspase-3 and suppressing TGF-a/EGFR signaling in lung adenocarcinoma. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 lung adenocarcinoma C34 M8140/3 qPCR, Western blot etc. lung cancer tissues, cell lines (A549, H1299, H1975, HCC827) down-regulated Our results showed that GAS5 was significantly downregulated in lung adenocarcinoma tissues compared with the paired adjacent non-tumorous tissue samples. Furthermore, lower GAS5 expression levels were associated with larger tumor sizes, poor tumor differentiation, and advanced pathological stages. GAS5 overexpression was inversely correlated with the expression of the EGFR pathway and IGF-1R proteins. 25925741 2015 The long non-coding RNA, GAS5, enhances gefitinib-induced cell death in innate EGFR tyrosine kinase inhibitor-resistant lung adenocarcinoma cells with wide-type EGFR via downregulation of the IGF-1R expression. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 non small cell lung cancer C34 M8046/3 qPCR, Luciferase reporter assay, Western blot, RIP cell lines (A549, H23, H522, H1299, H460, 16HBE and HEK-293T) up-regulated MALAT1 was significantly upregulated in five human NSCLC cells.On the contrary,miR-124 was remarkably downregulated, which indicated a potential negative correlation between miR-124 and MALAT1.MALAT1can act as a competing endogenous lncRNA (ceRNA) to modulate miR-124/STAT3 in NSCLC. MALAT1/miR-124/STAT3 was involved in NSCLC development.MALAT1 can have interactions with estrogen receptor and indicate poor survival of breast cancer. 29215698 2017 The lncRNA MALAT1 contributes to non-small cell lung cancer development via modulating miR-124/STAT3 axis. MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT 440823 ENSG00000225783 NR_003491 GRCh38_22:26646428-26676475 lung cancer C34 NA RNA-seq, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP lung cancer tissues, human lung cancer cell lines (PC9, HCC827, A549, H1870, H1048, and H1299U87) up-regulated LncRNA MIAT expression was associated with tumor size, lymph node metastasis,distant metastasis and TNM stage.Univariate analysis and multivariate analysis revealed that the lncRNA MIAT to be an independent factor for predicating the prognosis of lung cancer patients.Low lncRNA MIAT have longer overall survival time and progression-free survival time than patients with high lncRNA MIAT expression. Moreover, the knockdown of MIAT significantly sensitized PC9 and gefitinib-resistant PC9 cells to gefitinib in vitro and in vivo, and increased the expression of miR-34a and inactivated PI3K/Akt signaling. MIAT interacted with miR-34a and epigenetically controlled the miR-34a expression by hyper-methylating its promotor. MiR-34a promoter methylation status was measured by MSP in tissues and BSP in cells. 29487526 2018 Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a. RHPN1-AS1 RHPN1-AS1, C8orf51 78998 ENSG00000254389 NR_026785 GRCh38_8:143366631-143368548 non small cell lung cancer C69.9 M8720/3 PCR, RNA pull-down assay, Luciferase reporter assay, Western blot analysis NSCLC samples and adjacent non-tumor tissues, The NSCLC cell lines (A549, H1975, H1299, HCC827, PC9) and human bronchial epithelial cells (16HBE) down-regulated RHPN1-AS1 was observed to be downregulated in gefitinib resistant patients and NSCLC cell lines.RHPN1-AS1 was found to positively regulate the expression of TNFSF12 by directly interacting with miR-299-3p.Collectively, RHPN1-AS1 modulates gefitinib resistance through miR-299-3p/TNFSF12 pathway in NSCLC. 30010468 2018 The lncRNA RHPN1-AS1 downregulation promotes gefitinib resistance by targeting miR-299-3p/TNFSF12 pathway in NSCLC. HOXA10 NA NA ENSG00000253293 NA GRCh38_7:27170591-27180261 lung adenocarcinoma C34 M8140/3 DNA methylation etc. cell line differential expression competing endogenous RNA network analysis inferred that lncRNA ENSG00000240990 competed with HOXA10 to absorb hsa-let-7a/b/f/g-6p and affected patient prognosis in LUAD. Last but not least, by integrating target information of miRNA we also provided a newperspective for the discovery of potential small molecule drugs. In summary, we systematically analyzed the regulatory role of SCNA lncRNAs. This work may facilitate cancer research and serve as the basis for future efforts to understand the role of SCNA lncRNAs, develop novel biomarkers and improve knowledge of tumor biology. We used strict approach to construct ceRNA network. The approach not only considered the lncRNAs/PCGs that acted as miRNA sponges, but also selected negative miRNA-target interactions. 29069717 2017 Integrated analysis of dosage effect lncRNAs in lung adenocarcinoma based on comprehensive network. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 lung adenocarcinoma C34 M8140/3 DNA methylation etc. cell lines differential expression competing endogenous RNA network analysis inferred that lncRNA ENSG00000240990 competed with HOXA10 to absorb hsa-let-7a/b/f/g-5p and affected patient prognosis in LUAD. Last but not least, by integrating target information of miRNA we also provided a new perspective for the discovery of potential small molecule drugs. Some small molecule drugs, such as Enoxacin and Etoposide, regulated the competitive relations of lncRNA-PCG pairs by influencing the expression of hsa-let-7a/b/f/g-5p, which provided novel clues for LUAD treatment. Therefore, we combined the information that was provided by SM2miR [67] with the module to infer potential small molecule drugs for LUAD treatment. In the ceRNA module, some potential drugs could up-regulate the hsa-let-7a/b/f/g-5p expression and further down-regulate the expression of related lncRNAs/PCGs and contribute to the treatment of LUAD ((Figure10)). 29069717 2017 Integrated analysis of dosage effect lncRNAs in lung adenocarcinoma based on comprehensive network. ENST00000507437 RNPS1P1 NA ENSG00000250896 NA GRCh38_4:11371975-11372892 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) up-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. ENST00000508827 RP11-47I22.2, LOC101927780 NA NA NA GRCh38_14:61556320-61570653 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) up-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioblastoma NA M9440/3 CHIP-PCR etc. GBM cell lines (U87, U87vIII), breast cancer cell line (MCF-7) up-regulated The level of HOTAIR expression in GBM was higher than in other low grade gliomas and normal brain tissues. NLK (Nemo-like kinase), a negative regulator of the B-catenin pathway, was negatively correlated with HOTAIR expression. When the B-catenin pathway was inhibited, GBM cells became susceptible to cell cycle arrest and inhibition of invasion. Introduction of the HOTAIR 5' domain in human glioma-derived astrocytoma induced B-catenin. An intracranial animal model was used to confirm that HOTAIR depletion inhibited GBM cell migration/invasion. In the orthotopic model, HOTAIR was required for GBM formation in vivo. 25823657 2015 HOTAIR is a therapeutic target in glioblastoma. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA Microarray, qPCR, Western blot, RNAi etc. cell line (MCF-7, MCF-7/Dox400, MCF-7/Dox800, MCF-7/Dox1600) up-regulated we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Moreover, we found that CUL4A, an ubiquitin ligase component, was a critical factor bridging H19 lncRNA to MDR1 expression, and a high tumor CUL4A expression was associated with low survival in breast cancer patients treated with chemotherapy. A similar trend was observed in ER-positive breast cancer patients treated with chemotherapy although it was not statistically significant in overall survival due to a small sample size 29190892 2017 LncRNA H19 is a major mediator of doxorubicin chemoresistance in breast cancer cells through a cullin4A-MDR1 pathway. DLEU2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 10301 ENSG00000176124 NR_002605 GRCh38_13:50082171-50723236 gastric cancer C16 NA qPCR, Western blot, RIP gastric cancer tissues, cell lines (AGS, SGC7901, MGC803, BGC823,GES-1) up-regulated DLEU1 was observably intensified in GC tissues and cell lines. And highly expressed DLEU1 was relevant to tumor size, advanced stage of pathology and lymph node metastasis in GC patients. Silenced DLEU1 obviously suppressed proliferation via leading to the cell cycle arrest and inducing cell apoptosis of GC.DLEU1 could recruit LSD1(lysine specific demethylase 1) to the promoter regions of KLF2 and then suppressed its transcription. the oncogenic function mediated by DLEU1 in GC was partly by regulating KLF2.highly expressed DLEU1 means a poorer survival ability for GC patients. 29282356 2017 Long non-coding RNA DLEU1 predicts poor prognosis of gastric cancer and contributes to cell proliferation by epigenetically suppressing KLF2. ENST00000457390 RP11-14N7.2, LOC100996732 NA NA NA GRCh38_1:144245027-144245821 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. ENST00000476909 LINC00856 NA NA NA GRCh38_10:78267410-78280213 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. ENST00000553559 SNHG10, C14orf62, LINC00063, NCRNA00063 283596 ENSG00000247092 NR_001459 GRCh38_14:95532914-95534872 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) up-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. ENST00000565617 KB-1460A1.5 NA NA NA GRCh38_8:101166805-101169629 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. ENST00000568031 RP11-863P13.3 NA NA NA GRCh38_16:88177298-88178610 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) up-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. ENST00000576810 RP11-462G12.1, LOC102724927 NA NA NA GRCh38_16:3947609-3950444 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 400550 ENSG00000268388 NR_033925 GRCh38_16:86474529-86509099 osteosarcoma NA M9180/3 qPCR, Western blot etc. osteosarcoma tissues, cell lines (MG63, SaoS2 and HOS) down-regulated FENDRR expression was down-regulated in the doxorubicin-resistant OS cell lines and tissues and negatively correlated to the poor prognosis of OS patients. Together, our study demonstrated that lncRNA FENDRR may act as an inhibitory molecule of doxorubicin-resistance through down-regulating the expression of ABCB1 and ABCC1 genes in osteosarcoma cells. 29069754 2017 LncRNA FENDRR sensitizes doxorubicin-resistance of osteosarcoma cells through down-regulating ABCB1 and ABCC1 FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 NA NA NA NA osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. FOXC2-AS1 FOXC2-AS1, ODRUL 103752587 ENSG00000260944 NR_125795 GRCh38_16:86565145-86567761 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) up-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. FOXC2-AS1 FOXC2-AS1, ODRUL 103752587 ENSG00000260944 NR_125795 GRCh38_16:86565145-86567761 osteosarcoma NA M9180/3 qPCR, RNAi, Western blot, RNA-FISH etc. osteosarcoma tissues, cell lines (MG63, SaoS2 and HOS) up-regulated FOXC2-AS1 and its antisense transcript FOXC2 are positively up-regulated in doxorubicin-resistant osteosarcoma cell lines and tissues, correlate with poor prognosis and promote doxorubicin resistance in osteosarcoma cells in vitro and in vivo. LncRNA FOXC2-AS1 may promote doxorubicin resistance in OS by increasing the expression of transcription factor FOXC2, further facilitating ABCB1 expression. 28323030 2017 Antisense lncRNA FOXC2-AS1 promotes doxorubicin resistance in osteosarcoma by increasing the expression of FOXC2. FOXC2-AS1 FOXC2-AS1, ODRUL 103752587 ENSG00000260944 NR_125795 GRCh38_16:86565145-86567761 osteosarcoma NA M9180/3 qPCR, microarray, Western blot, Luciferase reporter assay etc. cell lines (SaoS2, HOS, U2-OS, MG63, 143B) up-regulated ODRUL is upregulated in OS tissues and cell lines and correlates with poor prognosis. A microarray screen combined with online database analysis showed that miR-3182 is upregulated and MMP2 is downregulated in sh-ODRUL-expressing MG63 cells and that miR-3182 harbors potential binding sites for ODRUL and the 30 UTR of MMP2 mRNA. In addition, miR-3182 expression and function are inversely correlated with ODRUL expression in vitro and in vivo. A luciferase reporter assay demonstrated that ODRUL could directly interact with miR-3182 and upregulate MMP2 expression via its competing endogenous RNA activity on miR-3182 at the posttranscriptional level. 28750740 2017 LncRNA ODRUL Contributes to Osteosarcoma Progression through the miR-3182/MMP2 Axis FOXC2-AS1 FOXC2-AS1, ODRUL 103752587 ENSG00000260944 NR_125795 GRCh38_16:86565145-86567761 osteosarcoma NA M9180/3 microarray, qPCR, RNAi, Western blot etc. cell lines (MG-63, SaoS2, U-2OS) up-regulated lncRNA ODRUL was higher in different doxorubicin-resistant OS cell lines and lower in different doxorubicin-sensitive OS cell lines. Moreover, we showed that lncRNA ODRUL was increased in specimens of OS patients with a poor chemoresponse and lung metastasis. We further demonstrated that lncRNA ODRUL inhibition could inhibit OS cell proliferation, migration, and partly reversed doxorubicin resistance in vitro. In addition, we found that the expression of classical drug resistance-related ATP-binding cassette, subfamily B, member 1 (ABCB1) gene was decreased after the lncRNA ODRUL knockdown. Thus, we concluded that lncRNA ODRUL may act as a pro-doxorubicin-resistant molecule through inducing the expression of the classical multidrug resistance-related ABCB1 gene in osteosarcoma cells. 26408180 2015 A long non-coding RNA contributes to doxorubicin resistance of osteosarcoma. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 bladder cancer C67 NA qPCR, RNAi, Western blot etc. BTCC tissues, cell lines (T24, J82) down-regulated In this study, we found that GAS5 low-expressed in BTCC tissues and cells, and its low expression level had positive correlation with higher pathological grades of BTCC. Moreover, GAS5 was a prognostic biomarker of disease free survival for BTCC patients. GAS5 over-expression could inhibit cell proliferation of BTCC J82 and T24 cells significantly. The IC50 to doxorubicin in T24/DOX cells (resistance to doxorubicin) presented a conspicuous depression, GAS5 enhancement reduced the chemotherapy resistance to doxorubicin. GAS5 over-expression promoted apoptosis induced by doxorubicin in T24/DOX cells, and depressed the expression of anti-apoptosis protein Bcl-2. 27878359 2017 Long noncoding RNA GAS5 inhibits malignant proliferation and chemotherapy resistance to doxorubicin in bladder transitional cell carcinoma. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 hepatocellular carcinoma C22.0 M8170/3 MSP-PCR, Northern blot etc. cell lines (HepG2, R-HepG2, Hep3B) up-regulated Overexpression of multi-drug resistance 1 (MDR1) gene and its protein product P-glycoprotein, accompanied with a decrease in doxorubicin accumulation level, was observed in doxorubicin-resistant R-HepG2 cells, a subline derived by selection of human hepatocellular carcinoma HepG2 cells with doxorubicin. In addition, Northern-blot analysis revealed an eight fold upregulation of the imprinted H19 mRNA in R-HepG2 cells. H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. 17297456 2007 Riboregulator H19 induction of MDR1-associated drug resistance in human hepatocellular carcinoma cells. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 bladder cancer C67 NA qPCR, RNAi, Western blot etc. cell lines (TCC, T24 and J82) up-regulated HOTAIR was up-regulated in bladder transitional cell carcinoma (TCC) tissues and cell lines compared with normal bladder transitional cell (NBTC) tissues and bladder epithelial immortalized SV-HUC-1 cells, and its expression level had positive correlation with histological grades of TCC. In T24 and J82 cells, HOTAIR over-expression promoted cell proliferation and inhibited chemosensitivity to doxorubicin and cell apoptosis induced by doxorubicin; silence of HOTAIR showed opposite regulative effects. 26781446 2016 Long noncoding RNA HOTAIR is a prognostic biomarker and inhibits chemosensitivity to doxorubicin in bladder transitional cell carcinoma. LINP1 NA 108570035 ENSG00000223784 NR_138480 GRCh38_10:6737382-6739026 breast cancer C50 NA qPCR, Western blot breast cancer tissues, Human breast cancer cells (MDA-MB-231, MDA-MB-468 and MCF7) up-regulated LINP1 knockdown mitigated breast cancer cell growth by inducing G1-phase cell cycle arrest and apoptosis. LINP1 also promoted breast cancer cell metastasis and influenced the expression of epithelial-mesenchymal transition-related markers. We identified p53 as a regulator of LINP1, and LINP1 overexpression could restore the metastatic effects of p53. Furthermore, LINP1 was upregulated in doxorubicin- and 5-fluorouracil-resistant cells and induced chemoresistance. We also observed that LINP1 enrichment played a critical functional role in chemoresistance by inhibiting chemotherapeutics-induced apoptosis. Moreover, LINP1 in tumors was associated with lower overall survival and disease-free survival. 29293402 2018 Long noncoding RNA LINP1 acts as an oncogene and promotes chemoresistance in breast cancer. NR_033878 LINC00944 387895 ENSG00000256128 NR_033878 GRCh38_12:126752164-126761045 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) up-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. NR_040001 LINC01116, TALNEC2 375295 ENSG00000163364 NR_040001 GRCh38_2:176629589-176637931 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. SOX2OTV7 NA NA NA NA NA osteosarcoma NA M9180/3 qPCR, Western blot, in vitro knockdown cell lines (U2OS and SaoS2, U-87 MG ) down-regulated EGCG targeting LncRNA SOX2OT variant 7 produced synergistic effects with Doxorubicin on osteosarcoma cell growth inhibition. On the one hand, EGCG could reduce the Doxorubicin-induced pro-survival autophagy through decreasing SOX2OT variant 7 to improve the growth inhibition of Doxorubicin. On the other hand, EGCG could partially inactivate Notch3/DLL3 signaling cascade targeting SOX2OT variant 7 to reduce the stemness then abated drug-resistance of osteosarcoma cells. 29475441 2018 SOX2OT variant 7 contributes to the synergistic interaction between EGCG and Doxorubicin to kill osteosarcoma via autophagy and stemness inhibition. LINC00707 NA 100507127 ENSG00000238266 NR_038291 GRCh38_10:6779598-6842906 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, RNAi lung adenocarcinoma tissues, cell lines(SPCA1, A549, H1299, H1975,16HBE) up-regulated The expression level of LINC00707 was clearly upregulated in LAD tissues compared to that in corresponding normal tissues.Its overexpression was related to advanced TNM stage, larger tumor size, lymphatic metastasis, and poor prognosis.LINC00707 knockdown repressed LAD cell proliferation both in vitro and in vivo. This process may involve the inducing of G1 arrest and apoptosis.cell migration was impaired after LINC00707 inhibition.Cdc42 is an important target gene involved in the carcinogenesis of LINC00707.LINC00707 is a noncoding oncogene that exerts important regulatory functions in LAD, suggesting its potential as a biomarker in the prognosis and treatment of LAD.patients expressing higher levels of LINC00707 had poorer disease-free survival and overall survival. 29482190 2018 The Long Intergenic Noncoding RNA 00707 Promotes Lung Adenocarcinoma Cell Proliferation and Migration by Regulating Cdc42. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 multiple myeloma C42.1 M9732/3 qPCR, Luciferase reporter assay, Western blot cell lines (RPMI8226, JJN-3, U266, ANBL6, OPM-2, MM1S, and MM1R) up-regulated upregulation of NEAT1 was tightly linked to poor prognosis. knockdown of NEAT1, the DEX-induced sensitivity was enhanced in the resistant cells.Meanwhile, overexpression of NEAT1 increased the DEX-induced resistance in the sensitive cells.the NEAT1/miR-193a/MCL1 pathway is closely associated with the development of DEX resistance in myeloma cells,and knockdown of NEAT1 can significantly improve DEX sensitivity in MM.Patientswith elevatedNEAT1 expression showed reduced survival times compared with patients with low levels of NEAT1 expression. 29205703 2017 LncRNA NEAT1 promotes dexamethasone resistance in multiple myeloma by targeting miR-193a/MCL1 pathway. GAS6-AS2 NA NA ENSG00000272695 NA NA acute myeloid leukemia NA M9861/3 qPCR etc. cell lines (MOLM14, K562, HEK293, HL60) up-regulated Transcriptional activation of the GAS6-AS2 lncRNA, identified in our analysis, leads to hyperactivation of the GAS6/TAM pathway, a resistance mechanism in multiple cancers including AML. 29677511 2018 An Integrated Genome-wide CRISPRa Approach to Functionalize lncRNAs in Drug Resistance. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 gastric cancer C16 NA qPCR, drugs sensitivity Plasma, gastric adenocarcinoma cell lines (MGC-803 and MKN-45) up-regulated HULC was highly expressed in the plasma and tissues of the GC patients compared with controls, with HULC high expression indicating lower survival rate. HULC knockdown enhanced cisplatin-induced apoptosis in GC cells.We observed that HULC knockdown in both MGC-803 and MKN-45 cells significantly decreased the IC50 values of CDDP, ADR, and 5-FU 28356873 2016 Silencing of LncRNA HULC Enhances Chemotherapy Induced Apoptosis in Human Gastric Cancer MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 melanoma NA M8720/3 qPCR etc. melanoma tissues, cell lines (A375, WM35, SK-MEL-5, and SK-MEL-2) differential expression The level of MEG3 was significantly associated with poor prognosis. MEG3 could bind to miR-499-5p and CYLD mRNA contained a binding site of miR-499-5p. Importantly, overexpression of MEG3 suppressed the growth of xenograft tumor and improved chemotherapy sensitivity of A375 cells to cisplatin and 5-FU treatment. 29808164 2018 lncRNA-MEG3 Suppresses the Proliferation and Invasion of Melanoma by Regulating CYLD Expression Mediated by Sponging miR-499-5p H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 ovarian cancer C56.9 NA RNA-seq, qPCR, Western blot etc. cell lines (A2780, A2780-DR) up-regulated We verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. 27193186 2016 The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot etc. lung adenocarcinoma tissues, cell lines (A549/DDP, SPC-A1 etc.) up-regulated In this study, we show that HOTAIR expression was significantly upregulated in cisplatin-resistant A549/DDP cells compared with in parental A549 cells. Knockdown of HOTAIR by RNA interference could resensitize the responses of A549/DDP cells to cisplatin both in vitro and in vivo. In contrast, overexpression of HOTAIR could decrease the sensitivity of A549 and SPC-A1 cells to cisplatin. 24155936 2013 The long noncoding RNA HOTAIR contributes to cisplatin resistance of human lung adenocarcinoma cells via downregualtion of p21(WAF1/CIP1) expression. LINC00261 LINC00261, ALIEN, C20orf56, DEANR1, HCCDR1, NCRNA00261, onco-lncRNA-17 140828 ENSG00000259974 NR_001558 GRCh38_20:22547671-22578642 colon cancer C18 NA qPCR, Western blot colon cancer tissues, cell lines (HCT116, HCT8, HT29, SW480, FHC) down-regulated LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability,migration, and invasion.LINC00261 might down-regulate nuclear B-catenin through restraining B-catenin from cytoplasm into nuclei or it could also promote B-catenin degradation and inhibit activation of Wnt pathway.LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.Overexpression of LINC00261 in SW480/DDP cells inhibited the survival rate. 29267503 2017 Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 lung cancer C34 NA qPCR, Luciferase reporter assay, Western blot, RIP lung cancer tissues, cell lines (A549, H1299, H469, SPC-A1 and A549/DDP, NHBE) up-regulated Lung cancer patients with high MALAT1 levels were associated with cisplatin resistance and low overall survival.MALAT1 knockdown in lung cancer cells resulted in miR-101-3p upregulation and increased cisplatin sensitivity.miR-101-3p decreased myeloid cell leukemia 1(MCL1) expression by binding to the 3'-untranslated region (3'-UTR) of its mRNA. MALAT1/miR-101-3p/MCL1 signaling underlies cisplatin resistance in lung cancer. 29484127 2017 MALAT1/miR-101-3p/MCL1 axis mediates cisplatin resistance in lung cancer. NMR NA 100505887 ENSG00000228750 NR_104620 GRCh38_1:6724637-6730012 esophageal squamous cell cancer NA NA in vitro knockdown esophageal squamous cell carcinoma tissues down-regulated We identified a novel NSUN2 methylated lncRNA (NMR), which was significantly upregulated in esophageal squamous cell carcinoma (ESCC), functioned as a key regulator of ESCC tumor metastasis and drug resistance. Upregulation of NMR correlated with tumor metastasis and indicated poor overall survival in ESCC patients. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1B and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. 29763634 2018 Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 oesophageal cancer NA M8070/3 qPCR oesophageal cancer tissues, cell lines (KYSE30, KYSE450, and Eca109) up-regulated PCAT-1, showed higher expression in OC tissues, especially higher in secondary OC compared with normal mucosa tissues. Overexpression of PCAT-1 increased the proliferation rate and growth of OC cells. Inhibition of PCAT-1 decreased proliferation and growth of OC cells, and increased cisplatin chemosensitivity. PCAT-1 may potentially serve as a therapeutic target for treating OC.PCAT-1 promotes development of OC and represses the chemoresistance of OC to cisplatin, and silencing of PCAT-1 may be a therapeutic strategy for treating OC.the expression of HOTAIR in oesophageal squamous cell carcinoma was significantly higher than that in adjacent tissues, and it was significantly correlated with the metastasis, high stage, and survival rate of oesophageal carcinoma. 29314203 2017 LncRNA PCAT-1 promotes tumour growth and chemoresistance of oesophageal cancer to cisplatin. RP11-135L22.1 NA NA NA NA NA ovarian cancer C56.9 NA qRT-PCR, Western blot ovarian cancer tissues, ovarian cancer cell lines (A2780, HEY, HO8910) down-regulated RP11-135L22.1 was lowly expressed in ovarian cancer.RP11-135L22.1 expression was negatively correlated with the treating time and dose of cisplatin. Western blot showed that cisplatin induced autophagy in ovarian cancer cells in a time- and dose-dependent manner. Cisplatin combined with RP11-135L22.1 can reduce autophagy, increase the apoptosis and inhibit its activity of ovarian cancer cells to a certain extent. 29509240 2018 Cisplatin suppresses tumor proliferation by inhibiting autophagy in ovarian cancer via long non-coding RNA RP11-135L22.1. SFTA1P SFTA1P, SFTPF NA ENSG00000225383 NA GRCh38_10:10784437-10794980 lung squamous cell carcinoma C34 M8070/3 qPCR, Western blot etc. cell lines (NCl-H226, SK-MES-1, NCl-H1299, A549, A549-DDP) up-regulated Here, we found that lncRNA SFTA1P (surfactant associated 1, pseudogene), highly expressed in lung, was down-regulated in LSCC tissues and could be induced upon cisplatin treatment in LSCC cells. Elevated SFTA1P induced apoptosis and enhanced the sensitivity to cisplatin of LSCC cells. We further identified that hnRNP-U (heterogeneous nuclear ribonucleoprotein U) was down-regulated in LSCCs and positively correlated with patients’ poor prognosis as well as SFTA1P. Mechanistic studies revealed that SFTA1P could up-regulate hnRNP-U expression. In addition, we identified that hnRNP-U enhanced cisplatin-induced apoptosis through up-regulation of GADD45A, high expression of which was correlated with good prognosis in LSCC patients. 29228625 2017 Long noncoding RNA SFTA1P promoted apoptosis and increased cisplatin chemosensitivity via regulating the hnRNP-U-GADD45A axis in lung squamous cell carcinoma SNHG8 SNHG8, LINC00060, NCRNA00060 100093630 ENSG00000269893 NR_003584 GRCh38_4:118278709-118279823 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). MIR100HG MIR100HG, AGD1, linc-NeD125, lncRNA-N2 399959 ENSG00000255248 NR_024430 GRCh38_11:122028327-122556721 colorectal cancer C19.9 NA qPCR etc. cell lines up-regulated MIR100HG, miR-100 and miR-125b overexpression was also observed in cetuximab-resistant colorectal cancer and head and neck squamous cell cancer cell lines and in tumors from colorectal cancer patients that progressed on cetuximab. miR-100 and miR-125b coordinately repressed five Wnt/B-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness. Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6. These findings identify a clinically actionable, epigenetic cause of cetuximab resistance. 29035371 2017 lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/B-catenin signaling lnc-SCD-1:13 NA NA NA NA NA gastric cancer C16 NA qPCR etc. cell line (NCI-N87) differential expression a low dose of celecoxib may exert an anti-cancer effect by regulating the cell cycle and apoptosis independent of COX-2 in GC cells. ITGA3 and/or DVL1 co-expressed with lnc-SCD-1:13 and lnc-PTMS-1:3 may be involved in the effects of a low dose of celecoxib on GC. 28789408 2017 Anti-cancer effect of low dose of celecoxib may be associated with lnc-SCD-1:13 and lnc-PTMS-1:3 but not COX-2 in NCI-N87 cells. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR etc. ovarian cancer tissues up-regulated HOTAIR expression was significantly associated with poor survival in carboplatin-treated patients with adjusted hazard ratios for death of 3.64 in the discovery and 1.63 in the validation set. This effect was not seen in patients who did not receive carboplatin. HOTAIR expression or its surrogate DNAme signature predicted poor outcome in all additional sets of carboplatin-treated ovarian cancer patients while HOTAIR expressors responded preferentially to cisplatin. 26497652 2015 HOTAIR and its surrogate DNA methylation signature indicate carboplatin resistance in ovarian cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 multiple myeloma C42.1 M9732/3 qPCR, Western blot bone marrow tissues, cell lines ( OPM-2, U266, KM3, XG1, JJN3, RPMI, U1996, H929, and MM1S) up-regulated H19 knockdown induced by shRNA transfection significantly inhibited proliferation, viability and colony formation in MM cells, as well as inactivated NF-kB pathway.combination treatment of H19 knockdown and NF-kB suppression (induced by specific inhibitor PDTC) produced synergistically inhibitory effects.patients with high expression of H19 had a lower survival rate.H19 was involved in MM cell growth. The linkage between H19 and NF-kB pathway may provide a novel interpretation for the mechanism of H19's growth regulation in MM. 29273733 2017 Knockdown of long non-coding RNA H19 inhibits multiple myeloma cell growth via NF-kB pathway. BDLNR NA NA NA NA NA cervical cancer C53 NA qPCR, Western blot, RIP cervical cancer tissues, cell lines (HeLa, SiHa, ME-180, and Caski,H8) up-regulated BDLNR physically bound to YBX1, recruited YBX1 to PIK3CA promoter, activated PIK3CA expression and PI3K/Akt pathway.BDLNR was upregulated in cervical cancer and associated with poor prognosis of cervical cancer patients. BDLNR mediated the anti-cancer effects of baicalein in cervical cancer via activating PI3K/Akt pathway and BDLNR would be potential therapeutic target for enhancing the anti-cancer effects of baicalein in cervical cancer.upregulated BDLNR expression indicated poor overall survival of cervical cancer patients. 29175387 2017 Baicalein inhibits cervical cancer progression via downregulating long noncoding RNA BDLNR and its downstream PI3K/Akt pathway. PAX8-AS1-N NA NA NA NA NA breast cancer C50 NA qPCR, Western blot etc. breast cancer tissue, cell lines (MDA-MB-231 and MCF-7) down-regulated we identified a novel isoform of lncRNA PAX8-AS1 (PAX8-AS1-N), which is activated by baicalein in a dose- and time-dependent manner.PAX8-AS1-N reduced cell viability,inhibited cell-cycle progression,and induced apoptosis of breast cancer cells in vitro.Depletion of PAX8-AS1-N promoted breast xenograft tumor growth in vivo. Furthermore, depletion of PAX8-AS1-N attenuated the suppressive roles of baicalein on cell viability,the apoptosis induced by baicalein, and also the suppressive roles of baicalein on tumor growth in vivo. Mechanistically, PAX8-AS1-N bound to miR-17-5p, and up-regulated miR-17-5p targets,such as PTEN, CDKN1A, and ZBTB4. In addition, PAX8-AS1-N was down-regulated in breast cancer and reduced expression of PAX8-AS1-N indicated poor survival of breast cancer patients. 29693272 2018 Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8-AS1-N. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown breast cancer cell lines (MDA-MB-231,MCF-7, SK-BR-3 and HEK293T) up-regulated Furthermore, H19 knockdown decreases PDK1 xpression in hypoxia, and ablation of PDK1 counteracts H19-mediated glycolysis and self-renewal ability in vitro and in vivo.Reprogramming is referred to as the conversion of differentiated cells to a stem-like state. Ectopic expression of four transcription factors (Oct4, Klf4, Sox2 and c-Myc) reprograms various types of somatic cells to induced pluripotent stem cells. Accordingly, H19 and PDK1 expression exhibits strong correlations in primary breast carcinomas. H19 acting as a competitive endogenous RNA sequesters miRNA let-7 to release Hypoxia-inducible factor 1a, leading to an increase in PDK1 expression. Lastly, aspirin markedly attenuates glycolysis and cancer stem-like characteristics by suppressing both H19 and PDK1. 29106390 2017 Glycolysis gatekeeper PDK1 reprograms breast cancer stem cells under hypoxia. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 prostate cancer C61.9 NA qPCR, Western blot, RIP, Luciferase reporter assay cell lines (DU145 and LNCaP) up-regulated UCA1 was up-regulated in prostate cancer tissues compared to hyperplastic prostatic tissues,and a higher UCA1 level predicted poor prognosis in PCa patients.Then we determined that the miR-184/Bcl-2 axis might be the downstream signaling pathway of UCA1 upon ART treatment. UCA1 binds to miR-184 through its seed sequences and may function as a sponge for miR-184. 28209917 2017 Artesunate suppresses the viability and mobility of prostate cancer cells through UCA1, the sponge of miR-184 lncRNA-PRLB NA NA NA NA NA breast cancer C50 NA Microarray, qPCR, Western blot, RIP etc. breast cancer tissues, cell lines lncRNA-PRLB was upregulated in human breast cancer tissues and breast cancer cell lines.Further evaluation verified that lncRNA-PRLB was positively correlated with the extent of metastasis, and its expression was correlated with shorter survival time of breast cancer patients. We identified microRNA miR-4766-5p as an inhibitory target of lncRNA-PRLB.Both lncRNA-PRLB overexpression and miR-4766-5p knockdown could remarkably enhance cell growth, metastasis, and chemoresistance. We also determined that sirtuin 1 (SIRT1) was an inhibitory target of miR-4766-5p, and that SIRT1 was inhibited by both lncRNA-PRLB knockdown and miR-4766-5p overexpression. The subcellular distribution assay revealed that lncRNA-PRLB is predominately located in the plasma. 29752439 2018 A novel long non-coding RNA-PRLB acts as a tumor promoter through regulating miR-4766-5p/SIRT1 axis in breast cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, RNAi etc. gastric cancer tissues, cell lines (MKN7, MKN45, MKN74, NUGC4, AZ521, AGS, KATOIII) up-regulated Expression of both lncRNAs was significantly higher in cancerous tissues than in corresponding normal mucosa, and higher expression of these lncRNAs significantly correlated with peritoneal metastasis in GC patients. In addition, elevated HOTAIR expression emerged both as an independent prognostic and risk factor for peritoneal dissemination. SiRNA knockdown of HOTAIR in GC cells significantly inhibited cell proliferation, migration and invasion, but concurrently enhanced the anoikis rate in transfetced cells. 25280565 2014 Metastasis-associated long non-coding RNA drives gastric cancer development and promotes peritoneal metastasis. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colorectal cancer C19.9 NA qPCR colorectal cancer tissues up-regulated The expression level of lncRNA CCAT2 in CRC tissues was increased significantly compared with adjacent normal tissues or non-cancerous tissues. CCAT2 expression was observed to be progressively increased between tumor-node-metastasis (TNM) stages I and IV. A high level of CCAT2 expression was revealed to be associated with poor cell differentiation, deeper tumor infiltration, lymph node metastasis,distance metastasis, vascular invasion and advanced TNM stage. patients with high levels of CCAT2 expression had shorter disease-free survival and overall survival times.high CCAT2 expression was an independent poor prognostic factor. 29181105 2017 Overexpression of long non-coding RNA colon cancer-associated transcript 2 is associated with advanced tumor progression and poor prognosis in patients with colorectal cancer. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 colorectal cancer C19.9 NA qPCR, Western blot etc, cell lines (HCT8, HT29, LoVo, HCT116, SW480, SW620) up-regulated LINC00152 was overexpressed in CRC tissues and negatively related to the survival time of CRC patients. Functional analyses revealed that LINC00152 could promote cell proliferation. LINC00152 could increase the resistance of CRC cells to 5-fluorouracil (5-FU) by suppressing apoptosis. We also discovered that LINC00152 could enhance cell migration and invasion. 29180678 2017 Long non-coding RNA LINC00152 promotes cell proliferation, metastasis, and confers 5-FU resistance in colorectal cancer by inhibiting miR-139-5p MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gastric cancer C16 NA qPCR, Western blot etc. cell lines (SGC7901, BGC823) up-regulated Chemoresistant GC cells had higher levels of MALAT1 and increased autophagy compared with parental cells. Silencing of MALAT1 inhibited chemo-induced autophagy, whereas MALAT1 promoted autophagy in gastric cancer cells. Knockdown of MALAT1 sensitized GC cells to chemotherapeutics. MALAT1 acts as a competing endogenous RNA for miR-23b-3p and attenuates the inhibitory effect of miR-23b-3p on ATG12, leading to chemo-induced autophagy and chemoresistance in GC cells. 29162158 2017 Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR gastric cancer tissues, cell lines (BGC-823 and MKN-45) up-regulated lncRNA HOTAIR had an extremely high expression level in GC cells, and predicted poor prognosis in patients.Down-regulation of HOTAIR could promote chemosensitivity, induce apoptosis of GC cells, and significantly inhibit GC cell proliferation, invasion and metastasis in vivo and in vitro. 29236333 2017 Effect and mechanism of lncRNA HOTAIR on occurrence and development of gastric cancer. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, Luciferase reporter assay, Western blot breast cancer tissues, cell lines (MCF-10A, MCF-7, MDA-MB-231, T-47-D and ZR-75-1) up-regulated lncRNA NEAT1 was up-regulated in breast cancer cell lines and tissues.NEAT1 promoted invasion through inducing Epithelial-mesenchymal transition (EMT) and NEAT1 played a role in 5-fluorouracil (5-FU) resistance.the EMT-inducer HMGA2 was identified as a down-stream target of miR-211.LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis.breast cancer patients with low levels of NEAT1 expression had better overall survival time than those with high levels. 28720546 2017 The lncRNA NEAT1 facilitates cell growth and invasion via the miR-211/HMGA2 axis in breast cancer. ENST00000547547 NA NA NA GRCh38_12:69946543-69947081 colorectal cancer C19.9 NA qPCR, Western blot, RIP cell lines (HCT116 and LoVo) down-regulated Overexpression of ENST00000547547 promoted 5-FU-induced cell apoptosis and reduced the chemoresistance of 5-FU in-vitro.ENST00000547547 was a target of miR-31, miR-31 was upregulated in 5-FU-resistant CRC cells, and knockdown of miR-31 increased the chemosensitivity of 5-FU-resistant CRC cells. ENST00000547547 reduced chemoresistance in 5-FU of 5-FU-resistant CRC cells through competitive binding to miR-31 and has the potential to serve as a therapeutic target in CRC patients. 29115526 2017 The long non-coding RNA ENST00000547547 reduces 5-fluorouracil resistance of colorectal cancer cells via competitive binding to microRNA-31. SNHG6 SNHG6, HBII-276HG, NCRNA00058, U87HG 641638 ENSG00000245910 NR_002599 GRCh38_8:66921684-66926398 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RNAi etc. HCC tissues, cell lines (BEL-7402, SMMC-7721, MHCC-97H, SK-Hep-1, Huh7 and HCC-LM3) up-regulated We found that five SNHG6 transcripts were differentially expressed in HCC tissues while only the SNHG6-003 had an oncogenic function.Ectopic expression of SNHG6-003 in HCC cells promoted cell proliferation and induced drug resistance, whereas SNHG6-003 knockdown promoted apoptosis.Moreover, SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-26a/b and thereby modulating the expression of transforming growth factor-B-activated kinase 1 (TAK1).Importantly, expression analysis revealed that both SNHG6-003 and TAK1 were upregulated in human cancers, exhibiting a co-expression pattern. 27530352 2017 The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma. SLC6A9-5:2 SLC6A9, GCENSG, GLYT1 NA NA NA NA papillary thyroid cancer NA M8260/3 microarray, qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. PTC tissues, cell lines (TPC-1 and BCPAP) down-regulated We demonstrated that SLC6A9-5:2 was remarkably downregulated in 131I-resistant thyroid cancer cell lines and 131I-insensitive patients and was positively correlated with Poly (ADP-ribose) polymerase 1 (PARP-1) expression and its activation. After downregulating SLC6A9 or blocking PARP-1 artificially, the sensitive thyroid cancer cells mostly displayed a tolerant phenotype under 131I exposure. Furthermore, SLC6A9-5:2 overexpression was positively correlated with PARP-1 mRNA and protein levels, which restored the sensitivity of resistant thyroid cancer cells. 28086241 2017 LncRNA-SLC6A9-5:2: A potent sensitizer in 131I-resistant papillary thyroid carcinoma with PARP-1 induction. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 cervical cancer C53 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. cell lines (SiHa, HeLa, DoTc2 4510) up-regulated Our results demonstrate that PVT1 expression is significantly increased in ICC tissue versus normal cervix and that higher expression of PVT1 correlates with poorer overall survival. In cervical cancer cell lines, PVT1 knockdown resulted in significantly decreased cell proliferation, migration and invasion, while apoptosis and cisplatin cytotoxicity were significantly increased in these cells. Finally, we show that PVT1 expression is augmented in response to hypoxia and immune response stimulation and that this lncRNA associates with the multifunctional and stress-responsive protein, Nucleolin. 27232880 2016 The lncRNA PVT1 Contributes to the Cervical Cancer Phenotype and Associates with Poor Patient Prognosis. SLC25A25-AS1 SLC25A25-AS1 100289019 ENSG00000234771 NR_033374 GRCh38_9:128108581-128118693 colorectal cancer C19.9 NA qPCR, RNAi, Western blot etc. CRC tissues, cell lines (HCT-116 and HT-29) down-regulated We demonstrated that the expression of SLC25A25-AS1, which has not been reported previously, was significantly decreased in both the tumor tissues (27 out of 30) and serum of CRC patients. SLC25A25-AS1 overexpression significantly inhibited proliferation and colony formation in colorectal cancer cell lines, and downregulation of SLC25A25-AS1 obviously enhanced chemoresistance and promoted EMT process in vitro associated with Erk and p38 signaling pathway activation. 27553025 2016 Decreased expression of LncRNA SLC25A25-AS1 promotes proliferation, chemoresistance, and EMT in colorectal cancer cells. lncRNA-PRAL PRAL, lncRNA-PRAL 109245082 ENSG00000279296 NA GRCh38_17:6772831-6776116 multiple myeloma C42.1 M9732/3 qPCR, Western blot, Flow cytometry, etc. cell lines (NCI-H929, ARH77, PRMI8226, OPM2, JJN3) down-regulated Survival curves showed that MM patients with low PRAL expression had a significantly shorter disease-free survival (DFS) and overall survival (OS) than the patients with high PRAL expression. We further identified and confirmed that miR-210 was the target of PRAL, and miR-210 overexpression overturned the potentiation effect of PRAL on BTZ efficacy. bone morphogenetic protein 2 (BMP2) was confirmed to be the target of miR-210. 29944867 2018 LncRNA PRAL is closely related to clinical prognosis of multiple myeloma and the bortezomib sensitivity. AF251187 NA NA NA NA GRCh38_2:168846243-168846834 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. AK123408 NA NA NA NA GRCh38_9:5832649-5835435 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) down-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. AK127565 LINC00683 NA ENSG00000266256 NA GRCh38_18:76615212-76625940 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. AL832444 NA NA NA NA GRCh38_8:123523808-123525468 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) down-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. AL833160 NA NA NA NA GRCh38_8:22679015-22684009 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. BALR-2 NA NA NA NA NA B cell acute lymphoblastic leukemia NA M9826/3 microarray, qPCR etc. blood (mononuclear cells) up-regulated Importantly, high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. BALR-2 plays a functional role in the pathogenesis and/or clinical responsiveness of B-ALL and that altering the levels of particular lncRNAs may provide a future diretcion for therapeutic development. 25681502 2015 LncRNA Expression Discriminates Karyotype and Predicts Survival in B-lymphoblastic Leukemia. BALR-2 NA NA NA NA NA B-lymphoblastic leukemia NA M9811/3 microarray, qPCR, Western blot etc. blood, cell line (HEK 293T) differential expression high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. In line with a function for this lncRNA in regulating cell survival, BALR-2 knockdown led to reduced proliferation, increased apoptosis, and increased sensitivity to prednisolone treatment. Conversely, overexpression of BALR-2 led to increased cell growth and resistance to prednisone treatment. Interestingly, BALR-2 expression was repressed by prednisolone treatment and its knockdown led to upregulation of the glucocorticoid response pathway in both human and mouse B-cells 25681502 2015 LncRNA Expression Discriminates Karyotype and Predicts Survival in B-Lymphoblastic Leukemia BC016787 DEPDC1-AS1 NA ENSG00000234264 NA GRCh38_1:68496676-68538627 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. BC036599 GUCY1A2, GC-SA2, GUC1A2 NA NA NA GRCh38_11:106674027-106676271 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) down-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. BC038366 LINC02158 729083 ENSG00000225611 NR_122070 GRCh38_3:42770612-42773635 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. BC038580 LINC01293 NA ENSG00000230836 NA GRCh38_2:74940258-74942670 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. BC039678 LOC101928047 NA NA NA GRCh38_6:6724886-6725300 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. BC040572 NA NA NA NA GRCh38_8:90646441-90646633 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. BC040587 LINC00901, LSAMP-AS4, TCONS_00005428 100506724 ENSG00000242385 NR_121607 GRCh38_3:116921431-116932238 osteosarcoma NA M9180/3 microarray, qPCR, FISH etc. osteosarcoma tissues, cell lines (U2OS, SAOS-2, HOS etc.) down-regulated The osteo3q13.31 genes LOC285194, BC040587, and LSAMP commonly show loss of expression in primary osteosarcoma samples and cell lines. Depleting either LSAMP or LOC285194 promoted proliferation of normal osteoblasts by regulation of apoptotic and cell-cycle transcripts and also VEGF receptor 1. Moreover, genetic deletions of LOC285194 or BC040587 were also associated with poor survival of osteosarcoma patients. 20048075 2010 Recurrent focal copy-number changes and loss of heterozygosity implicate two noncoding RNAs and one tumor suppressor gene at chromosome 3q13.31 in osteosarcoma. BC041455 LINC01671 101928233 ENSG00000225431 NR_131192 GRCh38_21:42599280-42615058 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) down-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. Overexpression of BC041455 prevented ERK1/2 phosphorylation. The effects of BC041455 on hormone-dependent MAPK signalling were observed in both MCF-7 and T-47D cells. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. BOKAS BOK-AS1, BOK-AS, BOKAS, NAToB, NCRNA00151 NA NA NA NA esophageal squamous cell cancer NA NA qPCR, Western blot, RIP etc. ESCC tissues up-regulated LncRNA BOKAS was up-regulated following radiation and promoted WISP1 expression and resultant radioresistance.WISP1 facilitated its own expression in response to radiation, creating a positive feedback loop and increased radioresistance. Our study revealed WISP1 as a potential target to overcome radioresistance in ESCC. 25749038 2015 Targeting WISP1 to sensitize esophageal squamous cell carcinoma to irradiation. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated The expression of CCAT1, CCAT1-L, CCAT2, PVT1, and CASC19 were elevated in cancer tissues. Among these, high expression of CCAT1 and CCAT2 was significantly associated with poor RFS (P=0.049 and 0.022, respectively) and OS (P=0.028 and 0.015, respectively). These results were validated in an independent patient cohort, in which combined expression of CCAT1 and CCAT2 expression was significantly associated with a poor RFS (HR:2.60, 95% confidence interval [CI]: 1.04-6.06, P=0.042) and a poor OS (HR:8.38, 95%CI: 2.68-37.0,<0.001).High expression of CCAT1 and CCAT2 significantly associates with poor RFS and OS. The expression of these two lncRNAs independently, or in combination, serves as important prognostic biomarkers in CRC. 28838211 2017 CCAT1 and CCAT2 long noncoding RNAs, located within the 8q.24.21 ‘gene desert’, serve as important prognostic biomarkers in colorectal cancer CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colorectal cancer C19.9 NA qPCR etc. CRC tissue up-regulated The expression of CCAT1, CCAT1-L, CCAT2, PVT1, and CASC19 were elevated in cancer tissues. Among these, high expression of CCAT1 and CCAT2 was significantly associated with poor RFS (P=0.049 and 0.022, respectively) and OS. 28838211 2017 CCAT1 and CCAT2 long noncoding RNAs, located within the 8q.24.21 ‘gene desert’, serve as important prognostic biomarkers in colorectal cancer GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 myeloid leukemia NA M9860/3 qPCR, luciferase reporter assay etc. cell line (PBMCs) up-regulated Meanwhile, GAS5 is downregulated in breast cancer cells.Survival analysis indicated that GAS5 rs55829688 (T > C) was significantly associated with prognosis of AML (p=0.018).Patients with rs55829688 CC genotype showed higher GAS5 expression in peripheral blood mononuclear cells (PBMCs) (p=0.025) and harbored a longer platelets recovery (p=0.040) than carriers of rs55829688T allele. In conclusion, rs55829688 polymorphism could increase GAS5 expression by interacting with TP63, which might aggravate the myelosuppression and in turn lead to poor prognosis in AML. GAS5 is observed to be a key mediator of glucocorticoids (GCs) resistance rather than a growth arrest-specific transcript in PBMCs. 27951730 2017 Long non-coding RNA GAS5 polymorphism predicts a poor prognosis of acute myeloid leukemia in Chinese patients via affecting hematopoietic reconstitution. HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 prostate cancer C61.9 NA Microarray Analysis, western blot, RNAi, GhIP etc. cell lines (LNCaP and PC-3) up-regulated we discovered that an lncRNA HOXD-AS1 is highly expressed in CRPC cells and correlated closely with Gleason score, T stage, lymph nodes metastasis, and progression-free survival. Knockdown of HOXD-AS1 inhibited the proliferation and chemo-resistance of CRPC cells in vitro and in vivo. Furthermore, we identified several cell cycle, chemo-resistance, and castration-resistance- related genes, including PLK1, AURKA, CDC25C, FOXM1, and UBE2C, that were activated transcriptionally by HOXD-AS1. Further investigation revealed that HOXD-AS1 recruited WDR5 to directly regulate the expression of target genes by mediating histone H3 lysine 4 tri-methylation (H3K4me3). In conclusion, our finndings indicate that HOXD-AS1 promotes proliferation, castration resistance, and chemo-resistance in prostate cancer by recruiting WDR5. This sheds a new insight into the regulation of CRPC by lncRNA and provides a poten-tial approach for the treatment of CRPC. 28487115 2017 lncRNA HOXD-AS1 Regulates Proliferation and Chemo-Resistance of Castration-Resistant Prostate Cancer via Recruiting WDR5 linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 colon cancer C18 NA qPCR, Western blot, luciferase reporter assay etc. cell lines (HB56, HB96,TSCC, Tca8113, SCC-9 and CAL27, HEK-293T), Oral cancer tissues up-regulated LincRNA-ROR was frequently up-regulated and inversely correlated with miR-145 down-regulation in the colon cancer specimens. The levels of CD44, CD133, Oct4, Sox2, Nanog, lincRNA-ROR in CD44(+) CD133(+) cells were significantly increased,while miR-145 was decreased compared with CD44(-)CD133(-)cells(P<0.05). The levels of CD44,CD133,lnc-ROR in CD44(+) CD133(+) cells were significantly reduced upon cell adherence, while miR-145 was significantly increased. Bioinformatics analysis revealed that lincRNA-ROR shared miRNA response elements with core transcription factors Oct4,Sox2 and Nanog. MiR-145 significantly inhibited the expression of lincRNA-ROR, Oct4, Sox2 and Nanog. Silencing lincRNA-ROR significantly inhibited colon cancer stem cells proliferation and increased the sensitivity to chemotherapy. Linc-ROR functions as a key ceRNA to prevent core TFs,e.g.Oct4, Sox2, Nanog, from miR-145-mediated suppression in colon cancer stem cells and regulates cell proliferation and chemosensitivity. 29690669 2018 LincRNA-ROR functions as a ceRNA to regulate Oct4, Sox2, and Nanog expression by sponging miR-145 and its effect on biologic characteristics of colonic cancer stem cells linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 breast cancer C50 NA qPCR breast cancer cell lines, breast cancer tissues and plasma up-regulated Among lncRNAs, large intergenic non-coding RNA regulator of reprogramming (lincRNA-ROR or linc-ROR) is a member of subvariety of lncRNAs, was first discovered in induced pluripotent stem cells (iPSCs), and plays a central role in promoting survival in iPSCs and embryonic stem cells (ESCs) through preventing the activation of cellular stress pathways.And linc-ROR also acts as a ceRNA to increase stemness gene Nanog expression by sponging miR-145 in cancer cells. 28869448 2017 Large intergenic non-coding RNA-ROR as a potential biomarker for the diagnosis and dynamic monitoring of breast cancer MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assays etc. cell lines (U251 and U87) up-regulated MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101. The present study elucidates a novel MALAT1-miR-101-Rap1B regulatory axis in glioma, contributing to a better understanding of the glioma pathogenesis and providing a promising therapeutic target for glioma patients. MALAT1 was found to be upregulated in glioma tissues and correlated with the progression of glioma.Although enormous efforts have been made to improve therapeutic strategies, the mortality of malignant glioma remains high and the median survival is less than 14 months. At present, the main treatment methods of glioma include surgical techniques, radiotherapy and chemotherapy, however, these traditional treatments obtain a poor prognosis due to the highly invasive nature and resistance to radiation and chemotherapy of glioma. 28551849 2017 Long non-coding RNA MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, Luciferase report assay etc. PDAC tissues, cell lines (Panc-1, Aspc-1, Mia Paca-2 and Bxpc-3) up-regulated MALAT1 is expressed at higher levels in pancreatic ductal adenocarcinoma (PDAC) tissues than in nontumour tissues and in metastatic PDAC than in localized tumours. Plasma levels of MALAT1-derived fragments are significantly elevated in patients with prostate cancer compared with those without prostate cance. MALAT1 regulates KRAS expression by influencing the spatial distribution of miR-217. MALAT1 inhibits the translocation of miR-217 from the nucleus to the cytoplasm. Patients with PDAC and high MALAT1 expression levels have shorter overall survival than patients with PDAC and low MALAT1 expression levels. Resistance to KRAS inhibition has been observed experimentally in studies regarding pancreatic cancer treatment34; thus, targeting MALAT1 may be another way to achieve KRAS/MAPK pathway inactivation. 28701723 2017 The lncRNA MALAT1 acts as a competing endogenous RNA to regulate KRAS expression by sponging miR-217 in pancreatic ductal adenocarcinoma. AB019562 NA NA NA NA NA hypopharyngeal squamous cell carcinoma C13 M8070/3 microarray, qPCR etc. primary HSCC tissues up-regulated AB209630 expression was significantly lower in carcinomas than in adjacent nontumor tissues. AB019562 expression was significantly higher in carcinomas than in adjacent nontumor tissues. 26131061 2015 Gene microarray analysis of lncRNA and mRNA expression profiles in patients with hypopharyngeal squamous cell carcinoma. AB209630 NA NA NA NA GRCh38_9:69248696-69251364 hypopharyngeal squamous cell carcinoma C13 M8070/3 microarray, qPCR etc. primary HSCC tissues down-regulated AB209630 expression was significantly lower in carcinomas than in adjacent nontumor tissues. AB019562 expression was significantly higher in carcinomas than in adjacent nontumor tissues. 26131061 2015 Gene microarray analysis of lncRNA and mRNA expression profiles in patients with hypopharyngeal squamous cell carcinoma. AC090952.4.1 RHBDF1P1 NA ENSG00000234123 NA GRCh38_3:14572852-14574792 non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. AC156455.1 AC156455.1, LOC100506691 NA ENSG00000256546 NA GRCh38_12:122063306-122068616 childhood acute lymphoblastic leukemia NA M9835/3 qPCR etc. cell lines (Reh, NALM-6) up-regulated We validated that five such lncRNA transcripts overexpressed in pre-B cALL samples (RP11-137H2.4, RP11-68I18.10, AC156455.1, KB-208E9.1, and CTA-331P3.1) were also overexpressed in the Reh and NALM-6 pre-B cALL cell lines that had significant impacts on cancer hallmark traits such as cell proliferation, migration, apoptosis, and treatment response. 27980230 2017 A childhood acute lymphoblastic leukemia-specific lncRNA implicated in prednisolone resistance, cell proliferation, and migration. AF268386 DDR2, MIG20a, NTRKR3, TKT, TYRO10, uc001gch.1 NA NA NA GRCh38_1:162785489-162786465 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Flow cytometry assay etc. HCC cell lines (SMCC7721 and HepG2) up-regulated We found that increased expression of AFAP1-AS1 was significantly correlated with pathological staging and lymph-vascular space invasion (LVSI) in HCC patients. Multivariate analyses indicated that AFAP1-AS1 represented an independent predictor for overall survival of HCC. Further experiments showed that knockdown of AFAP1-AS1 by si-AFAP1-AS1 decreased the proliferation and invasion in vitro and in vivo, induced cell apoptosis and blocked cell cycle in S phase via inhibition of the RhoA/Rac2 signaling 26892468 2016 Long noncoding RNA AFAP1-AS1 indicates a poor prognosis of hepatocellular carcinoma and promotes cell proliferation and invasion via upregulation of the RhoA/Rac2 signaling AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 esophageal squamous cell cancer NA NA qPCR, MTT assay etc. ESCC tissues, cell lines (KYSE30, KYSE70, KYSE150, KYSE450, KYSE510, and TE10) up-regulated Three lncRNAs (AFAP1-AS1, UCA1, HOTAIR) were found to be deregulated in cisplatin-resistant cells compared with their parent cells. AFAP1-AS1 was significantly up-regulated in tumor tissues compared with adjacent normal tissues. Furthermore, overexpression of AFAP1-AS1 was closely associated with lymph node metastasis, distant metastasis, advanced clinical stage, and response to dCRT. 26756568 2016 High expression of long non-coding RNA AFAP1-AS1 predicts chemoradioresistance and poor prognosis in patients with esophageal squamous cell carcinoma treated with definitive chemoradiotherapy. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 non small cell lung cancer C34 M8046/3 qPCR, etc. lung cancer tissues, normal tissues. up-regulated In conclusion, it was demonstrated that lncRNA AFAP1?AS1 is overexpressed in NSCLC and an unfavorable biomarker for patients with NSCLC. Upregulation of HOTAIR in lung tumor tissues is associated with metastasis, drug resistance and poor survival time in patients with lung cancer. 29963138 2018 Long noncoding RNA AFAP1-AS1 is upregulated in NSCLC and associated with lymph node metastasis and poor prognosis. AK022798 C1orf74, URLC4, FLJ25078 148304 ENSG00000162757 NA GRCh38_1:209779208-209784559 gastric cancer C16 NA qPCR, Western blot etc. cell lines (SGC7901, BGC823, SGC7901/DDP, BGC823/DDP etc.) up-regulated The expression of lncRNA AK022798 was significantly higher in all pcDNA3-Notch 1 plasmid treatment groups than in the pcDNA3 plasmid treatment group. Overexpression of lncRNA AK022798 promotes SGC7901/DDP and BGC823/DDP cells apoptosis.the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8. 25763542 2015 Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. AK054908 SNORA17B, ACA43, SNORA43 677824 ENSG00000276161 NA GRCh38_9:136726105-136726234 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). AK096725 LBX2-AS1 151534 ENSG00000257702 NR_024606 GRCh38_2:74502595-74504678 renal cell carcinoma C64.9 NA microarray, qPCR etc. RCC tissues up-regulated We chose the lncRNAs AK096725 (upregulated) and ENST00000453068 (downregulated) to confirm their differential expression levels in 70 paired RCC tissues and adjacent non-tumor tissues. Levels of AK096725 were significantly greater in RCC tissues while those of ENST00000453068 was significantly lower compared to the non-tumor tissues. These results are consistent with the microarray data. 24905231 2014 Expression pattern of long non-coding RNAs in renal cell carcinoma revealed by microarray. AK123263 LOC100506974 NA NA NA GRCh38_17:13776832-13777349 non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. AK126698 NA NA NA NA NA non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. AK129685 NA NA NA NA GRCh38_19:13837806-13840186 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). AK130275 PAX8-AS1 654433 ENSG00000189223 NR_015377 GRCh38_2:113211522-113276581 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). AK130977 NA NA NA NA GRCh38_20:36550794-36551444 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). ANRASSF1 RASSF1-AS1, ANRASSF1 102060282 ENSG00000281358 NR_109831 GRCh38_3:50337511-50338300 prostate cancer C61.9 NA RNA-seq, qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. cell lines (HeLa, MDA-MB-231, LNCaP and MCF-8) up-regulated ANRASSF1 endogenous expression is higher in breast and prostate tumor cell lines compared with non-tumor, and an opposite pattern is observed for RASSF1A. ANRASSF1 ectopic overexpression reduces RASSF1A abundance and increases the proliferation of HeLa cells, whereas ANRASSF1 silencing causes the opposite effects. These changes in ANRASSF1 levels do not affect the RASSF1C isoform abundance. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region. 23990798 2013 The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation. ANRASSF1 RASSF1-AS1, ANRASSF1 102060282 ENSG00000281358 NR_109831 GRCh38_3:50337511-50338300 cervical cancer C53 NA RNA-seq, qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. cell lines (HeLa, MDA-MB-231, LNCaP and MCF-9) differential expression Overexpression of ANRASSF1 increases the cell proliferation rate and decreases cell death. 23990798 2013 The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation. ANRASSF1 RASSF1-AS1, ANRASSF1 102060282 ENSG00000281358 NR_109831 GRCh38_3:50337511-50338300 breast cancer C50 NA RNA-seq, qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. cell lines (HeLa, MDA-MB-231, LNCaP and MCF-7) up-regulated ANRASSF1 endogenous expression is higher in breast and prostate tumor cell lines compared with non-tumor, and an opposite pattern is observed for RASSF1A. ANRASSF1 ectopic overexpression reduces RASSF1A abundance and increases the proliferation of HeLa cells, whereas ANRASSF1 silencing causes the opposite effects. These changes in ANRASSF1 levels do not affect the RASSF1C isoform abundance. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region. 23990798 2013 The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 gastric cancer C16 NA qPCR, RNAi etc. primary gastric cancer tissues, cell line (BGC823) up-regulated ANRIL was highly expressed in gastric cancer tissues of cisplatin-resistant and 5-fluorouracil (5-FU)-resistant patients, and the same upregulation trends were observed in cisplatin-resistant cells (BGC823/DDP) and 5-FU-resistant cells (BGC823/5-FU). In addition, BGC823/DDP and BGC823/5-FU cells transfected with ANRIL siRNA and treated with cisplatin or 5-FU, respectively, exhibited significant lower survival rate, decreased invasion capability, and high percentage of apoptotic tumor cells. The influence of ANRIL knockdown on MDR was assessed by measuring IC50 of BGC823/DDP and BGC823/5-FU cells to cisplatin and 5-FU, the result showed that silencing ANRIL decreased the IC50 values in gastric cancer cells. Moreover, qRT-PCR and western blotting revealed that ANRIL knockdown decreased the expression of MDR1 and MRP1, both of which are MDR related genes; regression analysis showed that the expression of ANRIL positively correlated with the expression of MDR1 and MRP1 27121324 2016 Silencing of long non-coding RNA ANRIL inhibits the development of multidrug resistance in gastric cancer cells AOC4P AOC4P, AOC4, UPAT 90586 ENSG00000260105 NA GRCh38_17:42865922-42874369 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RNA pull-down assay etc. HCC tissues, cell lines (J7 and SK-Hep1) down-regulated we identified a differentially expressed novel tumor suppressive lncRNA termed amine oxidase, copper containing 4, pseudogene (AOC4P). The level of AOC4P expression was significantly downregulated in 68% of HCC samples and negatively correlated with advanced clinical stage, capsule invasion and vessel invasion. Low AOC4P expression correlated with poor prognostic outcomes, serving as an independent prognostic factor for HCC. In vitro functional assays indicated that AOC4P overexpression significantly reduced cell proliferation, migration and invasion by inhibiting the epithelial-mesenchymal transition (EMT). 26160837 2015 Long non-coding RNA AOC4P suppresses hepatocellular carcinoma metastasis by enhancing vimentin degradation and inhibiting epithelial-mesenchymal transition AP000221.1 LOC105372753 NA ENSG00000229962 NA GRCh38_21:25515473-25518338 pancreatic cancer C25 NA microarray, qPCR etc. cell lines (SW1990, SWl990/GZ etc.) up-regulated Six lncRNAs (RP11-58D2.1, lincRNA-ZNF532, AP000221.1, CTC-338M12.5, CR619813, DDX6P) were selected to validate the microarray consistency by using qPCR. The results demonstrated that RP11-58D2.1, lincRNA-ZNF532 and AP000221.1 were upregulated and that CTC-338M12.5, DDX6P and CR619813 were downregulated in the SW1990/GZ cells compared with SW1990 cells. 25755691 2015 Genomic analysis of drug resistant pancreatic cancer cell line by combining long non-coding RNA and mRNA expression profling. ASHGA5P014130 ULK4P2, D-X, FAM7A1 89838 ENSG00000260128 NA GRCh38_15:30572738-30600647 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. ASHGA5P014632 AL589743.1, PCAN-2 NA ENSG00000244306 NA GRCh38_14:19284653-19337730 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. ASHGA5P018902 LRRC75A-AS1, C17orf45, C17orf76-AS1, FAM211A-AS1, NCRNA00188, TSAP19 125144 ENSG00000175061 NA GRCh38_17:16438822-16478678 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues down-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. ASHGA5P022276 NA NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. ASHGA5P028603 NA NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. ASHGA5P036884 HAR1B, HAR1R, LINC00065, NCRNA00065 NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. ASHGA5P039672 ANP32C, PP32R1 NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues down-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. ASHGA5P043753 LOC100133091 NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. ASHGA5P051732 TIPARP-AS1 100287227 ENSG00000243926 NR_027954 GRCh38_3:156671862-156674378 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. AX746718 NA NA NA NA NA malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). BACE1-AS BACE1-AS, BACE1-AS1, BACE1AS, NCRNA00177 100379571 ENSG00000278768 NR_037803 GRCh38_11:117290874-117293571 ovarian cancer C56.9 NA qPCR, Western blot, Northern blot, MTT assay etc. ovarian cancer stem cell up-regulated The mRNA expression levels of BACE1-AS were significantly increased in anisomycin-treated OCSCs compared to controls. In addition, mRNA and protein levels of BACE1 and AB1-42 were increased in anisomycin-treated OCSCs compared to controls. We confirmed that anisomycin suppressed the growth of xenograft tumors formed by OCSCs in vivo. Finally, when expression of lncRNA BACE1-AS was silenced using siRNA, BACE1 expression was downregulated and the antiproliferative and anti-invasive effects of anisomycin were reduced. 26783004 2016 Long non-coding RNA BACE1-AS is a novel target for anisomycin-mediated suppression of ovarian cancer stem cell proliferation and invasion. BC047917 TMEM179, C14orf90, TMEM179A NA NA NA GRCh38_14:104590865-104592156 renal cell carcinoma C64.9 NA microarray, qPCR etc. RCC tissues up-regulated From five paired samples we identified hundreds of significantly differentiated lncRNAs. Specifically, the most upregulated lncRNAs were: uc001vjj.1, ENST00000414223, BC047917, uc003erl.1, and uc009wkz.1, of which uc001vjj.1 was the highest. The most highly downregulated were: ENST00000507950, uc001aka.2, NR_026860, NR_024256, and BC070168, of which ENST00000507950 showed the largest downregulation. 24905231 2014 Expression pattern of long non-coding RNAs in renal cell carcinoma revealed by microarray. BC070168 TSPAN8, CO-029, TM4SF3 NA ENSG00000127324 NA GRCh38_12:71125085-71441898 renal cell carcinoma C64.9 NA microarray, qPCR etc. RCC tissues down-regulated From five paired samples we identified hundreds of significantly differentiated lncRNAs. Specifically, the most upregulated lncRNAs were: uc001vjj.1, ENST00000414223, BC047917, uc003erl.1, and uc009wkz.1, of which uc001vjj.1 was the highest. The most highly downregulated were: ENST00000507950, uc001aka.2, NR_026860, NR_024256, and BC070168, of which ENST00000507950 showed the largest downregulation. 24905231 2014 Expression pattern of long non-coding RNAs in renal cell carcinoma revealed by microarray. BC087858 NA NA NA NA NA non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Cell proliferation assay, Cell apoptosis assay etc. NSCLC tissues, cell lines (PC9, H1975, H460 and H23) up-regulated Over-expression was observed in NSCLC cells and patients with acquired resistance to EGFR-TKIs and significantly associated with a shorter progression-free survival (PFS) in tumors with respond to EGFR-TKIs. The significant relationship was not observed in patients with T790M mutation but in patients with non-T790M. Down-regulation of BC087858 could significantly promote PC9/R and PC9/G2 cells invasion. BC087858 knockdown restored gefitinib sensitivity in acquired resistant cells with non-T790M and inhibited the activation of the PI3K/AKT and MEK/ERK pathways and epithelial-mesenchymal transition (EMT) via up-regulating ZEB1 and Snail. 27409677 2016 Long non-coding RNA BC087858 induces non-T790M mutation acquired resistance to EGFR-TKIs by activating PI3K/AKT and MEK/ERK pathways and EMT in non-small-cell lung cancer. BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 glioma NA M9380/3 qPCR etc. cell lines (U251, U87) down-regulated MEG3 and ST7OT1 are up-regulated in both cell lines under apoptosis induced using both agents. The induction of GAS5 is only clearly detected during DOX-induced apoptosis, whereas the up-regulation of neat1 and MIR155HG is only found during RES-induced apoptosis in both cell lines. However, TUG1, BC200 and MIR155HG are down regulated when necrosis is induced using a high dose of DOX in both cell lines. 25645334 2015 Altered expression of long non-coding RNAs during genotoxic stress-induced cell death in human glioma cells BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 breast cancer C50 NA qPCR, ChIP etc. cell lines (MCF-7, T47D, MDA-MB-231) up-regulated In this study, we show that BC200 is upregulated in breast cancer; among breast tumor specimens there is a higher level of BC200 in estrogen receptor (ER) positive than in ER-negative tumors. Further experiments show that activation of estrogen signaling induces expression of BC200. 27277684 2016 Regulation of alternative splicing of Bcl-x by BC200 contributes to breast cancer pathogenesis. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA microarray, qPCR, RNAi etc. cell lines (ZR-75-1, MCF7, BCAR4 etc.) differential expression As BCAR4 expression in cell lines did not change the sensitivity to different chemotherapeutic agents, the increased sensitivity to lapatinib is not due to a general mechanism of drug resistance. Also in our BCAR4-expressing cell models, the combination of lapatinib and antioestrogens was more potent in inhibiting cell growth than lapatinib alone; indicating that blocking the ERBB2 pathway with lapatinib re-sensitises BCAR4-expressing cells to antioestrogens. BCAR4 expression strongly sensitised ZR-75-1 and MCF7 breast cancer cells to the combination of lapatinib and antioestrogens. 22892392 2012 BCAR4 induces antioestrogen resistance but sensitises breast cancer to lapatinib. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA qPCR etc. cell line (ZR-75-1) up-regulated Forced expression of BCAR4 in human ZR-75-1 and MCF7 breast cancer cells resulted in cell proliferation in the absence of estrogen and in the presence of various antiestrogens. Inhibition of estrogen receptor 1 (ESR1) expression with small interfering RNA (siRNA), implied that the BCAR4-induced mechanism of resistance is independent of ESR1. BCAR4 is a strong transforming gene causing estrogen-independent growth and antiestrogen resistance, and induces tumor formation in vivo. Due to its restricted expression, BCAR4 may be a good target for treating antiestrogen-resistant breast cancer. 21506106 2011 Characterization of BCAR4, a novel oncogene causing endocrine resistance in human breast cancer cells. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA qPCR, Western blot etc. cell lines (ZR-75-1, BCAR3, EGFR etc.) up-regulated Multivariate analyses established high BCAR4 mRNA levels as an independent predictive factor for poor PFS after start of tamoxifen therapy for recurrent disease. BCAR4 may have clinical relevance for tumour aggressiveness and tamoxifen resistance. Our cell model suggests that BCAR4-positive breast tumours are driven by ERBB2/ERBB3 signalling. Patients with such tumours may benefit from ERBB-targeted therapy. 20859285 2010 Relevance of BCAR4 in tamoxifen resistance and tumour aggressiveness of human breast cancer. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA qPCR etc. cell line (ZR-75-1) up-regulated We showed that ectopic expression of this gene, designated as breast cancer antiestrogen resistance 4 (BCAR4), caused OH-TAM resistance and anchorage-independent cell growth in ZR-75-1 cells and that the intact open reading frame was required for its function. We conclude that retroviral transfer of cDNA libraries into human breast cancer cells is an efficient method for identifying genes involved in tamoxifen resistance. 16778085 2006 Functional screen for genes responsible for tamoxifen resistance in human breast cancer cells. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA qPCR, Western blot, Cell proliferation assay etc. primary breast cancer tissues, cell lines (ZR-75-1,IPH-926 etc.) up-regulated Relative high BCAR4 mRNA expression was identified in IPH-926, a cell line derived from an endocrine-resistant lobular breast cancer. Moderate BCAR4 expression was evident in MDA-MB-134 and MDA-MB-453 breast cancer cells. BCAR4 protein was detected in breast cancer cells with ectopic (ZR-75-1-BCAR4) and endogenous (IPH-926, MDA-MB-453) BCAR4 mRNA expression. Knockdown of BCAR4 inhibited cell proliferation. 26317614 2015 Breast Cancer Anti-Estrogen Resistance 4 (BCAR4) Drives Proliferation of IPH-926 lobular Carcinoma Cells. BE244504 NA NA NA NA GRCh38_20:856476-856922 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) down-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. CAR10 ADAM12, ADAM12-OT1, CAR10, MCMP, MCMPMltna, MLTN, MLTNA 8038 ENSG00000148848 NA GRCh38_10:126012381-126388455 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated To identify lncRNAs that are critical to lung carcinogenesis, we selected three lncRNAs, CAR intergenic 10 (hereafter, CAR10), AK311218, and RP11-480I12.3, from the most up-regulated lncRNAs in the HPR NSCLCs (Table S3) and tested their expression by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The expression of these lncRNAs was consistent with the microarray analysis. 27322209 2016 Long non-coding RNA stabilizes the Y-box-binding protein 1 and regulates the epidermal growth factor receptor to promote lung carcinogenesis. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 glioma NA M9380/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, MTT assay etc. glioma tissues, cell lines (U251, U373, SNB19, U118, and LN229) down-regulated CASC2 expression was down-regulated in glioma tissues and cell lines. Exogenous CACS2 alone was sufficient to inhibit glioma cells' proliferation and amplified TMZ-induced repression of cell proliferation, while CACS2 knockdown could reverse this process. CASC2 up-regulates PTEN through direct inhibiting miR-181a and plays an important role in glioma sensitivity to TMZ and may serve as a potential target for cancer diagnosis and treatment. 28121023 2017 LncRNA CASC2 Interacts With miR-181a to Modulate Glioma Growth and Resistance to TMZ Through PTEN Pathway. CCAL NA NA NA NA NA colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues up-regulated We identified colorectal cancer-associated lncRNA (CCAL) as a key regulator of CRC progression. Patients whose tumours had high CCAL expression had a shorter overall survival and a worse response to adjuvant chemotherapy than patients whose tumours had low CCAL expression.Our results suggest that CCAL is a crucial oncogenic regulator involved in CRC tumorigenesis and progression. 25994219 2015 Long non-coding RNA CCAL regulates colorectal cancer progression by activating Wnt/B-Catenin signalling pathway via suppression of activator protein 2a. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues down-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. CES1P1-001 CES1P1, CES1A2, CES1A3, CES4, CESR, PCE-3 NA NA NA NA non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. CILA1 NA NA NA NA NA tongue squamous cell carcinoma C02 M8070/3 qPCR, Western blot etc. cell lines (CAL27, SCC9), TSCC tissues up-regulated lncRNA 1 (CILA1) was discovered by using microarrays and was functionally identified as a regulator of chemo-sensitivity in TSCC cells. Upregulation of CILA1 promotes EMT, invasiveness, and chemo-resistance in TSCC cells, whereas the inhibition of CILA1 expression induces mesenchymal-epithelial transition (MET) and chemo-sensitivity, and inhibits the invasiveness of cisplatin-resistant cells both in vitro and in vivo. We also found that CILA1 exerts its functions via the activation of the Wnt/B-catenin signaling pathway. High CILA1 expression levels and low levels of phosphorylated B-catenin were closely associated with cisplatin resistance and advanced disease stage, and were predictors of poor prognosis in TSCC patients. These findings provided a new biomarker for the chemo-sensitivity of TSCC tumors and a therapeutic target for TSCC treatment. 29699939 2018 Chemotherapy-Induced Long Non-coding RNA 1 Promotes Metastasis and Chemo-Resistance of TSCC via the Wnt/B-Catenin Signaling Pathway. CRALA NA NA NA NA NA breast cancer C50 NA qPCR etc. breast tissues up-regulated CRALA is upregulated in chemoresistant breast cancer cell lines compared to their parental lines. Silencing of CRALA in chemoresistant breast cancer cells resensitizes the cells to chemotherapy in vitro. Furthermore, univariate and multivariate analysis showed that higher CRALA expression was significantly associated with poor prognosis in 144 breast cancer patients. 28834648 2017 Long non-coding RNA CRALA is associated with poor response to chemotherapy in primary breast cancer CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 bladder cancer C67 NA qPCR, in vitro knockdown etc. cell lines (5637,T24), BC tissues up-regulated CRNDE was significantly increased in bladder cancer, and overexpressed expression of CRNDE was positively related with advanced TNM stage of bladder cancer patients. In addition, in vitro experiments showed that CRNDE strengthened cell migration/proliferation and inhibited cell apoptosis in bladder cancer.CRNDE can suppress E2F3 expression to increase miR-145 expression. 29710461 2018 Overexpression of CRNDE promotes the progression of bladder cancer. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, RIP lung adenocarcinoma tissues, cell lines (A549, H1299) up-regulated In our present study, we identified that CRNDE was significantly upregulated in LAD tissue and radio-resistant LAD cell lines. And high level of CRNDE expression was significantly correlated with poor differentiation, TNM stage and lymph node metastasis, radiotherapy response and high level of CRNDE expression had a significantly shorter overall survival. 28550688 2017 Long Noncoding RNA CRNDE/PRC2 Participated in the Radiotherapy Resistance of Human Lung Adenocarcinoma Through Targeting p21 Expression CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay, FISH, MTT assay etc. CRC tissues, cell lines (HCT116 and SW480) up-regulated The expression levels of the CRNDE were upregulated in CRC clinical tissue samples. Significantly, we found that the repression of cell proliferation, the reduction of chemoresistance, and the inhibition of Wnt/B-catenin signaling induced by CRNDE knockdown would require the increased expression of miR-181a-5p. 28086904 2017 The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/B-catenin signaling. ENST00000447565 Lnc-LIF-AS NA NA NA GRCh38_22:30239194-30240538 cervical cancer C53 NA qPCR, Western blot, Microarray hybridization etc. cervical tissues, cell lines (SiHa and ME-180) down-regulated ENST00000422259, ENST00000447565 (Lnc-LIF-AS) and ENST00000469965, together with their related antisense mRNA DPYD (dihydropyrimidine dehydrogenase, a pyrimidine catabolic pathway gene), LIF (leukemia inhibitor factor) and FLNC (filamin C) were all notably differentially expressed in both ΔNp63a overexpression cells and knockdown cells.An inverse interaction of LIF and ΔNp63a expression was as well validated in clinical samples of cervical cancer, and high level of LIF in cervical cancers was related with poor patient survival. 28391028 2017 LncRNA expression profile of ΔNp63a in cervical squamous cancers and its suppressive effects on LIF expression. ENST01108 NA NA NA NA NA glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (U251 and U87), glioma tissues up-regulated lncRNA ENST01108 (ENST01108) has oncogenic role in glioma. Clinical data suggest that ENST01108 is closely associated with the malignant status in glioma. In vitro experiment demonstrated that overexpression of ENST01108 promoted glioma cell proliferation, migration, invasion, EMT process and survival, while knockdown of ENST01108 has an opposite effect,indicating that ENST01108 serves as an oncogenic property in glioma carcinogenesis.Further, we identified miR-489 as a direct target of ENST01108 and ENST01108 negatively regulate miR-489 by act as a sponge. SIK1 is verified as the direct target of miR-489 and it is negatively regulated by miR-489. ENST01108 also positively regulate SIKI and it promotes SIKI expression by suppressing miR-489. Taken together, the reciprocal repression of ENST011081 and miR-489 may be served as potential targets for cancer therapeutics in glioma. 29421578 2018 Long non-coding RNA ENST01108 promotes carcinogenesis of glioma by acting as a molecular sponge to modulate miR-489. FTH1P3 FTH1P3,FTHL3,FTHL3P NA ENSG00000213453 NA GRCh38_2:27392784-27393367 breast cancer C50 NA qPCR,Flow cytometry assay,Western blot,Luciferase reporter assay,etc. Human breast cancer cell lines (MCF-7,MDA-MB-231,MDA-MB-468,MDA-MB-453) and normal human breast epithelial cell (MCF-10A) were purchased from ATCC (Manassas,VA,USA). breast cancer tumorous tissue. up-regulated Bioinformatics tools and luciferase reporter assay validated that,FTH1P3 promoted ABCB1 protein expression through targeting miR-206,acting as,a miRNA sponge. In summary,our results reveal the potential regulatory mechanism ,of FTH1P3 on breast cancer paclitaxel resistance through miR-206/ABCB1,providing a novel insight for the breast cancer chemoresistance. However,the occurrence of chemoresistance causes the poor prognosis,high recurrence rate and low 5-year survival rate.In the present study,we investigate the role of lncRNA FTH1P3 in breast cancer paclitaxel resistance and explore the underlying mechanism for the drug resistance generation. 29971911 2018 Long non-coding RNA FTH1P3 activates paclitaxel resistance in breast cancer through miR-206/ABCB1. FTX FTX, LINC00182, MIR374AHG, NCRNA00182 100302692 ENSG00000230590 NR_028379 GRCh38_X:73946555-74293574 acute myeloid leukemia NA M9861/3 Microarray, qPCR, Western blot, Flow cytometry assay, RIP, etc. AML cell lines(U937, THP-1). up-regulated The observation suggested that high-mannose N-glycans and mannosyltransferase ALG3 affected drug-resistance in AML cells. FTX/miR-342/ALG3 axis could potentially be used for the targets to overcome therapeutic resistance in AML. Functionally, we found that FTX directly interacted with miR-342 to regulate ALG3 expression and function, including ADR-resistant cell growth and apoptosis. Kaplan–Meier overall survival curves (OS) was observed based on ALG3 level. Data were the means±SD of triplicate determinants (*p < 0.05). 29880818 2018 Aberrant mannosylation profile and FTX/miR-342/ALG3-axis contribute to development of drug resistance in acute myeloid leukemia. GAPLINC GAPLINC, LINC01540 100505592 ENSG00000266835 NR_110429 GRCh38_18:3466250-3478978 colorectal cancer C19.9 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell line (HCT116), CRC tissue up-regulated GAPLINC expression was obviously increased in CRC tissues.In HCT116, silencing of GAPLINC weakened cell migration and invasion, while overexpression of GAPLINC significantly promoted cell migration and invasion. Through dual-luciferase, RNA pull-down, and Transwell assays, we verified that miR-34a was the downstream molecule of GAPLINC and that miR-34a negatively regulated the migration and invasion of HCT116 cell.Furthermore, we found that GAPLINC positively regulated the miR-34a target gene c-MET in CRC tissues. 29427222 2017 Long Noncoding RNA GAPLINC Promotes Cells Migration and Invasion in Colorectal Cancer Cell by Regulating miR-34a/c-MET Signal Pathway. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 prostate cancer C61.9 NA qPCR, RNAi etc. cell lines (22Rv1, PC-3 etc.) up-regulated GAS5 promotes the apoptosis of prostate 34 cells, and exonic sequence, i.e. GAS5 lncRNA, is sufficient to mediate this activity. Abnormally low levels of 35 GAS5 expressionmay therefore reduce the effectiveness of chemotherapeutic agents. 23676682 2013 Long non-coding RNA GAS5 regulates apoptosis in prostate cancer cell lines. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA Microarray, qPCR, Western blot, RIP, luciferase reporter assay, Flow cytometry assay, etc. human breast cancer cell line (MCF-7, MCF-7R). breast cancer tissues. down-regulation Collectively, our study demonstrates that GAS5 enhances the efficacy of tamoxifen in the treatment of breast cancer and could be a novel prognostic biomarker. Tamoxifen is a frequently used drug for hormonal therapy in patients with breast cancer, however, development of resistance to tamoxifen remains a serious clinical problem.Kaplan-Meier survival analysis was used to analyze the relationship between the expression of GAS5 and survival rate. P < 0.05 indicates a significant difference. Moreover, GAS5 increased sensitivity of breast cancer cells to tamoxifen by serving as a molecular sponge for miR-222, contributing to suppression of phosphatase and tensin homologs (PTEN) (one endogenous target of miR-222). 29969658 2018 Downregulation of lncRNA GAS5 confers tamoxifen resistance by activating miR-222 in breast cancer. GHET1 GHET1, lncRNA-GHET1 102723099 ENSG00000281189 NR_130107 GRCh38_7:148987527-148989432 gastric cancer C16 NA qPCR, Western blot etc. gastric carcinoma tissues, cell lines (BGC823 and SGC7901) up-regulated Highly expressing GHET1 promoted the development of MDR which was related to the Bax, Bcl-2, MDR1 and MRP1 genes expression in gastric cancer cells. In the BGC823 and SGC7901 cell, overexpression of GHET1 downregulated Bax expression and upregulated Bcl-2, MDRA and MRP1 expression, which resulted in increasing cisplatin resistance and inhibiting cell apoptosis. In the BGC823/DPP and SGC7901/DDP cell, knockdown of GHET1 leaded to increase cisplatin sensitivity and promote cell apoptosis. In the present study, we examined the GHET1 expression level in gastric carcinoma tissues of cisplatin sensitive patients and drug-resistant patients, as well as the MDR gastric cancer cell lines and their chemo-sensitive parental line. We also identified the function of GHET1 in cisplatin resistant strains (BGC823/DPP and SGC7901/ DDP cells) and their parental line (BGC823 and SGC7901 cells) using gain-of-function and loss-of-function approaches in vitro. 28578256 2017 Overexpression of long non-coding RNA GHET1 promotes the development of multidrug resistance in gastric cancer cells. GRP78 NA 3309 ENSG00000044574 NA GRCh38_9:125234853-125241330 prostate cancer C61.9 NA qPCR etc. cell line (PC3PCA+ ) up-regulated Three proteins were found down-regulated and 7 proteins up-regulated in PC3PCA+ cells compared to PC3NC cells,including GRP78.Higher GRP78 was also found in PCa clinical specimens.This study confirmed that in PCa, PCA3 plays a pro-cancer role through promoting cell proliferation, migration and invasion while inhibiting cell apoptosis. This process might involve the up-regulation of GRP78.GRP78 was also reported to be preferentially expressed in the camptothecin (CPT)- resistant PC3 prostate cancer cell line in comparison to the CPT-sensitive LNCaP prostate cancer cell line, which indicated its involvement in chemotherapy resistant in PCa. 28739722 2017 GRP78 Participates in PCA3-regulated Prostate Cancer Progression. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. LUAD tissues, cell lines (A549, A549/DDP) up-regulated In our study, the expression of H19 in cisplatin-resistant A549/DDP cells was unregulated. Knockdown of H19 restored the response of A549/DDP cells to cisplatin. H19-mediated chemosensitivity enhancement was associated with metastasis, induction of G0/G1 cell-cycle arrest, cell proliferation, and increased apoptosis. Furthermore, lncRNA H19 expression was significantly related to TNM stage and metastasis. Overexpression of H19 was negatively correlated with cisplatin-based chemotherapy response in patients. 27911863 2017 Correlation of long non-coding RNA H19 expression with cisplatin-resistance and clinical outcome in lung adenocarcinoma. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tumor tissue, cell line (A549) up-regulated H19 and miR-21 expression was measured in tumor tissues and corresponding non-tumor lung tissues from 200 patients by quantitative reverse transcription polymerase chain reaction. Expression of both H19 and miR-21 was significantly higher in lung tissues from patients with NSCLC than in normal lung tissues. Increased expression of H19 and miR-21 was positively correlated with advanced tumor-node-metastasis stage and tumor size. miR-21 expression was highest in stage I and II NSCLC, whereas H19 expression was highest in stage III and IV NSCLC. The results show that H19 may mainly contributes to the progression of NSCLC, and its expression levels can reflect the invasive and metastatic status to some extent. New H19 and miR-targeting anticancer drugs will soon enter the clinical stage of development and ultimately become available for the treatment of patients with lung cancer. 28799568 2017 Association of long non-coding RNA H19 and microRNA-21 expression with the biological features and prognosis of non-small cell lung cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, Western blot, RIP, ChIP etc. cell lines (MCF-7, ZR-75-1) up-regulated In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERa-positive breast cancer cells, but not in ERa-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. 27845892 2016 LncRNA H19 confers chemoresistance in ERa-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, e luciferase reporter assay, etc. Human HCC cell lines (ie, Bel-7402, HepG2, Hep3b, QGY7703, SMMC-7721). HCC tissues. up-regulated In conclusion, the miR-193a-3p targeted by lncRNA H19 tended to master the chemo- and radio- resistances of HCC by modulation of PSEN1, which might assist in supplying novel biomarkers to improve the treatment efficacy for HCC for that chemo- and radio-resistances themselves could make the efficacies be poor. The following drugs were taken into application, including docetaxel (DT) (Sanofi-Aventis, Paris, France), paclitaxel (Pt) (Taijipharmaceutical Co. Xi'an, China), vinorelbine (Vb) (Pierre Fabre, Castres, France), and 5-fluorouracil (5-Fu) (Macklin, Shanghai, China). The restrained lncRNA H19 and over-expressed miR-193a-3p expressions tended to significantly elevate the survival rate and proliferation of Bel-7402 cells, when they were exposed to radiation and subject to chemo-therapies. PSEN1 appeared to be subject to the modification of lncRNA H19 and miR-193a-3p in its acting on the survival rates and proliferative abilities of HCC cells. The lncRNA H19/miR-193a-3p/PSEN1 axis could be regarded as the treatment targets for HCC, so as to further improve the treatment efficacy of chemo- and radio-therapies for HCC. 29968942 2018 The LncRNA H19/miR-193a-3p axis modifies the radio-resistance and chemotherapeutic tolerance of hepatocellular carcinoma cells by targeting PSEN1. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, etc. breast cancer cell line, breast cancer tumor tissues. down-regulation Our results suggest that the combined let-7a and H19 signature is a novel prognostic factor for breast cancer patients treated with neoadjuvant chemotherapy.H19 is associated with drug-resistance in breast cancer cells.Univariate and multivariate survival analyses were conducted using the Cox proportional hazards regression method. As determined using X-tile, the optimal cutoff value for the risk score to assess progression-free survival (PFS) based on the combined signature was -0.1. Several miRNAs and lncRNAs, including let-7a and H19, provide prognostic information for many cancers. 29963109 2018 Combined Let-7a and H19 Signature: A Prognostic Index of Progression-Free Survival in Primary Breast Cancer Patients. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 prostate cancer C61.9 NA qPCR, RIP, ChIP, RNA pull-down assay etc. prostate cancer tissues up-regulated Here, we report HOTAIR as an androgen-repressed lncRNA, and, as such, it is markedly upregulated following androgen deprivation therapies and in CRPC. Functionally, HOTAIR overexpression increases, whereas HOTAIR knockdown decreases, prostate cancer cell growth and invasion. Taken together, our results provide compelling evidence of lncRNAs as drivers of androgen-independent AR activity and CRPC progression, and they support the potential of lncRNAs as therapeutic targets. 26411689 2015 LncRNA HOTAIR Enhances the Androgen-Receptor-Mediated Transcriptional Program and Drives Castration-Resistant Prostate Cancer HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 head and neck squamous cell carcinoma C76.0 M8070/3 in vitro knockdown, Luciferase reporter assay, qPCR,Western blot, RNA-seq etc. cell lines (SCC25, Cal27,UM-SCC1,SCC15, Tscca, Tca8113,Hep-2,Tb3.1), HNSCC tumor tissues up-regulated STAT3 inhibition with WP1066 decreased HOTAIR level and sensitized HNSCC to cisplatin or cetuximab. STAT3 promoted HOTAIR transcription and its interaction with pEZH2-S21, resulting in enhanced growth of HNSCC cells.STAT3 signaling promotes HNSCC progression via regulating HOTAIR and pEZH2-S21 in HNSCC with PI3K overexpression/activation. 29540490 2018 STAT3/HOTAIR Signaling Axis Regulates HNSCC Growth in an EZH2-dependent Manner. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 esophageal squamous cell cancer NA NA qPCR, MTT assay etc. ESCC tissues, cell lines (KYSE30, KYSE70, KYSE150, KYSE450, KYSE510, and TE10) up-regulated Three lncRNAs (AFAP1-AS1, UCA1, HOTAIR) were found to be deregulated in cisplatin-resistant cells compared with their parent cells. AFAP1-AS1 was significantly up-regulated in tumor tissues compared with adjacent normal tissues. Furthermore, overexpression of AFAP1-AS1 was closely associated with lymph node metastasis, distant metastasis, advanced clinical stage, and response to dCRT. 26756568 2016 High expression of long non-coding RNA AFAP1-AS1 predicts chemoradioresistance and poor prognosis in patients with esophageal squamous cell carcinoma treated with definitive chemoradiotherapy. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, RNAi, Luciferase reporter assay cell lines (MCF-7, MDA-MB-231 and SKBR3) differential expression Treatment of mice harboring platinum-resistant ovarian tumor xenografts with pHLIP-PNA constructs suppressed HOTAIR activity, reduced tumor formation and improved survival. 28420874 2017 Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. cell lines (MCF7, T47D, ZR-751, MDA-MB-453 and MDA-MB-468) up-regulated HOTAIR expression is negatively regulated by oestrogen, positively regulated by FOXA1 and FOXM1, and is inversely correlated with oestrogen receptor and directly correlated with FOXM1 in breast tumours. The combination of HOTAIR and FOXM1 enables greater discrimination of endocrine therapy responders and non-responders in patients with oestrogen receptor positive breast cancer. Consistent with this, HOTAIR expression is increased in cell-line models of endocrine resistance. 27378691 2016 Long-range regulators of the lncRNA HOTAIR enhance its prognostic potential in breast cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi etc. HCC tissues, cell lines (SMMC-7721, HepG2, Hep3B etc.) up-regulated The expression level of HOTAIR in cancer tissues was higher than in adjacent noncancerous tissues. High expression level of HOTAIR was an independent prognostic factor for predicting HCC recurrence in LT patients. Furthermore, in patients exceeding the Milan criteria, those with a high expression level of HOTAIR revealed a significantly shorter recurrence-free survival. 21327457 2011 Overexpression of long non-coding RNA HOTAIR predicts tumor recurrence in hepatocellular carcinoma patients following liver transplantation. HOTAIRM1 HOTAIRM1, HOXA-AS1, HOXA1-AS1, NCRNA00179 100506311 ENSG00000233429 NA GRCh38_7:27095647-27100265 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 10984 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 lung adenocarcinoma C34 M8140/3 qPCR, Western blot etc. LAD tissues, cell line (A549) up-regulated the expression of KCNQ1OT1 was confrmed to be highly expressed in LAD tissues and cells contrast to control tissues and cells, and high KCNQ1OT1 expression correlated to malignant behaviors of LAD, including big tumor size, poor differentiation, positive lymphatic metastasis and high TNM stages. The transfection of si-KCNQ1OT1 could effectually knockdown the expression of KCNQ1OT1 in A549 and A549/PA cells. 28600629 2017 Knockdown of long non-coding RNA KCNQ1OT1 depressed chemoresistance to paclitaxel in lung adenocarcinoma. KCNQ1OT1 KCNQ1OT1,KCNQ1-AS2,KCNQ10T1,Kncq1,KvDMR1,KvLQT1-AS,LIT1,NCRNA00012 10984 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 hypopharyngeal squamous cell carcinoma C13 M8070/3 Microarray,qPCR,Western blot,Cell proliferation assay,Luciferase reporter assay,RIP,etc. TSCC samples and cell lines(CAL27,SCC9),normal tissues,chemo-sensitive samples and chemo-insensitive TSCC tissues. up-regulated Finally, miR-211-5p inhibition in sh-KCNQ1OT1-expressing TSCC cells rescued the suppressed cell proliferation and cisplatin resistance induced by KCNQ1OT1 knockdown. In summary, our study has elucidated the role of the oncogenic lncRNA KCNQ1OT1 in TSCC growth and chemo-resistance, which may serve as a new target for TSCC therapy.he stable cisplatin-resistant cell lines, CAL27-res and SCC9-res, were established by the selection of CAL27 or SCC9 colonies treated with 10?7 to 10?5?M cisplatin (Sigma, Carlsbad, CA, USA) as described previously.Kaplan-Meier survival analysis indicated that increased KCNQ1OT1 expression in TSCC tissues was significantly associated with a lower rate of overall survival (p?5 cm. Additionally, the knockdown of 91H expression inhibited osteosarcoma cells' proliferation and promoted their apoptosis in vitro. 27555785 2016 Clinical implication of long noncoding RNA 91H expression profile in osteosarcoma patients. AC007271.3 ENST00000428188 NA ENSG00000226925 NA GRCh38_2:102172621-102182108 oral squamous cell carcinoma C06.9 M8070/3 qPCR etc. oral squamous cell carcinomatissues, cell lines (SCC9, SCC15, and SCC25) up-regulated A total of 691 lncRNAs (433 upregulated and 258 downregulated) were differentially expressed in OSCC tissues compared with normal controls (p< 0.05). Based on Gene Ontology and pathway analysis, we selected four differentially expressed lncRNAs (AC007271.3, AC007182.6, LOC283481, and RP11-893F2.9), and showed that aberrant AC007271.3 levels in OSCC patients were significantly associated with clinical stage, especially in early-stage disease, in an expanded case-control study. The combination of AC007271.3 and SCCA (AUC=0.902, p< 0.001) showed significantly better ability to discriminate between OSCC and controls compared with SCCA or AC007271.3 alone. Serum AC007271.3, SCCA, and TSGF levels could also discriminate between OSCC and normal controls with sensitivities of 77.6%, 55.0%, and 63.3%, and specificities of 84.5%, 93.3%, and 66.7%, respectively. These results suggest that AC007271.3, SCCA, and TSGF could be novel circulating biomarkers for the determination of OSCC. 29763905 2018 SCCA, TSGF, and the Long Non-Coding RNA AC007271.3 are Effective Biomarkers for Diagnosing Oral Squamous Cell Carcinoma. AC012065.7 NA NA ENSG00000279307 NA GRCh38_2:20529467-20529976 chronic lymphocytic leukemia NA M9823/3 qPCR, etc. CLL peripheral blood mononuclear cells, CLL cell lines (HG3, MEC2), Burkitt lymphoma B cell line (RAMOS) differential expression Finally, two novel lncRNAs (hypermethylated CRNDE and hypomethylated AC012065.7) were validated in an independent CLL sample cohort (48 samples) compared with 6 normal sorted B cell samples using quantitative pyrosequencing analysis.The methylation levels showed an inverse correlation to gene expression levels analyzed by real-time quantitative PCR. Notably, survival analysis revealed that hypermethylation of CRNDE and hypomethylation of AC012065.8 correlated with an inferior outcome 27777635 2016 Global DNA methylation profiling reveals new insights into epigenetically deregulated protein coding and long noncoding RNAs in CLL AK001091 PQLC3, C2orf22, MGC33602 NA ENSG00000162976 NA GRCh38_2:11155372-11178874 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated The expression levels of AK001091 and AK024171 in gastric cancerous tissues were lower than those in non-cancerous gastric tissues, while the expression levels of AK093735, BC003519 and NR_003573 in gastric cancerous tissues were higher than those in non-cancerous gastric tissues. These results were consistent with those shown in the expression microarray data sets. 27460075 2016 Identification of a five-lncRNA signature for the diagnosis and prognosis of gastric cancer. AK024171 NA NA NA NA GRCh38_5:81400786-81403288 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated The expression levels of AK001091 and AK024171 in gastric cancerous tissues were lower than those in non-cancerous gastric tissues, while the expression levels of AK093735, BC003519 and NR_003573 in gastric cancerous tissues were higher than those in non-cancerous gastric tissues. These results were consistent with those shown in the expression microarray data sets. 27460075 2016 Identification of a five-lncRNA signature for the diagnosis and prognosis of gastric cancer. AK093735 CEP83, CCDC41, NPHP18, NY-REN-58 51134 ENSG00000173588 NA GRCh38_12:94306449-94459988 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues up-regulated The expression levels of AK001091 and AK024171 in gastric cancerous tissues were lower than those in non-cancerous gastric tissues, while the expression levels of AK093735, BC003519 and NR_003573 in gastric cancerous tissues were higher than those in non-cancerous gastric tissues. These results were consistent with those shown in the expression microarray data sets. 27460075 2016 Identification of a five-lncRNA signature for the diagnosis and prognosis of gastric cancer. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 oral cancer C06.9 NA qPCR,Luciferase reporter assay, in vitro knockdown etc. cell lines (HB56, HB96, TSCC, Tca8113, SCC-9 and CAL27,HIOEC，HEK-293T),oral cancer tissues up-regulated ANRIL showed significantly higher, while miR-125a showed lower, expression in OC tissues and sera than in normal controls. MTT, colony formation, flow cytometry analysis, wound-healing, transwell and mice xenograft model assays were used to detect the proliferation, migration, and invasion of ARNIL-overexpressing HB56 cells and ARNIL-knockdown CAL27 cells. The results showed that cell proliferation, migration, and invasion were significantly increased by ARNIL overexpression and decreased by ARNIL silencing in oral cancer cells. Furthermore, we found a negative correlation between ARNIL and miR-125a, and ARNIL acts as a miRNA-sponge by directly interacting with miR-125a. 29635126 2018 The role of long non-coding RNA ANRIL in the carcinogenesis of oral cancer by targeting miR-125a. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 breast cancer C50 NA microarray, qPCR etc. plasma, breast cancer tissues up-regulated Expression level of these 3 lncRNAs was determined in plasma samples of 60 patients with BC and 40 healthy individuals by performing real-time PCR. As expected, the relative expression of ANRIL, HIF1A-AS2, and UCA1 was significantly higher in patients with TNBC than in patients with NTNBC, which was consistent with the results of microarray analysis. 28248879 2017 A three-long noncoding RNA signature as a diagnostic biomarker for differentiating between triple-negative and non-triple-negative breast cancers. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 non small cell lung cancer C34 M8046/3 qPCR etc. non-small cell lung cancer tissues up-regulated We assessed the expressions of the 12 lncRNAs in 92 serum samplesand identified two lncRNAs [SOX2OT and ANRIL] that were overexpressed in tumor serum samples compared with healthy controls. Kaplan-Meier analysis demonstrated that low expressions of SOX3OT and ANRIL were both associated with higher OS rate (P = 0.008 and 0.017, respectively), and SOX2OT could be used as an independent prognostic factor (P = 0.036). 29504701 2018 Circulating long noncoding RNA act as potential novel biomarkers for diagnosis and prognosis of non-small cell lung cancer. AOC4P AOC4P, AOC4, UPAT 90586 ENSG00000260105 NA GRCh38_17:42865922-42874369 gastric cancer C16 NA microarray, qPCR etc. plasma, gastric cancer tissues, cell lines (SGC-7901 and BGC-823) up-regulated Five (TINCR, CCAT2, AOC4P, BANCR and LINC00857) were significantly upregulated in plasma, tumor tissues and GC cell lines. 28042329 2017 Genome-Wide lncRNA Microarray Profiling Identifies Novel Circulating lncRNAs for Detection of Gastric Cancer. ASBEL NA 110806272 ENSG00000280594 NR_149073 GRCh38_21:17611744-17633199 breast cancer C50 NA qPCR, Western blot etc. breast cancer tissues, cell lines (MDA-MB-231) down-regulated LncRNA ASBEL has been identified as an anti-sense transcript of BTG3 (B cell translocation gene 3) gene, which encodes an anti-proliferation protein. Remarkable down-regulation of BTG3 has been reported in triple-negative breast cancer (TNBC). In the present study, a number of single-stranded modified anti-sense DNA oligonucleotides (antago) were designed, synthesized and screened for specific lncRNA ASBEL knockdown. We showed here that anti-ASBEL antago played a significant tumor suppressive role in TNBC by effective down-regulation of lncRNA ASBEL, which in turn led to increased BTG3 expression. The obtained data suggest lncRNA ASBEL as a novel therapeutic target in TNBC. antago3 has a great potential to be an useful therapeutic tool for TNBC treatment through targeting lncRNA ASBEL-related pathway. 28552529 2017 Targeting long non-coding RNA ASBEL with oligonucleotide antagonist for breast cancer therapy BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues up-regulated The expression of all 18 candidate lncRNAs was evaluated by RT-qPCR, using 80 pairs of CRC and control tissue samples. Among these, eight lncRNAs (MALAT-1, NR_029373, NR_046321, NR_034119, GAS5, BANCR, NR_026817 and PCAT-1) were found significantly dysregulated in CRC tumor tissues compared with controls. 27591862 2016 Identification of long noncoding RNAs as potential novel diagnosis and prognosis biomarkers in colorectal cancer. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 gastric cancer C16 NA microarray, qPCR etc. plasma, gastric cancer tissues, cell lines (SGC-7901 and BGC-823) up-regulated Five (TINCR, CCAT2, AOC4P, BANCR and LINC00857) were significantly upregulated in plasma, tumor tissues and GC cell lines. 28042329 2017 Genome-Wide lncRNA Microarray Profiling Identifies Novel Circulating lncRNAs for Detection of Gastric Cancer. BC003519 NA NA NA NA GRCh38_10:95873044-95875952 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues up-regulated The expression levels of AK001091 and AK024171 in gastric cancerous tissues were lower than those in non-cancerous gastric tissues, while the expression levels of AK093735, BC003519 and NR_003573 in gastric cancerous tissues were higher than those in non-cancerous gastric tissues. These results were consistent with those shown in the expression microarray data sets. 27460075 2016 Identification of a five-lncRNA signature for the diagnosis and prognosis of gastric cancer. BLACAT1 BLACAT1, LINC00912, UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 papillary thyroid cancer NA M8260/3 qPCR etc. PTC tissues down-regulated BLACAT1 could act as a possible suppressor gene in PTC and may serve as a potential biomarker for prognosis prediction of PTC. BLACAT1 expression was associated with LNM andgender 29599647 2018 Prognostic value of long non-coding RNA BLACAT1 in patients with papillary thyroid carcinoma. BLACAT1 BLACAT1, LINC00912, UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 colorectal cancer C19.9 NA qPCR colorectal cancer tissues, serum, cell lines (SW480, HT-29 and LS 174T) up-regulated The expression tendency of the five up-regulated lncRNAs (UCA1, CRNDE, H19, ZFAS1 and BLACAT1) and two down-regulated lncRNAs (DPP10-AS1 and HAGLR) were same as the results of microarray data 28406230 2017 Meta-signature LncRNAs serve as novel biomarkers for colorectal cancer: integrated bioinformatics analysis, experimental validation and diagnostic evaluation BORG NA NA NA NA NA breast cancer C50 NA qPCR etc. cell lines (D2.OR, D2.A1, 67NR, 4T07, 4T1) up-regulated Through in silico and biological analyses, we identifed a novel lncRNA, BMP/OP-Responsive Gene (BORG), whose expression directly correlates with aggressive breast cancer phenotypes, as well as with metastatic competence and disease recurrence in multiple clinical cohorts. Mechanistically, BORG elicits the metastatic outgrowth of latent breast cancer cells by promoting the localization and transcriptional repressive activity of TRIM28, which binds BORG and induces substantial alterations in carcinoma proliferation and survival. Moreover, inhibiting BORG expression in metastatic breast cancer cells impedes their metastatic colonization of the lungs of mice, implying that BORG acts as a novel driver of the genetic and epigenetic alterations that underlie the acquisition of metastatic and recurrent phenotypes by breast cancer cells. 28983112 2017 The lncRNA BORG Drives Breast Cancer Metastasis and Disease Recurrence CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 multiple myeloma C42.1 M9732/3 qPCR, Luciferase reporter assay, Western blot cell lines (RPMI-8226, U266, MM.1S, KM3 and H929) up-regulated the relative expression levels of CCAT1 were significantly upregulated in MM tissues and cell lines compared with healthy donors and normal plasma cells (nPCs). High expression of CCAT1 was correlated shorter overall survival of MM patients. CCAT1 knockdown significantly inhibited cell proliferation, induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis in vitro, and suppressed tumor growth in vivo. MiR-181a-5p was a direct target of CCAT1, and repression of miR-181a-5p could rescue the inhibition of CCAT1 knockdown on MM progression. In addition,CCAT1 positively regulated HOXA1 expression through sponging miR-181a-5p in MM cells. lncRNA CCAT1 exerted an oncogenic role in MM by acting as a ceRNA of miR-181a-5p. These results suggest that CCAT1 may serve as a novel diagnostic marker and therapeutic target for MM. 29228867 2017 Long non-coding RNA CCAT1 promotes multiple myeloma progression by acting as a molecular sponge of miR-181a-5p to modulate HOXA1 expression. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 prostate cancer C61.9 NA qPCR etc. blood, tissues up-regulated Our study employs Whole Genome DNA Sequence (WGS) data from tumor samples (n = 103) to comprehensively assess the role of the Knudson two hit genetic model in SCNA generation in prostate cancer. PCDH18 methylation is predictive of biochemical recurrence a 28945760 2017 Appraising the relevance of DNA copy number loss and gain in prostate cancer using whole genome DNA sequence data CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 colon cancer C18 NA qPCR, ISH etc. colonic adenoma-carcinoma tissues up-regulated CCAT1 is up-regulated across the colon adenoma-carcinoma sequence. This up-regulation is evident in pre-malignant conditions and through all disease stages, including advanced metastatic disease suggesting a role in both tumorigenesis and the metastatic process. 23594791 2015 Differential expression of colon cancer associated transcript1 (CCAT1) along the colonic adenoma-carcinoma sequence. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 colorectal cancer C19.9 NA qPCR etc. CRC tissues down-regulated we found that the levels of HOTAIR and CCAT1 were significantly higher in plasma of CRC patients than that of the healthy control. Moreover, the levels of lincRNA-p21 were obviously decreased in plasma of CRC patients as compared to those of healthy control. There was highly correlated for CCAT1, HOTAIR and lincRNA-p21 in plasma and serum. By receiver operating characteristic curve (ROC) analysis, plasma CCAT1 provided the higher diagnostic performance for detection of CRC. Moreover, CCAT1 combining with HOTAIR could provide a more effective diagnosis performance. Most importantly, this combination was effective to detect CRC at an early stage (85%). In conclusion, our results demonstrated that increased plasma HOTAIR and CCAT1 could be used as a predictive biomarker for CRC screening, and that combination of HOTAIR and CCAT1 had a higher positive diagnostic rate of CRC than HOTAIR or CCAT1 alone 26823726 2016 Combined identification of long non-coding RNA CCAT1 and HOTAIR in serum as an effective screening for colorectal carcinoma CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 breast cancer C50 NA qPCR, RNAi, Western blot etc. breast cancer tissues, cell lines (MDA-MB-231, MCF-7) up-regulated We first confirmed the high expression level of CCAT2 in breast cancer tissues and breast cancer cell lines by reverse transcription quantitative polymerase chain reaction (RT-qPCR) assay, and we further analyzed the relationship between CCAT2 expression and clinical prognostic factors. Also, the biological function of CCAT2 was explored and the results showed silencing of CCAT2 could suppress cell growth in vitro and tumor formation in vivo. Finally, our results revealed that the abnormal expression of CCAT2 could influence the Wnt signaling pathway. 26442763 2015 Long noncoding RNA CCAT2 promotes breast tumor growth by regulating the Wnt signaling pathway CFLAR-AS1 CFLAR-AS1, ALS2CR10 65072 ENSG00000226312 NR_040030 GRCh38_2:201140278-201157823 esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues up-regulated Further validation in a larger cohort including 205 ESCC patients, 82 patients suffering from esophagus dysplasia and 210 healthy controls confirmed that increased Linc00152, CFLAR-AS1 and POU3F3 might be potential biomarkers for predicting the early progress. We also revealed that circulating levels of three lncRNAs were associated with poor post-surgery prognosis of ESCC patients. 27855375 2016 Three Circulating LncRNA Predict Early Progress of Esophageal Squamous Cell Carcinoma. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 gastric cancer C16 NA qPCR, Western blot gastric cancer tissue, cell lines (MGC-803, MNK-45, SGC-7901, HGC-27, GES) up-regulated expression of CRNDE was higher in GC tissues and cells compared with the normal gastric tissue and normal gastric cell lines. High expression of CRNDE was correlated with invasion depth , TNM stage and lymph node metastasis. Furthermore, high CRNDE expression was associated with shorter overall survival of GC patients. high CRNDE expression was a significant independent predictor of poor survival in GC.knockdown of CRNDE inhibited cell proliferation, migration and invasion of GC.CRNDE exerted its oncogenic role by affecting PI3K/AKT signaling pathways. 29243780 2017 Long non-coding RNA CRNDE is a novel tumor promoter by modulating PI3K/AKT signal pathways in human gastric cancer. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 hepatocellular carcinoma C22.0 M8170/3 qPCR hepatocarcinoma tissues, cell lines (LM3, SMMC-7721, Mhepatocarcinoma97H and Mhepatocarcinoma97L, L-02) up-regulated The results indicated that the expression levels of both lncRNA CRNDE and LINC01419 in HCC patients group were obviously higher than that in healthy. It was found that CRNDE had high sensitivity and specificity in the diagnosis of HCC.The high expression of lncRNA CRNDE and GBAP1 suggested a poor prognosis. 29221168 2017 Diagnosis, prognosis and bioinformatics analysis of lncRNAs in hepatocellular carcinoma. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 colorectal cancer C19.9 NA qPCR, Western blot etc. serum, cell lines (HCT116, SW480 SW620, HT-29 and LoVo) up-regulated The increased expression of exosomal CRNDE-h was successfully validated in 148 CRC patients when compared with colorectal benign disease patients and healthy donors. Exosomal CRNDE-h level significantly correlated with CRC regional lymph node metastasis and distant metastasis. 27888803 2016 Exosomal long noncoding RNA CRNDE-h as a novel serum-based biomarker for diagnosis and prognosis of colorectal cancer. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 colorectal cancer C19.9 NA qPCR, Western blot etc. CRC tissues, cell lines (NCM460, HT-29, SW480, HCT-116, SW620, LoVo, SW48, DLD-1, Caco2 and HT-15) up-regulated high CRNDE-p and low miR-217 levels in exosomes released from CRC cells than in exosomes released from the control NCM460 cells. serum exosomal CRNDE-p and miR-217 levels show diagnostic and prognostic potential for CRC patients. 29137379 2017 Diagnostic potential of serum exosomal colorectal neoplasia differentially expressed long non-coding RNA (CRNDE-p) and microRNA-217 expression in colorectal carcinoma. DGCR5 DGCR5, LINC00037, NCRNA00037 26220 ENSG00000237517 NR_002733 GRCh38_22:18970514-18994628 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. serum, HCC tissues down-regulated DGCR5 was found down-regulated in HCC tissues and serum and low expression of DGCR5 was correlated with a poor cancer specific survival, as the overall 5-year CSS rates were 10.3% (low expression group) and 36.6% (high expression group), respectively. 27898409 2016 Down-Regulation of LncRNA DGCR5 Correlates with Poor Prognosis in Hepatocellular Carcinoma. DQ786243 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RIP hepatocellular carcinoma tissues, cell lines (Huh-7, HepG2, HepG3B, SMMC7721, L02) up-regulated LncDQ was upregulated in both HCC tissue samples and serum and was correlated with low survival rate and adverse clinical pathological characteristics.LncDQ expression was an independent prognostic factor for HCC. Knockdown of LncDQ induced inhibition of cell proliferation, migration, and invasion in vitro and in vivo.LncDQ regulated the epithelial-mesenchymal transition pathway by interacting with EZH2, to epigenetically repress the expression of E-cadherin in HCC cells. 29669339 2018 Upregulation of LncDQ is Associated with Poor Prognosis and Promotes Tumor Progression via Epigenetic Regulation of the EMT Pathway in HCC. ENST00000415582 ELF3-AS1 102723465 ENSG00000234678 NR_146472 GRCh38_1:202000101-202001283 papillary thyroid cancer NA M8260/3 microarray, qPCR etc. blood up-regulated Compared with 131I-avid lung metastases, we discovered that two lncRNAs (ENST00000462717 and ENST00000415582) were upregulated and two (TCONS_00024700 and NR_028494) were downregulated in the non-131I-avid lung metastases of PTC. Low (ENST00000462717 and ENST00000415582) and high plasma lncRNA levels (TCONS_00024700and NR_028494) were also found to be associated with better prognosis of PTC patients with lung metastases. 27997908 2016 Circulating Long Non-Coding RNAs Act as Biomarkers for Predicting 131I Uptake and Mortality in Papillary Thyroid Cancer Patients with Lung Metastases. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (LO2, SMMC-7721, Huh7, HepG2, HepG2.2.15), HCC tissues up-regulated lncRNA FAL1 was up-regulated in HCC tissues and functioned as an oncogene in HCC.LncRNA FAL1 could accelerate cell proliferation and metastasis as a ceRNA mechanism by competitively binding to miR-1236. Moreover,lncRNA FAL1 was also up-regulated in serum exosome of HCC patients and could transfer lncRNA FAL1 to HCC cells to increase their abilities of cell proliferation and migratio. 29421439 2018 LncRNA FAL1 promotes cell proliferation and migration by acting as a CeRNA of miR-1236 in hepatocellular carcinoma cells. FER1L4 FER1L4, C20orf124 NA ENSG00000088340 NA GRCh38_20:35558737-35607562 colon cancer C18 NA qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc. colon cancer tissues, cell lines (NCM460, RKO, Lovo, HCT116, SW480 and SW620) down-regulated The results showed the aberrant expression of FER1L4 and miR-106a-5p in colon cancer tissues. In addition, significant negative correlation between FER1L4 and miR-106a-5p expression levels was observed. Among the colon cancer cell lines, FER1L4 levels were relatively lower, with concurrent high levels of miR-106a-5p. Restoration of FER1L4 decreased the expression of miR-106a-5p, and had a significant influence on colon cancer cell proliferation, migration and invasion. The FER1L4 expression was correlated with depth of tumor invasion, lymph node metastasis, vascular invasion and clinical stage. Circulating FER1L4 and miR-106a-5p levels were decreased and increased, respectively, in colon cancer patients after surgery. 26224446 2015 Long non-coding RNA Fer-1-like protein 4 suppresses oncogenesis and exhibits prognostic value by associating with miR-106a-5p in colon cancer. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, Luciferase reporter assay,in vitro knockdown etc. cell lines (SPCA-1, NCI-H1299, A549, NCI-H441,LTEP-a2,BEAS-2B), LAD tissues up-regulated FEZF1 antisense RNA1 (FEZF1-AS1) is markedly upregulated in human lung adenocarcinoma (LAD) tissues,cell lines and associated with poor prognosis.Loss-of-function revealed that deletion of FEZF1-AS1 expression significantly inhibited the LAD cells proliferation,invasion and migration. Further studies revealed that downregulation of FEZF1-AS1 reduced mRNA and protein expression of its sense-cognate gene FEZF1(forebrain embryonic zinc finger protein 1) in LAD cells, and vice versa. 29510777 2018 LincRNA FEZF1-AS1 is associated with prognosis in lung adenocarcinoma and promotes cell proliferation, migration and invasion. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 head and neck cancer C76.0 NA qPCR etc. blood down-regulated LincRNA-p21 and GAS5 levels were found to be significantly lower in plasma of the HNC patients than in healthy individuals with median values 0.008 vs. 0.571 and 0.126 vs. 0.910, respectively. 26482616 2016 Do circulating long non-coding RNAs (lncRNAs) (LincRNA-p21, GAS 5, HOTAIR) predict the treatment response in patients with head and neck cancer treated with chemoradiotherapy. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 gastric cancer C16 NA qPCR etc. GC tissues differential expression Genotype del/del was significantly associated with a higher survival rate. Patients with late tumor stage were found to have a significantly lower rate of genotype del/del than those with an early tumor stage . Patients with UICC III and IV were found to have a significantly lower rate of genotype del/del than those with UICC I and II. The variant rs145204276 of GAS5 is associated with the development and prognosis of GC.The allele del of rs145204276 is associated with a remarkably lower incidence of cancer progression and metastasis. Methylation percentage of the 7th CpG site significantly correlated with GAS5 expression in the tumor tissues 29557411 2018 The Variant rs145204276 of GAS5 is Associated with the Development and Prognosis of Gastric Cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 colorectal cancer C19.9 NA qPCR etc. cell line (SW480), CRC tissues up-regulated LncRNA GAS5 is upregulated while the miR-221 is downregulated in the tissues,plasma and exosomes of patients with CRC. The results of ROC showed that the expressions of both lncRNA GAS5 and miR-221 in the tissues, plasma and exosomes had diagnostic value in CRC. While the LncRNA GAS5 expression in tissues, plasma and exosomes were associated with the tumor node metastasis (TNM) stage,Dukes stage,lymph node metastasis (LNM),local recurrence rate and distant metastasis rate,the MiR-221 expression in tissues, plasma and exosomes were associated with tumor size, TNM stage, Dukes stage, LNM, local recurrence rate and distant metastasis rate.LncRNA GAS5 and miR-221 expression in tissues, plasma and exosomes were found to be independent prognostic factors for CRC. Following the overexpression of GAS5, the GAS5 expressions was up-regulated and miR-221 expression was down-regulated;the rate of cell proliferation,migration and invasion were decreased. 29630521 2018 Prognostic and predictive value of long non-coding RNA GAS5 and mircoRNA-221 in colorectal cancer and their effects on colorectal cancer cell proliferation, migration and invasion. GAS5-AS1 NA 100506046 ENSG00000270084 NR_037605 GRCh38_1:173863248-173863941 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC surgical tissues down-regulated GAS5-AS1 was down-regulated in HCC tissues .Expression of GAS5-AS1 was notably associated with differentiation, tumor-node-metastasis (TNM) stage (I～II vs III～IV, P= 0.020) and glucose levels (< 6.2 vs≧ 6.2, P= 0.047) in HCC patients. GAS5-AS1 expression had a relatively poor prognosis. Univariate and multivariate analysis elaborated that GAS5-AS1 was an independent prognostic factor for HCC patients. 29660898 2018 Down-regulation of long non-coding RNA GAS5-AS1 and its prognostic and diagnostic significance in hepatocellular carcinoma. GIHCG NA NA NA NA NA renal cell carcinoma C64.9 NA qPCR renal cell carcinoma tissues, cell lines (786-O and Caki-1) up-regulated Increased expression of GIHCG is positively correlated with advanced TNM stages, Fuhrman grades, and poor prognosis.knockdown of GIHCG significantly represses proliferation and migration of RCC cells.high GIHCG expression in RCC tissues is correlated with a reduction in overall survival. 29364470 2018 Long noncoding RNA GIHCG is a potential diagnostic and prognostic biomarker and therapeutic target for renal cell carcinoma. HIF1A-AS1 HIF1A-AS1, 5'aHIF-1A, 5'aHIF1alpha 100750246 ENSG00000258777 NR_047116 GRCh38_14:61681041-61695823 colorectal cancer C19.9 NA qPCR colon cancer tissues up-regulated differentiation degree, tumor size, TNM stage, T stage, N stage, M stage and serum level of HIF1A-AS1 were all linked to CRC prognosis.Compared to CRC patients with low HIF1A-AS1 expression, high expression of patients were associated with a shorter 5-year-survival rate. lower differentiation degree, tumor > 5cm and higher expression of HIF1A-AS1 were independent risk factors affecting the survival rate of patients with CRC. 28946548 2017 Elevated serum level of lncRNA-HIF1A-AS1 as a novel diagnostic predictor for worse prognosis in colorectal carcinoma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 acute myeloid leukemia NA M9861/3 qPCR etc. blood up-regulated The expression of HOTAIR was significantly upregulated in the AML patients compared with the healthy controls, and markedly decreased in the patients post-treatment compared with pre-treatment. Moreover, high levels of HOTAIR were associated with higher white blood cell and BM blast counts, and lower hemoglobin and platelet counts. Patients with a high level of HOTAIR expression had relatively poor overall survival and relapse-free survival times compared with those with a low level of HOTAIR expression. 26622861 2015 Overexpression of long non-coding RNA HOTAIR predicts a poor prognosis in patients with acute myeloid leukemia. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR etc. blood (serum) up-regulated Compared with normal control, the expression of HOTAIR was significantly upregulated in the sera of cervical cancer patients. In addition, elevated HOTAIR was associated with advanced tumor stages, adenocarcinoma, lymphatic vascular space invasion, and lymphatic node metastasis. In addition, our follow-up data showed that high HOTAIR was notably correlated with tumor recurrence and short overall survival. 25366139 2015 A high level of circulating HOTAIR is associated with progression and poor prognosis of cervical cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cardia adenocarcinoma C16.0 M8140/3 qPCR, RFLP-PCR etc. blood up-regulated Among three htSNPs of the HOTAIR gene (rs12826786 C>T, rs4759314 A>G, and rs10783618 C>T), only the T allele of rs12826786 was found to increase the risk of developing GCA and was associated with smoking habit and tumor-node-metastasis (TNM) stage. In addition, higher expression levels of HOTAIR were found in tumor tissues and rs12826786 SNP has a genotype-specific effetc on HOTAIR expression. A high HOTAIR expression level was associated with poor GCA patients' survival. 25476857 2014 Associations between polymorphisms of HOTAIR and risk of gastric cardia adenocarcinoma in a population of north China. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 malignant glioma NA M9380/3 RNA-seq, Microarray, qPCR GBM clinical specimens and cell lines (GBM-L18, SNB19, U87MG, SW1783, A172) up-regulated Mechanistically, HOTAIR was overexpressed in a gene dosage-independent manner, while DNA methylation levels of particular CpGs in HOTAIR locus were associated with HOTAIR expression levels in GBM clinical specimens and cell lines. Concordantly, the demethylating agent 5-Aza-2'-deoxycytidine affected HOTAIR transcriptional levels in a cell line-dependent manner. Importantly, HOTAIR was frequently co expressed with HOXA9 in high-grade gliomas from TCGA, Oncomine, and our Portuguese and French datasets. Integrated in silico analyses, chromatin immunoprecipitation, and qPCR data showed that HOXA9 binds directly to the promoter of HOTAIR. 29644006 2018 The long non-coding RNA HOTAIR is transcriptionally activated by HOXA9 and is an independent prognostic marker in patients with malignant glioma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 thyroid cancer C73.9 NA qPCR thyroid tumor tissue, plasma, cell lines (WRO, TPC-1 and SW579) up-regulated Furthermore, the expression of HOTAIR is significantly upregulated in human thyroid carcinoma cells compared with normal human thyroid cells. 28565838 2017 HOTAIR is a promising novel biomarker in patients with thyroid cancer HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colorectal cancer C19.9 NA qPCR etc. CRC tissues, blood up-regulated CRC patients had higher HOTAIR expression in blood than healthy controls, whereas there was no difference in HOTAIR levels between tumor and adjacent mucosa of CRC patients. HOTAIR levels positively correlated between blood and tumor. High HOTAIR levels in tumors were associated with higher mortality of patients. The hazard ratio was even higher when blood HOTAIR levels were taken into account. Upregulated HOTAIR relative expression in primary tumors and in blood of CRC patients is associated with unfavorable prognosis. 24583926 2014 HOTAIR long non-coding RNA is a negative prognostic factor not only in primary tumors, but also in the blood of colorectal cancer patients. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colorectal cancer C19.9 NA qPCR, RIP,Western Blot etc. colorectal cancer tissues, colorectal cancer cell lines ( HT29, SW480, FHC) down-regulated HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-kB signaling in CRC. HOTAIR was reported to act as a prognostic circulating marker and potential therapeutic target in patients with tumor diseases,while its chemotherapeutic value has rarely been discussed in clinical research. Previous research has found that HOTAIR negatively regulated the expression of miRNAs mainly by functioning as a competing endogenous RNA (ceRNA) sponge, such as miR-145 and miR-331-3p in breast and gastric cancer, respectively. 28918035 2017 lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-kB/TS Signaling in Colorectal Cancer. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 gastric cancer C16 NA qPCR etc. blood (serum), cell lines (AGS, SGC-7901, MGC-803, MKN-45 etc.) up-regulated HULC is upregulated in GC patients. A high serum HULC level correlated with tumor size, lymph node metastasis, distant metastasis, tumor-node-metastasis stage, and H. pylori infection. 27322075 2016 Long non-coding RNA HULC as a novel serum biomarker for diagnosis and prognosis prediction of gastric cancer. JPX JPX, DCBALD06, ENOX, LINC00183, NCRNA00183 554203 ENSG00000225470 NR_024582 GRCh38_X:73944184-74070408 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. blood, HCC tissues down-regulated JPX and XIST levels were significantly decreased in HCC and associated with histological grade and tumor-node-metastasis stage. Low JPX and XIST expression resulted in significantly poor overall survival of HCC. Moreover, plasma JPX levels in patients were lower than that in controls. 27776968 2017 Downregulation of long non-coding RNAs JPX and XIST is associated with the prognosis of hepatocellular carcinoma. KCCAT199 NA NA NA NA NA prostate cancer C61.9 NA qPCR etc. blood, frozen tissue differential expression Our study employs Whole Genome DNA Sequence (WGS) data from tumor samples (n = 103) to comprehensively assess the role of the Knudson two hit genetic model in SCNA generation in prostate cancer. PCDH19 methylation is predictive of biochemical recurrence a 28945760 2017 Appraising the relevance of DNA copy number loss and gain in prostate cancer using whole genome DNA sequence data KCCAT91 NA NA NA NA NA prostate cancer C61.9 NA qPCR etc. blood, frozen tissue differential expression Our study employs Whole Genome DNA Sequence (WGS) data from tumor samples (n = 103) to comprehensively assess the role of the Knudson two hit genetic model in SCNA generation in prostate cancer. PCDH20 methylation is predictive of biochemical recurrence a 28945760 2017 Appraising the relevance of DNA copy number loss and gain in prostate cancer using whole genome DNA sequence data LAMA5-AS1 NA 101928158 ENSG00000228812 NR_109922 GRCh38_20:62352995-62356480 multiple myeloma C42.1 M9732/3 Microarray, qRT-PCR bone marrow up-regulated the lncRNA ST3GAL6-AS1, ZNF663P, LAMA5-AS1 and RP11-175D17.3 were significantly upregulated in newly diagnosed MM and R/R MM samples compared with IDA controls and MM patients who got CR (P < 0.05) (Fig. 6). There was no significant differences between newly diagnosed MM patients and R/R ones, or MM patients who received CR and IDA controls (P > 0.05)(Fig. 6). the expression level of ST3GAL6-AS1 was associated with D-S (P = 0.021), ISS (P = 0.038), R-ISS stage (P = 0.027), mSMART risk status (P = 0.013) and the percentage of malignant plasma cells in bone marrow (P = 0.031). 29459023 2018 Focusing on long non-coding RNA dysregulation in newly diagnosed multiple myeloma. LINC00310 C21orf82, NCRNA00310 114036 ENSG00000227456 NR_027266 GRCh38_21:34157724-34190244 breast cancer C76.0 NA qRT-PCR, Western blot analysis Human cell lines (MCF-7, MDA-MB-231, HMLE and HEK-293T), LM-4142 cells, breast cancer cell lines (MCF-7, MDA-MB-231 and LM-4142), breast cancer tissue and the normal tissues up-regulated LINC00310 was increased as breast cancer progressed, and the deregulation of LINC00310 was significantly associated with patients' survival. LINC00310 promoted cell proliferation by regulating c-Myc expression in?vitro. LINC00310 KO significantly suppressed tumour growth in?vivo. serum LINC00310 expression was significantly up-regulated in patients with breast cancer, LINC00310 had a powerful capability of distinguishing patients with breast cancer from healthy individuals 29993199 2018 The oncogenic potentials and diagnostic significance of long non-coding RNALINC00310 in breast cancer. LINC0086 LED, LINC0086, LINC00086, NCRNA00086,SMIM10L2A 399668 ENSG00000178947 NA GRCh38_X:135421943-135428074 nasopharyngeal cancer C11 NA qPCR, Cell transfection, Luciferase reporter assay, Flow cytometry assay, CCK-8 assay etc. serum, NPC tissues, cell lines (C666-1 and HK-1) down-regulated LINC0086 decreased in NPC patient serum samples and tissues.Upregulation of LINC0086 inhibited cancer cell proliferation and promoted apoptosis. In addition, Upregulation of LINC0086 dramatically decreased the expression of miR-214 in C666-1 and HK-1 cells.We also validated that both miR-214 and LINC0086 presented in the RISC complex, demonstrating that LINC0086 could decrease miR-214 expression by directly interacting with miR-214. Furthermore, the suppressive effects of LINC0086 on NPC cell growth were reversed by overexpression miR-214 expression in vitro and in vivo. 28245169 2017 Long Non-Coding RNA LINC0086 Functions as a Tumor Suppressor in Nasopharyngeal Carcinoma By Targeting miR-214. LINC-PINT LINC-PINT, LincRNA-Pint, MKLN1-AS1, PINT 378805 ENSG00000231721 NR_015431 GRCh38_7:130938963-131110176 lung adenocarcinoma C34 M8140/3 qPCR, microarry, RIP etc. cell lines (HCT116, A549) down-regulated Here we characterize the function of the p53-regulated human lncRNA LINC-PINT in cancer. We find that LINC-PINT is downregulated in multiple types of cancer and acts as a tumor suppressor lncRNA by reducing the invasive phenotype of cancer cells. A cross-species analysis identifies a highly conserved sequence element in LINCPINT that is essential for its function. This sequence mediates a specific interaction with PRC2, necessary for the LINC-PINT-dependent repression of a pro-invasion signature of genes regulated by the transcription factor EGR1. 29078818 2017 The human lncRNA LINC-PINT inhibits tumor cell invasion through a highly conserved sequence element LINC-PINT LINC-PINT, LincRNA-Pint, MKLN1-AS1, PINT 378805 ENSG00000231721 NR_015431 GRCh38_7:130938963-131110176 pancreatic cancer C25 NA qPCR, ISH etc. pancreatic cancer tissues, blood down-regulated Linc-pint expression is lower in plasma samples from PCa patients than from healthy individuals. Linc-pint levels are lower in PCa tumors than in adjacent tissues, carcinoma of the ampulla of Vater (CAV) and cholangiocarcinoma (CCA), and suggest that Linc-pint could be used for distinguishing the cause of malignant obstructive jaundice. Low plasma Linc-pint levels correlate with tumor recurrence, while low tumor Linc-pint levels correlate with poor prognosis for PCa patients after pancreatectomy. 27708234 2016 Plasma and tumor levels of Linc-pint are diagnostic and prognostic biomarkers for pancreatic cancer. lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 102800311 NA NA NA B-cell lymphoma NA M9591/3 qPCR, Western blot etc. B cell lymphoma tissues, DLBCL cell lines (SU-DHL-2, OCI-LY-3, OCILY-10, SU-DHL-4, OCI-LY-7) down-regulated We found that lincRNA-p21 levels were markedly decreased in DLBCL tissues compared with normal. Its expression level was significantly correlated with Ann Arbor stages, B symptoms, performance status, IPI score and serum LDH. Moreover, patients with high levels of LincRNA-p21 expression had a favorable overall survival and progression-free survival. Furthermore, ectopic expression of lincRNA-p21 inhibited cell proliferation, arrested cycle progression and modulated cyclin D1, CDK4 and p21 expression in DLBCL cell lines. These results demonstrated lincRNA-p21 can be identified as a potential novel prognostic biomarker for prognosis in DLBCL and regulate cell proliferation and cycle in vitro 26475621 2015 LincRNA-p21 predicts favorable clinical outcome and impairs tumorigenesis in diffuse large B cell lymphoma patients treated with R-CHOP chemotherapy linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 breast cancer C50 NA qPCR breast cancer tissues, cell lines (MCF-7, MDA-MB-231, SK-BR-3, BT549, MCF10A) up-regulated Plasma lincRNA-ROR levels were associated with estrogen receptors and lymph node metastasis.Plasma lincRNA-ROR may be a potential biomarker for BC diagnosis and a dynamic monitor.LincRNA-ROR is reportedly overexpressed in triple-negative (ER-, PR-, HER2-) breast cancer and could serve as a biomarker or therapeutic target for improving survival. 29090518 2017 Detection and analysis of circulating large intergenic non-coding RNA regulator of reprogramming in plasma for breast cancer. linc-UFC1 UFC1, HSPC155 NA ENSG00000143222 NA GRCh38_1:161152776-161158856 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, etc. Human GC cell lines MGC-803, BGC-823, SGC-7901, HGC-27, MKN-45, GES-1, BGC-823, SGC-7901, MKN-45cells. tumor tissues, non-tumor tissues. up-regulated UFC1 has a promoting role in GC progression, at least in part, by acting as a miR-498 sponge and derepressing Lin28b expression, which would provide a novel biomarker for GC diagnosis and prognosis and offer a potential target for GC therapy.Suppression of Lin28b by miR-498 could be rescued by UFC1 overexpression, whereas Lin28b overexpression partially rescued UFC1 knockdown-mediated inhibition of GC cell function. Lin28b expression was increased in GC and suggested a co-expression pattern with UFC1. The circulating lncRNAs provide a blood-based biomarker for cancer detection.Survival time was analyzed by Kaplan–Meier method and log-rank test. P values less than 0.05 was considered statistically significant.The circulating lncRNAs provide a blood-based biomarker for cancer detection. 29970131 2018 Long non-coding RNA UFC1 promotes gastric cancer progression by regulating miR-498/Lin28b. lnc00462717 PSMD6-AS1, lnc00462717 109729140 ENSG00000243410 NA GRCh38_3:64011964-64016246 papillary thyroid cancer NA M8260/3 microarray, qPCR etc. blood up-regulated Compared with 131I-avid lung metastases, we discovered that two lncRNAs (ENST00000462717 and ENST00000415582) were upregulated and two (TCONS_00024700 and NR_028494) were downregulated in the non-131I-avid lung metastases of PTC. Low (ENST00000462717 and ENST00000415582) and high plasma lncRNA levels (TCONS_00024700 and NR_028494) were also found to be associated with better prognosis of PTC patients with lung metastases. 27997908 2016 Circulating Long Non-Coding RNAs Act as Biomarkers for Predicting 131I Uptake and Mortality in Papillary Thyroid Cancer Patients with Lung Metastases. lnc-GNAT1-1 NA 2779 ENSG00000114349 NA GRCh38_3:50191612-50196516 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. CRC tissues, cell lines (SW480, SW620, HT29, LoVo, HCT116, and RKO) down-regulated Expression of lnc-GNAT1-1 was decreased in liver metastasis than the primary tumor, while the later one is lower than the paired normal mucosa. Decreased lnc-GNAT1-1 expression was associated unfavorable clinicopathological features and a poor prognosis of CRC patients. Overexpression of lnc-GNAT1-1 could suppress the liver metastasis of CRC cells. Finally, we explored the underlying mechanism of the role lnc-GNAT1-1 plays in CRC, and found a positive correlation between lnc-GNAT1-1 and Raf kinase inhibitor protein (RKIP) expression both in cells and in patients' tissues. 27912775 2016 A novel long non-coding RNA lnc-GNAT1-1 is low expressed in colorectal cancer and acts as a tumor suppressor through regulating RKIP-NF-kB-Snail circuit. lncRNA00544 NA NA NA NA NA breast cancer C50 NA Microarray, qPCR luminal BC tissues, breast cancer cell lines (MCF-7, ZR751, T47D, BCAP37, SKBR3, MDA-MB-453, MDA-MB-436, MDA-MB-231, MDA-MB-231HM) up-regulated Here, we aim to identify the lncRNAs which are involved in the particular type luminal BC progression. By Gene Chips analysis, we found a novel lncRNA00544, which was highly expressed in the metastatic axillary nodes compared with corresponding luminal BC tissues (fold change=2.26, P=0.043).Many differentially expressed lncRNAs including circulating lncRNA and lncRNA signatures 28959047 2017 Long non-coding RNA00544 serves as a potential novel predictive and prognostic marker for HR+HER2 subtype breast cancer lncRNA-CIR NA NA NA NA NA bladder cancer C67 NA qPCR, in vitro knockdown 52 cancerous tissues and bladder cancer cell lines(T24, SW780, UBC-40, 5637 and UM-UC-3 ) up-regulated upregulating lncRNA-CIR was demonstrated to promote viability and invasion in T24 and SW780 cells, whereas siRNA-mediated lncRNA-CIR-knockdown consistently exhibited the opposite effects. High lncRNA-CIR levels also dictated poor overall survival among patients with bladder cancer. Furthermore, in vivo implantation experiments also supported a tumorigenic function for lncRNA-CIR, as decreasing lncRNA-CIR levels markedly attenuated Ki-67 staining and xenograft tumor growt 29435036 2017 Long non-coding RNA cartilage injury-related promotes malignancy in bladder cancer. lncRNA-WRAP53 WRAP53, DKCB3, TCAB1, WDR79 NA ENSG00000141499 NA GRCh38_17:7686071-7703502 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated We found that lncRNA-UCA1 and lncRNA-WRAP53 were significantly higher in sera of HCC than those with chronic HCV infection or healthy volunteers. Our data suggested that the increased expression of UCA1 and WRAP53 was associated with advanced clinical parameters in HCC. 26551349 2015 Investigation of long noncoding RNAs expression profile as potential serum biomarkers in patients with hepatocellular carcinoma. Lnc-Tim3 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. hepatocellular carcinoma tissues up-regulated we show that Lnc-Tim3 is upregulated and negatively correlates with IFN-γ and IL-2 production in tumor-infiltrating CD8 T cells of HCC patients. Lnc-Tim3 plays a pivotal role in stimulating CD8 T exhaustion and the survival of the exhausted CD8 T cells. Mechanistically, Lnc-Tim3 specifically binds to Tim-3 and blocks its interaction with Bat3, thus suppressing downstream Lck/ NFAT1/AP-1 signaling, leading to nuclear localization of Bat3, and enhancing p300-dependent p53 and RelA transcriptional activation of anti-apoptosis genes including MDM2 and Bcl-2. 29706626 2018 Long non-coding RNA Lnc-Tim3 exacerbates CD8 T cell exhaustion via binding to Tim-3 and inducing nuclear translocation of Bat3 in HCC. M26317 NA NA NA NA NA gastric cancer C16 NA Microarray, qPCR etc. gastric cancer tissues up-regulated M26317 was upregulated in gastric cancer tissues.Moreover,expression of M26317 correlated with patient age,size of tumor, Lauren's classification,depth of invasion,lymph node and distant metastasis,TNM stage and poor prognosis, but was not associated with gender,location of tumor,and differentiation.M26317 may have an important role in malignant transformation and metastasis of gastric cancer. 29698700 2018 Upregulation of long non-coding RNA M26317 correlates with tumor progression and poor prognosis in gastric cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 epithelial ovarian cancer C56.9 NA qPCR etc. plasma, EOC tissues up-regulated The results showed that levels of plasma MALAT1 were significantly increased in the EOC/DM group compared with the EOC/NDM and HC groups. 27446438 2016 Plasma long non-coding RNA MALAT1 is associated with distant metastasis in patients with epithelial ovarian cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 epithelial ovarian cancer C56.9 NA qPCR, Western blot, RNAi etc. ovarian tissues, cell lines (SK-Ov-3, OvCAR-3, CAOv-3, ES-2, A2780 and HOSEpiC) up-regulated Quantitative RT-PCR analysis revealed that the expression of MALAT1 was higher in human ovarian malignant tumor tissues and EOC cells than in normal ovarian tissues and non-tumorous human ovarian surface epithelial cells, respectively. By analyzing the online database Kaplan-Meier Plotter, MALAT1 was identified to be correlated with the overall survival (OS) and progression free survival (PFS) of patients with ovarian cancer. Finally, dual-luciferase reporter assays demonstrated that MALAT1 interacted with miR-143-3p, a miRNA that plays a role in EOC as demonstrated in our previous study. In conclusion, our results indicated that MALAT1 was overexpressed in EOC. Silencing of MALAT1 decreased EOC cell viability and inhibited EOC cell migration and invasion. These data revealed that MALAT1 may serve as a new therapeutic target of human EOC. Elevated plasma MALAT1 was associated with distant metastasis in patients with EOC. 29693187 2018 MALAT1 affects ovarian cancer cell behavior and patient survival. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 bladder cancer C67 NA qPCR etc. serum, urine, bladder cancer tissues up-regulated MEG3 was significantly down-regulated, SNHG16 and MALAT1 were significantly up-regulated in healthy vs. BCs and benign disease vs. BCs comparisons. 27793008 2016 Identification of a serum circulating lncRNA panel for the diagnosis and recurrence prediction of bladder cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. Hepatocellular carcinoma tissues up-regulated Circulatory MALAT1 might represent a putative non-invasive prognostic biomarker indicating worse liver failure score in HCV-related HCC patients with traditional markers.Supporting our bioinformatics prediction, MALAT1 served as a competitive endogenous RNA (ceRNA)to miR-143-3p,which in turn,caused up-regulation of ZEB1 and promoted cancer growth and metastasis in Bel-7402 and HepG2 cell lines. 29604585 2018 Oncogenic long noncoding RNA MALAT1 and HCV-related hepatocellular carcinoma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, plasma up-regulated Plasma MALAT1 levels were progressively and significantly higher in HCC patients than hepatic disease patients, and higher in hepatic disease patients than healthy controls. The expression of MALAT1 in HCC tissue was slightly higher than that in paired non-cancerous liver tissue, but not significant. The expression of MALAT1 in the non-cancerous liver tissue of 20 HCC patients was significantly higher than that in normal liver tissue of 13 colorectal cancer patients. In contrast, plasma MALAT1 levels were significantly low in HCC patients with hepatitis B infection, and significantly high in patients with liver damage B or liver cirrhosis. 26614531 2016 Plasma level of metastasis-associated lung adenocarcinoma transcript 1 is associated with liver damage and predicts development of hepatocellular carcinoma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, in vitro knockdown etc. cell lines (MDA-MB-231 and MCF7) up-regulated We demonstrate that MALAT1 facilitates cell proliferation, tumor progression and metastasis of triple-negative breast cancer (TNBC) cells despite having a comparatively lower expression level than ER or HER2-positive breast cancer cells. Assessment of the prognostic significance of MALAT1 in human breast cancer (n=1992) revealed elevated MALAT1 expression was associated with decreased disease-specific survival in ER negative, lymph node negative patients of the HER2 and TNBC molecular subtypes. Multivariable analysis confirmed MALAT1 to have independent prognostic significance in the TNBC lymph node negative patient subset. 27250026 2016 Functional and prognostic significance of long non-coding RNA MALAT1 as a metastasis driver in ER negative lymph node negative breast cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gastric cancer C16 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. gastric cancer tissues, cell lines (SGC7901, MKN45 and BGC823) up-regulated Here, we reported that the tissue and plasma MALAT1 levels were significantly higher in gastric cancer patients with distant metastasis than patients without distant metastasis and the healthy controls. In addition, high levels of plasma MALAT1 independently correlated to a poor prognosis for gastric cancer patients. Functional studies revealed that knockdown of MALAT1 could inhibit cell proliferation, cell cycle progression, migration and invasion, and promote apoptosis in gastric cancer cells. Furthermore, the miR-122-IGF-1R signaling correlated with the dysregulated MALAT1 expression in gastric cancer. 27486823 2016 The lncRNA MALAT1 is a novel biomarker for gastric cancer metastasis. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, RNAi, Flow cytometry assay, MTT assay etc. breast cancer tissues, cell line (MDA-MB-231) up-regulated Results showed that MALAT1 expression was significantly up-regulated in 85.9% (67/78) of cancerous tissues compared with normal counterparts. Further, an elevated MALAT1 expression in BC tissue was significantly associated with lymph metastasis and adverse 5-year disease-free survival. Suppression of lncRNA MALAT1 significantly inhibited BC cells proliferation, migration and invasion, induced apoptosis and cell cycle G1 arrest. In addition, serum MALAT1 levels in BC patients were much higher than levels in patients with benign breast disease. 27466303 2016 Clinical Significance of Long Non-coding RNA MALAT1 Expression in Tissue and Serum of Breast Cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 retinoblastoma C69.2 M9510/3 qPCR, Western blot retinoblastoma tissues, cell lines (Weri-Rb1 and Y79) down-regulated Hypermethylation of MEG3 promoter was observed more frequently in retinoblastoma tissues and was highly associated with low MEG3 expression and poor survival of retinoblastoma patients.hypermethylation of MEG3 promoter depressed MEG3 expression, promoted proliferation, inhibited apoptosis and increased B-catenin expression of retinoblastoma cells in vitro.promoter silencing by hypermethylation may account for the loss of MEG3 expression and predict poor prognosis. 29287592 2017 Hypermethylation of MEG3 promoter correlates with inactivation of MEG3 and poor prognosis in patients with retinoblastoma. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 bladder cancer C67 NA qPCR etc. serum, urine, bladder cancer tissues down-regulated MEG3 was significantly down-regulated, SNHG16 and MALAT1 were significantly up-regulated in healthy vs. BCs and benign disease vs. BCs comparisons. 27793008 2016 Identification of a serum circulating lncRNA panel for the diagnosis and recurrence prediction of bladder cancer. MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT 440823 ENSG00000225783 NR_003491 GRCh38_22:26646428-26676475 chronic lymphocytic leukemia NA M9823/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. CLL tissues, leukemia/lymphoma cell lines up-regulated MIAT expression was upregulated in breast cancer cell lines and tissues.MIAT acted as a competing endogenous RNA (ceRNA) to regulate the expression of dual specificity phosphatase 7 (DUSP7) by taking up miR-155-5p in breast cancer. There were positive correlation between MIAT and DUSP7 expression in breast cancer patients.MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p in breast cancer. MIAT was specifically up-regulated in the plasma and aqueous humor of cataract patients. 27527866 2016 Upregulation of long noncoding RNA MIAT in aggressive form of chronic lymphocytic leukemias. MIR22HG MIR22HG, C17orf91 84981 ENSG00000186594 NR_028502 GRCh38_17:1711493-1717174 hepatocellular carcinoma C22.0 M8170/3 qPCR hepatocellular carcinoma tissues, cell lines (SMMC-7721, Huh-7 and Hep3B cells) down-regulated lncRNA MIR22HG expressed significantly lower in HCC tissues compared with non-tumorous tissues. Under-expression of lncRNAMIR22HG was an independent risk factor associated with the prognosis of patients with HCC.under-expression of MIR22HG was closely related to tumor encapsulation, microvascular invasion (MVI), and TNM stage. lncRNA MIR22HG under-expression was an independent risk factor associated with the prognosis of patients with HCC. 29371967 2017 Prognostic values of long non-coding RNA MIR22HG for patients with hepatocellular carcinoma after hepatectomy. MUC19 MUC19, MUC-19 NA ENSG00000205592 NA GRCh38_12:40393395-40570832 head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. blood differential expression To investigate the role of lncRNAs in HPV16 promoting MDSCs aggregation in HNSCC, we examined 4 lncRNAs (HOTAIR, PROM1, CCAT1 and MUC19) expression in 47 HPV-positive blood samples using qRT-PCR. It turns out that the expression of HOTAIR, PROM1, CCAT1, and MUC19 was negatively associated with the number of MDSCs in HPV-positive HNSCC. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 colorectal cancer C19.9 NA qPCR, Western blot, Flow cytometry assay etc. CRC tissues, cell lines (HCT116, LoVo, HT29 and SW480) up-regulated Results showed that NEAT1 was significantly overexpressed in CRC cells and tissues. Clinicpathologic detection verified that high NEAT1 expression associated with bulk in CRC. The serum contents of NEAT1 were observably elevated comparing with healthy cases. The levels of NEAT1 were elevated in distinguishing CRC from normal. Further experiments illustrated that of NEAT1 knockdown signally inhibited growth and facilitated apoptosis. 28013491 2016 LncRNA NEAT1 Impacts Cell Proliferation and Apoptosis of Colorectal Cancer via Regulation of Akt Signaling. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 colorectal cancer C19.9 NA qPCR, RNAi, Cell proliferation assay, Cell invasion assay etc. blood, CRC tissues, cell lines (HCT116, LOVO) up-regulated Whole blood NEAT1 expression was significantly higher in colorectal cancer patients than in NCs. NEAT1_v1 and NEAT1_v2 expression were highly accurate in distinguishing colorectal cancer patients from NCs (area under the curve: 0.787 and 0.871, respectively). Knockdown of NEAT1_v1 in vitro could inhibit cell invasion and proliferation, while knockdown of NEAT1_v2 promoted cell growth. 26552600 2015 Nuclear-enriched abundant transcript 1 as a diagnostic and prognostic biomarker in colorectal cancer. NR_028494 LYRM2, DJ122O8.2 NA NA NA NA papillary thyroid cancer NA M8260/3 microarray, qPCR etc. blood down-regulated Compared with 131I-avid lung metastases, we discovered that two lncRNAs (ENST00000462717 and ENST00000415582) were upregulated and two (TCONS_00024700 and NR_028494) were downregulated in the non-131I-avid lung metastases of PTC. Low (ENST00000462717 and ENST00000415582) and high plasma lncRNA levels(TCONS_00024700and NR_028494) were also found to be associated with better prognosis of PTC patients with lung metastases. 27997908 2016 Circulating Long Non-Coding RNAs Act as Biomarkers for Predicting 131I Uptake and Mortality in Papillary Thyroid Cancer Patients with Lung Metastases. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 diffuse large B-cell lymphoma NA NA HiSeq, qPCR, Western blot,Luciferase reporter assay, ChIP etc. lymph node tissues, cell lines (U2932, SUDHL-6, SUDHL-3, OCI-Ly3, and OCI-Ly8) down-regulated Luciferase reporter assay and chromatin immunoprecipitation assay suggested that lncRNA PANDA was induced by p53 and p53 interacts with the promoter region of PANDA.Cell functional assay further indicated that PANDA functioned as a tumor suppressor gene through the suppression of cell growth by a G0/G1 cell cycle arrest in DLBCL. More importantly, Cignal Signal Transduction Reporter Array and western blot assay showed that lncRNA PANDA inactivated the MAPK/ERK signaling pathway. In conclusion, our integrated approach demonstrates that PANDA in DLBCL confers a tumor suppressive function through inhibiting cell proliferation and silencing MAPK/ERK signaling pathway. Thus, PANDA may be a promising therapeutic target for patients with DLBCL. 29069778 2107 Discovery and validation of the tumor-suppressive function of long noncoding RNA PANDA in human diffuse large B-cell lymphoma through the inactivation of MAPK/ERK signaling pathway. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 clear cell renal cell carcinoma C64.9 M8005/0 qPCR etc. renal tumour tissues down-regulated After marker discovery, we used the training set to detect the levels of these promising lncRNAs by RT and quantitative polymerase chain reaction (RT-qPCR) in a cohort of 24 patients with ccRCC and 27 normal controls. Five lncRNAs (lncRNA-LET, PVT1, PANDAR, PTENP1 and linc00963) were significantly downregulated in the serum of patients compared to the healthy controls. 26878386 2016 A serum-circulating long noncoding RNA signature can discriminate between patients with clear cell renal cell carcinoma and healthy controls. PARTICLE NA 100630918 NA NR_038942 NA breast cancer C50 NA qPCR, RNAi etc. cell line (MDA-MB-361, 24 hr) differential expression In silico analysis identified additional regions for PARTICLE triplexes at >1600 genomic locations. Multiple PARTICLE triplexes are clustered predominantly within the human and mouse tumor suppressor WW Domain Containing Oxidoreductase (WWOX) gene. Surface plasmon resonance diffraction and electrophoretic mobility shift assays were consistent with PARTICLE triplex formation within human WWOX with high resolution imaging demonstrating its enrichment at this locus on chromosome 16. PARTICLE knockdown and over-expression resulted in inverse changes in WWOX transcripts levels with siRNA interference eliminating PARTICLEs elevated transcription to irradiation. The evidence for a second functional site of PARTICLE triplex formation at WWOX suggests that PARTICLE may form triplex-mediated interactions at multiple positions in the human genome including remote loci. 28769061 2017 PARTICLE triplexes cluster in the tumor suppressor WWOX and may extend throughout the human genome. PARTICLE NA 100630918 NA NR_038942 NA osteosarcoma NA M9180/3 qPCR etc. cell lines (U2OS, SJSA, MG63) down-regulated The long ncRNA PARTICLE (promoter of MAT2A antisense radiation-induced circulating long non-coding RNA) is transiently elevated in response to irradiation and influences epigenetic silencing modification within WWOX. It can be concluded that the lncRNA PARTICLE influences the WWOX tumor suppressor and in the absence of WWOX FRA16D breakage, it is associated with OS metastasis-free survival. 29152092 2017 The long non-coding RNA PARTICLE is associated with WWOX and the absence of FRA16D breakage in osteosarcoma patients. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 prostate cancer C61.9 NA qPCR etc. blood and frozen tissue up-regulated Our study employs Whole Genome DNA Sequence (WGS) data from tumor samples (n = 103) to comprehensively assess the role of the Knudson two hit genetic model in SCNA generation in prostate cancer. PCDH17 methylation is predictive of biochemical recurrence after radical prostatectomy [39,40].PCDH17 methylation is predictive of biochemical recurrence after radical prostatectomy [39,40].DNA from whole blood samples and frozen tissue. 28945760 2017 Appraising the relevance of DNA copy number loss and gain in prostate cancer using whole genome DNA sequence data PTENP1 PTENP1, PTEN-rs, PTEN2, PTENpg1, PTH2, psiPTEN 11191 ENSG00000237984 NA GRCh38_9:33673504-33677499 clear cell renal cell carcinoma C64.9 M8005/0 qPCR etc. renal tumour tissues down-regulated After marker discovery, we used the training set to detect the levels of these promising lncRNAs by RT and quantitative polymerase chain reaction (RT-qPCR) in a cohort of 24 patients with ccRCC and 27 normal controls. Five lncRNAs (lncRNA-LET, PVT1, PANDAR, PTENP1 and linc00963) were significantly downregulated in the serum of patients compared to the healthy controls. 26878386 2016 A serum-circulating long noncoding RNA signature can discriminate between patients with clear cell renal cell carcinoma and healthy controls. PTENP1 PTENP1, PTEN-rs, PTEN2, PTENpg1, PTH2, psiPTEN 11191 ENSG00000237984 NA GRCh38_9:33673504-33677499 gastric cancer C16 NA qPCR etc. cancerous gastric tissues, blood (serum) up-regulated A three-lncRNA signature, including CUDR, LSINCT-5 and PTENP1, was identified that may be potential diagnostic marker for GC. Moreover, a risk model for the serum three-lncRNA signature demonstrated that healthy samples can be distinguished from early GC samples. Three-lncRNA signature in serum was identified as diagnostic marker for GC. 25694351 2015 Circulating CUDR, LSINCT-5 and PTENP1 long noncoding RNAs in sera distinguish patients with gastric cancer from healthy controls. PTENP1-AS NA 101243555 ENSG00000281128 NR_103745 GRCh38_9:33677268-33688011 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN45), gastric adenocarcinomas tissues up-regulated In the present study, we observed a higher level of H19 which sponged out the low level expressed miR-148a leading to the overexpression of its target mRNA DNMT1. In this study, we observed upregulation of PTENP1-AS increased the EGFR and AGO4 level in tumors. In addition, we also observed that lncRNA GAS5 competes with AGO4 for miR-21. Compared to PTENP1-AS, 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 clear cell renal cell carcinoma C64.9 M8005/0 qPCR etc. renal tumour tissues down-regulated After marker discovery, we used the training set to detect the levels of these promising lncRNAs by RT and quantitative polymerase chain reaction (RT-qPCR) in a cohort of 24 patients with ccRCC and 27 normal controls. Five lncRNAs (lncRNA-LET, PVT1, PANDAR, PTENP1 and linc00963) were significantly downregulated in the serum of patients compared to the healthy controls. 26878386 2016 A serum-circulating long noncoding RNA signature can discriminate between patients with clear cell renal cell carcinoma and healthy controls. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 breast cancer C50 NA qPCR, Western blot etc. BC tissues, cell lines (MDA-MB-231, MDA-MB-468, SK-BR-3, MDA-MB-435, T47D, MCF-7, MCF-10A) down-regulated To achieve cognition into the biological functions of PVT1 on breast cancer, PVT1 expression was downregulated by transfecting PVT1 siRNA into the MCF-7 and MDA-MB-231 cells, employing the scramble siRNA as a negative control.PVT1 DNA in serum and found that circulating PVT1 DNA significantly increased in the serum of breast cancer patients. circulating PVT1 DNA fragments may be a convenient means to predict the prognosis of breast cancer patients.The results demonstrated that breast cancer patients with high PVT1 expression showed significant shorter 5-year overall survival (OS) compared with patients with low PVT1 expression. 28534994 2017 Amplification and the clinical significance of circulating cell-free DNA of PVT1 in breast cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 hepatocellular carcinoma NA M9380/3 qRT-PCR, Microarray, ect. The human HCC cell lines (Bel-7402 and QGY-7703) and the normliver cell line (L02), HCC tissues and non-tumor tissues up-regulated PVT1 was markedly overexpressed in HCC tissue than in normal liver tissues, PVT1 gained moderate value in discriminating HCC patients from normal controls, confirming the results of RT-qPCR. Additionally, the upregulation of PVT1 could promote HCC cell proliferation in vitro and vivo. Based on the competing endogenous RNA (ceRNA) theory, the PVT1/miR-424-5p/INCENP axis was finally selected for further research. The in silico prediction revealed that there were complementary sequences between PVT1 and miR-424-5p as well as between miR-424-5p and INCENP. Furthermore, a negative correlation trend was found between miR-424-5p and PVT1 based on RT-qPCR, whereas a positive correlation trend was found between PVT1 and INCENP based on data from TCGA. Also, INCENP small interfering RNA (siRNA) could significantly inhibit cell proliferation and viability. 29975928 2018 A Preliminary Investigation of PVT1 on the Effect and Mechanisms of Hepatocellular Carcinoma: Evidence from Clinical Data, a Meta-Analysis of 840 Cases, and In Vivo Validation. RP11-175D17.3. NA NA NA NA NA multiple myeloma C42.1 M9732/3 Microarray, qPCR bone marrow up-regulated the lncRNA ST3GAL6-AS1, ZNF663P, LAMA5-AS1 and RP11-175D17.3 were significantly upregulated in newly diagnosed MM and R/R MM samples compared with IDA controls and MM patients who got CR (P < 0.05) (Fig. 6). There was no significant differences between newly diagnosed MM patients and R/R ones, or MM patients who received CR and IDA controls (P > 0.05)(Fig. 6). the expression level of ST3GAL6-AS1 was associated with D-S (P = 0.021), ISS (P = 0.038), R-ISS stage (P = 0.027), mSMART risk status (P = 0.013) and the percentage of malignant plasma cells in bone marrow (P = 0.031). 29459023 2018 Focusing on long non-coding RNA dysregulation in newly diagnosed multiple myeloma. RP11-222K16.2 NA NA NA NA GRCh38_3:27712910-27714005 acute myeloid leukemia NA M9861/3 Microarray, qPCR Bone marrow differential expression RP11-222K16.2 might affect the differentiation of natural killer cells, and promote the immunized evasion of AML by regulating Eomesodermin expression. Analysis of this study revealed that dysregulated lncRNAs and mRNAs in AML vs IDA controls could affect the immune system and hematopoietic cell differentiation. 29220122 2018 Expression profile analysis of long non-coding RNA in acute myeloid leukemia by microarray and bioinformatics. RP11-567G11.1 LINC02041 NA ENSG00000228952 NA GRCh38_3:187448845-187449450 pancreatic cancer C25 NA microarray, qPCR etc. pancreatic cancer tissues, cell lines (PANC-1, BxPC-3, Capan2, MIAPaCa-2, SW1990, and AsPC-1) up-regulated Compared with the HPDE6 cells, all PC cell lines had higher HOTTIP-005, XLOC_006390, and RP11-567G11.1 expression. The most increased lncRNAs in PC tissues were HOTTIP-005, XLOC_006390, and RP11-567G11.1. Increased HOTTIP-005 and RP11-567G11.1 expression were poor prognostic factors for patients with PC. 26447755 2015 Expression profile of long non-coding RNAs in pancreatic cancer and their clinical significance as biomarkers. SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 100507246 ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 bladder cancer C67 NA qPCR etc. serum, urine, bladder cancer tissues up-regulated MEG3 was significantly down-regulated, SNHG16 and MALAT1 were significantly up-regulated in healthy vs. BCs and benign disease vs. BCs comparisons. 27793008 2016 Identification of a serum circulating lncRNA panel for the diagnosis and recurrence prediction of bladder cancer. SOX2OT SOX2-OT, NCRNA00043, SOX2OT 347689 ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 pancreatic ductal adenocarcinoma C25.3 M8500/3 Microarray, RIP etc. pancreatic ductal adenocarcinoma tissues, cell lines (BxPC-3, Capan-1, Hs766T and HPDE) up-regulated We identified a lncRNA-Sox2ot from exosomes of highly invasive PDAC cells, and analyzed the expression of Sox2ot in the plasma samples and found that the plasma exosomal Sox2ot expression was high and correlated with TNM stage and overall survival rate of PDAC patients. Further research showed that Sox2ot promotes epithelial-mesenchymal transition (EMT) and stem cell like properties by regulating Sox2 expression. Sox2ot competitively binds to the miR-200 family to regulate the expression of Sox2, thus promoting invasion and metastasis of PDAC.We also confirmed the transmission of the exosomes from producer cells to recipient PDAC cells,exosomal Sox2ot can promote tumor invasion and metastasis in vitro and in vivo. We further confirmed tumor generated exosomes could excrete to tumor cell or blood circulation in vivo condition. 29643475 2018 Tumor-derived exosomal lnc-Sox2ot promotes EMT and stemness by acting as a ceRNA in pancreatic ductal adenocarcinoma. SOX2OT SOX2-OT, NCRNA00043, SOX2OT 347689 ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 non small cell lung cancer C34 M8046/3 qPCR etc. non-small cell lung cancer tissues up-regulated We assessed the expressions of the 12 lncRNAs in 92 serum samplesand identified two lncRNAs [SOX2OT and ANRIL] that were overexpressed in tumor serum samples compared with healthy controls. Kaplan-Meier analysis demonstrated that low expressions of SOX2OT and ANRIL were both associated with higher OS rate (P = 0.008 and 0.017, respectively), and SOX2OT could be used as an independent prognostic factor (P = 0.036). 29504701 2018 Circulating long noncoding RNA act as potential novel biomarkers for diagnosis and prognosis of non-small cell lung cancer. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA melanoma NA M8720/3 qPCR etc. blood up-regulated SPRY4-IT1 expression is high in melanoma patients but low in healthy controls, and is closely associated with tumor site and tumor stage. Elevated SPRY4-IT1 significantly reduces overall survival rates of patients and is considered as an independent prognostic factor in patients with melanoma. 27239436 2016 Clinical significance of long noncoding RNA SPRY4-IT1 in melanoma patients. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA esophageal squamous cell cancer NA NA qPCR etc. blood (plasma and serum) up-regulated Furthermore, plasma levels of POU3F3, HNF1A-AS1 and SPRY4-IT1 were significantly higher in ESCC patients compared with normal controls.By receiver operating characteristic curve (ROC) analysis, among the three lncRNAs investigated, plasma POU3F3 provided the highest diagnostic performance for detection of ESCC (the area under the ROC curve (AUC), 0.842. 25608466 2015 Identification of the long non-coding RNA POU3F3 in plasma as a novel biomarker for diagnosis of esophageal squamous cell carcinoma. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA cervical cancer C53 NA qPCR etc. serum, cervical cancer tissues up-regulated The expression levels of SPRY4-IT1 were higher in cervical cancer tissues than in adjacent normal tissues. Patients with higher SPRY4-IT1 expression had advanced clinical characteristics and a shorter overall survival time than those with lower SPRY4-IT1 expression. Moreover, multivariate analysis showed that relative SPRY4-IT1 expression was an independent predictor of overall survival in patients with cervical cancer. 27642559 2016 Upregulation of long noncoding RNA SPRY4-IT1 correlates with tumor progression and poor prognosis in cervical cancer. ST3GAL6-AS1 NA 100874207 ENSG00000239445 NR_046683 GRCh38_3:98714330-98732651 multiple myeloma C42.1 M9732/3 Microarray, qPCR bone marrow up-regulated the lncRNA ST3GAL6-AS1, ZNF663P, LAMA5-AS1 and RP11-175D17.3 were significantly upregulated in newly diagnosed MM and R/R MM samples compared with IDA controls and MM patients who got CR (P < 0.05) (Fig. 6). There was no significant differences between newly diagnosed MM patients and R/R ones, or MM patients who received CR and IDA controls (P > 0.05)(Fig. 6). the expression level of ST3GAL6-AS1 was associated with D-S (P = 0.021), ISS (P = 0.038), R-ISS stage (P = 0.027), mSMART risk status (P = 0.013) and the percentage of malignant plasma cells in bone marrow (P = 0.031). 29459023 2018 Focusing on long non-coding RNA dysregulation in newly diagnosed multiple myeloma. TCONS_00024700 lnc-TK2-5, NONHSAT142989 NA NA NA NA papillary thyroid cancer NA M8260/3 microarray, qPCR etc. blood down-regulated Compared with 131I-avid lung metastases, we discovered that two lncRNAs (ENST00000462717 and ENST00000415582) were upregulated and two (TCONS_00024700 and NR_028494) were downregulated in the non-131I-avid lung metastases of PTC. Low (ENST00000462717 and ENST00000415582) and high plasma lncRNA levels(TCONS_00024700and NR_028494) were also found to be associated with better prognosis of PTC patients with lung metastases. 27997908 2016 Circulating Long Non-Coding RNAs Act as Biomarkers for Predicting 131I Uptake and Mortality in Papillary Thyroid Cancer Patients with Lung Metastases. TINCR TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16 NA ENSG00000223573 NA GRCh38_19:5558167-5578349 breast cancer C50 NA qPCR, Luciferase reporter assay, in vitro knockdown etc. cell lines (MDA-MB-231, MDA-MB-435, MDA-MB-453, MDA-MB-468,MCF-7), breast cancer tissue up-regulated TINCR was aberrantly up-regulated by SP1,which in turn stimulated cell proliferation,anchorage-independent growth and suppressed cell apoptosis in breast cancer.TINCR silencing significantly suppressed migration and invasion in vitro and xenograft tumor growth in vivo.Mechanistically, TINCR modulated KLF4 expression via competing with miR-7, which consequently contributed to its oncogenic potential.MiR-7 inhibition severely compromised TINCR silencing-elicited tumor repressive effects 29614984 2018 Up-regulation of ceRNA TINCR by SP1 contributes to tumorigenesis in breast cancer. TINCR TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16 NA ENSG00000223573 NA GRCh38_19:5558167-5578349 gastric cancer C16 NA microarray, qPCR etc. plasma, gastric cancer tissues, cell lines (SGC-7901 and BGC-823) up-regulated Five (TINCR, CCAT2, AOC4P, BANCR and LINC00857) were significantly upregulated in plasma, tumor tissues and GC cell lines. 28042329 2017 Genome-Wide lncRNA Microarray Profiling Identifies Novel Circulating lncRNAs for Detection of Gastric Cancer. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 acute myeloid leukemia NA M9861/3 qPCR, Western blot etc. cell lines (KG-1, MOLM-14, HL-60, NB-4 and THP-1) up-regulated LncRNA TUG1 expression was higher in AML patients compared to controls and correlated with higher white blood cell counts, monosomal karyotype, FLT3-ITD mutation, poor-risk stratification, and poor prognosis, which independently predicted worse event-free survival and overall survival. In vitro, lncRNA TUG1 expression was higher in AML cell lines (KG-1, MOLM-14, HL-60, NB-4, and THP-1 cells) compared to controls. LncRNA TUG1 mimic promoted cell proliferation and decreased cell apoptosis rate, while lncRNA TUG1 inhibitor repressed cell proliferation and increased cell apoptosis rate. Rescue experiment showed that AURKA attenuated the influence of lncRNA TUG1 on AML cell proliferation and apoptosis. In conclusion, lncRNA TUG1 associates with advanced disease and worse prognosis in adult AML patients, and it induces AML cell proliferation and represses cell apoptosis via targeting AURKA. 29654398 2018 Long non-coding RNA taurine-upregulated gene 1 correlates with poor prognosis, induces cell proliferation, and represses cell apoptosis via targeting aurora kinase A in adult acute myeloid leukemia. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 osteosarcoma NA M9180/3 qPCR etc. blood, osteosarcoma tissues up-regulated TUG1 was significantly overexpressed in the osteosarcoma tissues compared with matched adjacent normal tissues and was closely correlated with tumor size, post-operative chemotherapy, and Enneking surgical stage. Upregulation of TUG1 strongly correlated with poor prognosis and was an independent prognostic indicator for overall survival and progression-free survival. 26499949 2016 Upregulation of long non-coding RNA TUG1 correlates with poor prognosis and disease status in osteosarcoma. UBE2CP3 NA NA ENSG00000250384 NA GRCh38_4:57072683-57073132 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, Western blot etc. tissues, cell lines (HepG2, SMMC-7721) up-regulated Clinical data showed that high levels of lncRNA UBE2CP3 were correlated with poor prognosis in HCC patients. Functional studies demonstrated that over-expression of lncRNA UBE2CP3 promoted cell invasion and migration in vitro and in vivo.Our results suggest that lncRNA UBE2CP3 promotes the metastasis of HCC and that serum lncRNA UBE2CP3 may be a new biomarker for the diagnosis of HCC. 29029437 2017 Long non-coding RNA UBE2CP3 promotes tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma uc004cox.4 NA NA NA NA NA bladder cancer C67 NA Microarray, qPCR etc. bladder cancer tissues up-regulated In the training set, uc004cox.4 was up-regulated and GAS5 was down-regulated in BC patients. Moreover, the expression of urinary uc004cox.4 was an independent predictor for the recurrence of NMIBC patients. 29516641 2018 Cell-free lncRNA expression signatures in urine serve as novel non-invasive biomarkers for diagnosis and recurrence prediction of bladder cancer. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 glioma NA M9380/3 RT-PCR, Luciferase reporter assay, in vitro knockdown glioma tumor tissues, glioma cell lines (SHG44, U87, U251, and A172) up-regulated UCA1 was upregulated in glioma tissue and indicated a poor prognosis. UCA1 knockdown induced by si-UCA1 significantly suppressed the proliferative, migrative, and invasive activities of glioma cell lines (U87 and U251).the complementary binding within UCA1 and miR-122 at the 3'-UTR. Functional experiments revealed that UCA1 acted as an miR-122 sponge to modulate glioma cell proliferation, migration, and invasion via downregulation of miR-122. 28548636 2017 Long Noncoding RNA UCA1 Targets miR-122 to Promote Proliferation, Migration, and Invasion of Glioma Cells. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 pancreatic cancer C25 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. pancreatic carcinoma cell lines (PANC-1, SW1990, AsPC-1), pancreatic cancer tissues up-regulated The colocalization relationship between lncRNA UCA1 and miR-96 was detected by RNA FISH. Whether UCA1 could target miR-96 and whether miR-96 could target FOXO3 3'UTR were verified by dual-luciferase reporter gene assay. High expression of lncRNA UCA1 and FOXO3 and low expression of miR-96 were shown in pancreatic cancer. Inhibition of UCA1 suppressed pancreatic tumor cell proliferation, colony formation, and metastasis, while inhibition of miR-96 promoted pancreatic cancer cell progression. FOXO3 was the downstream target gene of miR-96 and showed the opposite effects. LncRNA UCA1 promoted cell proliferation, invasion, migration and inhibited cell apoptosis of pancreatic cancer through down-regulating miR-96 and up-regulating FOXO3 29500870 2018 LncRNA UCA1 impacts cell proliferation, invasion, and migration of pancreatic cancer through regulating miR-96/FOXO3. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 hepatocellular carcinoma C22.0 M8170/3 qPCR hepatocellular carcinoma tissues up-regulated High expression of serum UCA1 was significantly associated with a high tumor grade, large tumor size,positive vascular invasion, and advanced TNM stage.a high serum UCA1 level was an independent unfavorable prognostic factor for HCC. High levels of UCA1 in HCC tumor tissues are closely related to large tumor size, vascular invasion,advanced TNM stage, and poor postoperative survival. 28856933 2017 Serum long noncoding RNA urothelial carcinoma-associated 1: A novel biomarker for diagnosis and prognosis of hepatocellular carcinoma. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 gastric cancer C16 NA qPCR etc. cancerous gastric tissues, blood (serum) up-regulated A three-lncRNA signature, including CUDR, LSINCT-5 and PTENP1, was identified that may be potential diagnostic marker for GC. Moreover, a risk model for the serum three-lncRNA signature demonstrated that healthy samples can be distinguished from early GC samples. Three-lncRNA signature in serum was identified as diagnostic marker for GC. 25694351 2015 Circulating CUDR, LSINCT-5 and PTENP1 long noncoding RNAs in sera distinguish patients with gastric cancer from healthy controls. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. blood, HCC tissues down-regulated JPX and XIST levels were significantly decreased in HCC and associated with histological grade and tumor-node-metastasis stage. Low JPX and XIST expression resulted in significantly poor overall survival of HCC. Moreover, plasma JPX levels in patients were lower than that in controls. 27776968 2017 Downregulation of long non-coding RNAs JPX and XIST is associated with the prognosis of hepatocellular carcinoma. XLOC_006390 lnc-HOXA13-1, XLOC_006390, linc-HOXA11 NA NA NA NA pancreatic cancer C25 NA microarray, qPCR etc. pancreatic cancer tissues, cell lines (PANC-1, BxPC-3, Capan2, MIAPaCa-2, SW1990, and AsPC-1) up-regulated Compared with the HPDE6 cells, all PC cell lines had higher HOTTIP-005, XLOC_006390, and RP11-567G11.1 expression. The most increased lncRNAs in PC tissues were HOTTIP-005, XLOC_006390, and RP11-567G11.1. Increased HOTTIP-005 and RP11-567G11.1 expression were poor prognostic factors for patients with PC. 26447755 2015 Expression profile of long non-coding RNAs in pancreatic cancer and their clinical significance as biomarkers. ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 B cell acute lymphoblastic leukemia NA M9826/3 qPCR, Western blot, RIP B-lineage acute lymphoblastic leukemia blood, cells (BMSC, HS-5, BALL-1) up-regulated ZEB1-AS1 levels were aberrantly up-regulated in B-ALL. All correlated with STAT3 activation and IL-11 production.a high level of ZEB1-AS1 predicted poor prognosis of B-ALL patients. a high level of ZEB1-AS1 predicted poor prognosis of B-ALL patients. Mechanistically, ZEB1-AS1 could bind to IL-11 and promote IL-11 stability. Down-regulation of ZEB1-AS1 decreased IL-11 production of human bone marrow stromal cells (BMSCs), which led to suppressed proliferation and inhibited IL-11/STAT3 pathway in BALL-1 cells. ZEB1-AS1 promotes the activation of IL-11/STAT3 signaling pathway by associating with IL-11 in B-ALL. 28861713 2017 LncRNA ZEB1-AS1 contributes to STAT3 activation by associating with IL-11 in B-lymphoblastic leukemia. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 esophageal squamous cell cancer NA NA qPCR etc. ESCC tumor tissues up-regulated ZFAS1 expression was significantly higher in ESCC tissues compared with the corresponding adjacent normal tissues.clinicopathological factors and ZFAS1 expression,can accurately predict the prognosis of lymph node-negative ESCC patients without preoperative chemoradiotherapy. ZFAS1 was found to act as a competing endogenous RNA (ceRNA) in liver cancer by binding to miR-150 and inhibiting the tumor suppressor function of miR-150. ZFAS1 promoted the increased expression of SP1 in ovarian cancer by competitive antagonism against miR-150 to enhance the ability of cell proliferation and chemotherapy resistance for ovarian cancer cells. ZFAS1 acts as an oncogene in colorectal cancer.ZFAS1 was found to promote gastric cancer cell proliferation by inhibiting KLF2 and NKD2 expression. 28938617 2017 Development and validation of nomogram based on lncRNA ZFAS1 for predicting survival in lymph node-negative esophageal squamous cell carcinoma patients ZNF663P NA NA ENSG00000215452 NA GRCh38_20:46414228-46459276 multiple myeloma C42.1 M9732/3 Microarray, qPCR bone marrow up-regulated the lncRNA ST3GAL6-AS1, ZNF663P, LAMA5-AS1 and RP11-175D17.3 were significantly upregulated in newly diagnosed MM and R/R MM samples compared with IDA controls and MM patients who got CR (P < 0.05) (Fig. 6). There was no significant differences between newly diagnosed MM patients and R/R ones, or MM patients who received CR and IDA controls (P > 0.05)(Fig. 6). the expression level of ST3GAL6-AS1 was associated with D-S (P = 0.021), ISS (P = 0.038), R-ISS stage (P = 0.027), mSMART risk status (P = 0.013) and the percentage of malignant plasma cells in bone marrow (P = 0.031). 29459023 2018 Focusing on long non-coding RNA dysregulation in newly diagnosed multiple myeloma. 6p22lncRNAs NA NA NA NA NA neuroblastoma NA M9500/3 qPCR etc. cell line (SH-SY5Y, IMR32, SK-N-AS, SK-N-BE2) down-regulated A pair of sense/antisense lncRNA (6p22lncRNAs) encoded by CASC15 and NBAT1 located at the neuroblastoma (NB) risk-associated 6p22.3 locus are tumor suppressors and show reduced expression in high-risk NBs. Loss of functional synergy between 6p22lncRNAs results in an undifferentiated state that is maintained by a gene-regulatory network, including SOX9 located on 17q, a region frequently gained in NB. 6p22lncRNAs regulate SOX9 expression by controlling CHD7 stability via modulating the cellular localization of USP36, encoded by another 17q gene. This regulatory nexus between 6p22.3 and 17q regions may lead to potential NB treatment strategies. 29533783 2018 Sense-Antisense lncRNA Pair Encoded by Locus 6p22.3 Determines Neuroblastoma Susceptibility via the USP36-CHD7-SOX9 Regulatory Axis. 91H NA NA NA NA NA colorectal cancer C19.9 NA qPCR, RNAi etc. CRC tissues, cell lines (HCT8, HT29, HCT116, SW620 etc.) up-regulated 91H was significantly overexpressed in cancerous tissue and CRC cell lines compared with adjacent normal tissue and a normal human intestinal epithelial cell line. Moreover, 91H overexpression was closely associated with distant metastasis and poor prognosis in patients with CRC, except for CNV of 91H. Multivariate analysis indicated that 91H expression was an independent prognostic indicator, as well as distant metastasis. 91H played an important role in the molecular etiology of CRC and might be regarded as a novel prognosis indicator in patients with CRC. 25058480 2014 Up-regulation of 91H promotes tumor metastasis and predicts poor prognosis for patients with colorectal cancer. AA174084 NA NA NA NA NA gastric cancer C16 NA qPCR, RIP etc. gastric cancer tissues down-regulated Expression levels of AA174084 were down-regulated significantly in 95 of 134 GC tissues (71%) compared with the levels in paired, adjacent, normal tissues. AA174084 levels had significant, negative correlations with age, Borrmann type, and perineural invasion. Plasma AA174084 levels in patients with GC dropped markedly on day 15 after surgery compared with preoperative levels and were associated with invasion and lymphatic metastasis. AA174084 levels in gastric juice from patients with GC were significantly higher than the levels in normal mucosa or in patients with minimal gastritis, gastric ulcers, and atrophic gastritis. The area under ROC was up to 0.848. 24986041 2014 Gastric juice long noncoding RNA used as a tumor marker for screening gastric cancer. AB019562 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell lines (SMMC-7721, PLC/PRF/5, C3AHCC, THLE-3) up-regulated AB019652 is upregulated in HCC tissues and cultured HCC cells. AB019562 knockdown increased the apoptotic rates of the two cell lines and activated the expression of caspase3, but not caspase8.For patients in the late stage, the introduction of sorafenib can improve survival rates, but remains limited. 28534955 2017 Long non-coding RNA AB019562 promotes cell proliferation and metastasis in human hepatocellular carcinoma. AB073614 NA NA NA NA GRCh38_3:149173591-149175492 ovarian cancer C56.9 NA microarray, qPCR, RNAi, Western blot, Flow cytometry assay etc. ovarain cancer tissues, cell lines (A2780, Caov3, HO-8910, OVCAR3, SKOV3 etc.) up-regulated Results showed that AB073614 expression was significantly up-regulated in 85.3% (64/75) cancerous tissues compared with normal counterparts. Knockdown of AB073614 expression significantly inhibited cell proliferation and invasion, resulted in cell arrest in G1 phase of cell cycle and a dramatic increase of apoptosis. Finally, western blot assays indicated that lncRNA AB073614 may exert its function by targeting ERK1/2 and AKT-mediated signaling pathway. In conclusion, our study suggests that lncRNA AB073614 acts as a functional oncogene in OC development. 26299803 2015 A long noncoding RNA AB073614 promotes tumorigenesis and predicts poor prognosis in ovarian cancer. AB073614 NA NA NA NA GRCh38_3:149173591-149175492 glioma NA M9380/3 qPCR etc. glioma tissues up-regulated The expression of AB073614 was detected in 65 glioma tissues and 13 normal brain tissues by qRT-PCR, showing that lncRNA AB073614 expression was significantly up-regulated in cancerous tissues compared with normal brain tissues, and it was positively correlated with tumor grade in glioma patients. Kaplan-Meier analysis demonstrated that increased AB073614 expression contributed to poor overall survival. Further, univariate Cox regression analysis indicated that lncRNA AB073614 overexpression was an unfavorable prognostic factor in gliomas, regardless of the tumor grade. Finally, after adjustment with age, sex, tumor grade and tumor location, multivariate Cox regression analysis suggested that both highly expressed lncRNA AB073614 and high tumor grade could be considered independent poor prognostic indicators for glioma patients 27104549 2016 Up-Regulation of Long Non-Coding RNA AB073614 Predicts a Poor Prognosis in Patients with Glioma AB073614 NA NA NA NA GRCh38_3:149173591-149175492 glioma NA M9380/3 qPCR, Western blot etc. glioma tissues, cell line (U251) up-regulated AB073614 expression was found to be significantly upregulated in glioma tissues compared with adjacent normal tissues, with a higher level in high-grade glioma. AB073614 expression was significantly upregulated in both glioma tissues and cell lines, and glioma patients with high AB073614 expression had lower overall survival rates. AB073614 promoted the progression of glioma by targeting SOX7 to activate the Wnt/B-catenin signaling pathway, suggesting that the inhibition of AB073614 might be a potential target for therapeutic intervention in glioma patients. AB073614 induced Wnt/B-catenin signaling activity by repressing SOX7 expression. 29029454 2017 Long noncoding RNA AB073614 promotes the malignance of glioma by activating Wnt/B-catenin signaling through downregulating SOX7. AB209630 NA NA NA NA GRCh38_9:69248696-69251364 hypopharyngeal squamous cell carcinoma C13 M8070/3 microarray, qPCR etc. HSCC tissues up-regulated Our results demonstrated that AB209630 levels were markedly lower in HSCC tissues and cells than in normal tissues and cells, and increased expression of AB209630 level significantly inhibited growth, metastasis, and invasion and stimulated apoptosis in vitro. In addition, patients with decreased expression of AB209630 had a significantly poorer prognosis than those with high AB209630 expression. These data suggest that increased expression of AB209630 might either stimulate or inhibit biological activities involved in HSCC development, indicating a potential application of AB209630 in future treatment for this disease. This study suggest that AB209630 functions as a tumor suppressor in HSCC, and its decreased expression may help predict a poor prognostic outcome of HSCC. Our future work will focus on the mechanisms of whether and how AB209630 as a tumor suppressor gene is involved in HSCC development 26895099 2016 AB209630, a long non-coding RNA decreased expression in hypopharyngeal squamous cell carcinoma, influences proliferation, invasion, metastasis, and survival ABHD11-AS1 ABHD11-AS1, LINC00035, NCRNA00035, WBSCR26 171022 ENSG00000225969 NR_026690 GRCh38_7:73735038-73736158 ovarian cancer C56.9 NA qPCR, Western blot ovarian cancer tissue, ovarian carcinoma cell lines (A2780 ,OVCAR3) up-regulated This is the first study to demonstrate the role of RhoC in the tumor-promoting effects of the lncRNA ABHD11-AS1. The present findings shed light on new therapeutic targets for ovarian cancer treatment.Because of its hidden onset, poor prognosis and high fatality rate, the overall survival rate of this cancer is not satisfactory. 28818073 2017 Role of the lncRNA ABHD11-AS1 in the tumorigenesis and progression of epithelial ovarian cancer through targeted regulation of RhoC. AC004166.7 STAG3L2, STAG3L1, STAG3L2P, STAG3L3 NA ENSG00000174353 NA GRCh38_7:72969696-73005922 lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. lung adenocarcinoma tissues up-regulated We initially identified a number of interesting candidate lncRNAs for further analysis. Of these, LOC100132354 and RPLP0P2 exhibited the most significantly changed expression in our analysis of 100 pairs of lung adenocarcinoma and normal lung tissue samples. The expression of LOC100132354 was significantly higher in lung adenocarcinoma than in the adjacent tissues, while the expression of RPLP0P2 was significantly lower in lung adenocarcinoma than in the adjacent tissues. 25089627 2014 Long noncoding RNA expression profiles of lung adenocarcinoma ascertained by microarray analysis. AC008440.10 NA NA NA NA NA laryngeal squamous cell cancer C32.3 NA qPCR etc. laryngeal squamous cell cancer tissues down-regulated Significant downregulation of lncRNA AC008440.10 was detected in LSCC tumor and metastatic lymph node in advanced stage of patient samples compared with those in early stage. The pattern of differentially expressed AC008440.10 displayed a clear trend that significantly related to tumor progression. The downregulation of lncRNA AC008440.10 correlates with increasing risk of metastasis, poor prognosis and patient survival. 29775753 2018 Long non-coding RNA biomarker for human laryngeal squamous cell carcinoma prognosis. AC009014.3 AC009014.3, LOC389332, NR_024418 NA NA NA NA clear cell renal cell carcinoma C64.9 M8005/0 qPCR clear cell renal cell carcinoma tissues, cell lines (786-O, 769-P, CaKi-1 and RLC-310) down-regulated The results demonstrated that LOC389332 expression was markedly lower in ccRCC tissues compared with that in matched adjacent non-tumor tissues. Furthermore, patients with ccRCC with lower levels of LOC389332 expression had a shorter overall survival time than those with higher LOC389332 expression. 28450954 2017 Downregulation of a novel long non-coding RNA, LOC389332, is associated with poor prognosis and tumor progression in clear cell renal cell carcinoma AC013264.2 AC013264.2, LOC101927596 NA ENSG00000231621 NA GRCh38_2:197197991-197199273 non small cell lung cancer C34 M8046/3 microarray, qPCR etc. NSCLC tissues down-regulated we initially identified a number of significant candidate lncRNAs (including GUCY1B2, RP11-385J1.2, AC018865.8, RP11-909N17.3, GNAS-AS1, TUBA4B, Z82214.3, XLOC_000371, AC013264.2 and RP1-317E23.3) and verified the expression of these lncRNAs by RT-qPCR with GAPDH as the reference gene, by calculating the 2-CT values. 25394782 2014 Detection of long-chain non-encoding RNA differential expression in non-small cell lung cancer by microarray analysis and preliminary verification. AC024560.2 RP11-496H1.1 NA ENSG00000249626 NA GRCh38_3:197660565-197665757 cervical cancer C53 NA microarray, qPCR etc. cervical cancer tissues differential expression To validate the results of data mining and determine the clinical relevance of lncRNA dysregulation, we detected the expression levels of the above four lncRNAs in 35 clinical tissues with and without pelvic lymph node metastasis (PLNM) by qRT-PCR. The qRT-PCR result was consistent with our analysis, in that expression of all 4 lncRNAs had statistical difference with the same trend. 27035672 2016 Characterization of long non-coding RNA expression profiles in lymph node metastasis of early-stage cervical cancer. AC026166.2-001 MTCO1P5 NA ENSG00000233026 NA GRCh38_3:12165299-12165642 laryngeal squamous cell cancer C32.3 NA microarray, qPCR etc. LSCC tissues down-regulated AC026166.2-001 and RP11-169D4.1-001 were distinctly dysregulated, with AC026166.2-001 exhibiting lower expression in cancer tissues and RP11-169D4.1-001 higher expression. We verified that both AC026166.2-001 and RP11-169D4.1-001 were expressed at a lower level in cervical lymph nodes compared with paired laryngeal cancer tissues and paired normal tissues. RP11-169D4.1-001 levels were positively correlated with lymph node metastasis. 25243407 2014 Long non-coding RNA profiling in laryngeal squamous cell carcinoma and its clinical significance: potential biomarkers for LSCC. AC026166.2-001 MTCO1P5 NA ENSG00000233026 NA GRCh38_3:12165299-12165642 laryngeal squamous cell cancer C32.3 NA Microarray, qPCR, Western blot, Luciferase reporter assay, knockdown The LSCC cell line (AMC-HN-8, TU-212), xenograft tumor tissues down-regulated AC026166.2-001 inhibited LSCC cell proliferation and the clone-forming capacity.Cell cycle distribution and related protein changes were measured by flow cytometry. AC026166.2-001 arrested the cell cycle at the G1 phase and induced apoptosis. In addition, AC026166.2-001 decreased cell migration as measured by wound healing assays and transwell migration assays. Moreover, luciferase reporter assay and Western blotting results suggested that AC026166. 2-001 acts as a sponge of miR-24-3p and regulates the expression of p27 and cyclin D1. The in vivo results showed that AC026166.2-001 significantly suppressed the growth of LSCC xenografts and promoted apoptosis.overexpression of miR-24-3p significantly reduced the luciferase activity of AC026166.2-001 WT GP-miRGLO vectors but not of AC026166.2-001 MUT. Next, AC026166. 2-001 may act as a sponge for miR-24-3p. Quantitative RT-PCR was used to test our assumption and we found that miR-24-3p was down-regulated by AC026166.2-001. 29463827 2018 Long non-coding RNA AC026166.2-001 inhibits cell proliferation and migration in laryngeal squamous cell carcinoma by regulating the miR-24-3p/p27 axis. AC026904.1 NA NA NA NA NA breast cancer C50 NA Microarray, qPCR, RIP, Luciferase reporter assay etc. breast cancer tissue, cell line MDA-MB-231-luc-D3H2LN up-regulated We observed that TGF-B induced genome-wide changes in lncRNA levels in breast cancer cells, among which AC026904.1 and UCA1 were highly expressed in metastatic breast cancer and closely associated with poor prognosis. 29774079 2018 Long non-coding RNAs AC026904.1 and UCA1: a “one-two punch” for TGFB-induced SNAI2 activation and epithelial-mesenchymal transition in breast cancer AC079776.2 AC079776.1 105373615 ENSG00000250207 NR_149127 GRCh38_2:129825126-129877553 lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. lung adenocarcinoma tissues down-regulated We initially identified a number of interesting candidate lncRNAs for further analysis. Of these, LOC100132354 and RPLP0P2 exhibited the most significantly changed expression in our analysis of 100 pairs of lung adenocarcinoma and normal lung tissue samples. The expression of LOC100132354 was significantly higher in lung adenocarcinoma than in the adjacent tissues, while the expression of RPLP0P2 was significantly lower in lung adenocarcinoma than in the adjacent tissues. 25089627 2014 Long noncoding RNA expression profiles of lung adenocarcinoma ascertained by microarray analysis. AC093850.2 NA NA NA NA GRCh38_2:215718043-215719424 esophageal squamous cell cancer NA NA RNA-seq, Microarray, qPCR, in vitro knockdown ESCC tissues, Human esophageal cancer cell lines (KYSE150,KYSE180, KYSE450, KYSE70, KYSE140 and TE3) up-regulated A novel three-lncRNA signature, comprised of RP11-366H4.1.1 (ENSG00000248370), LINC00460 (ENSG00000233532) and AC093850.2 (ENSG00000230838), was identified. The signature classified patients into high-risk and low-risk groups with different overall survival (OS) and disease-free survival (DFS). The signature indicates that patients in the high-risk group show poor OS and DFS, whereas patients with a low-risk group show significantly better outcome. The independence of the signature was validated by multivariable Cox regression analysis. GO and KEGG pathway analysis for 588 protein-coding genes-associated with the three lncRNAs indicated that the three lncRNAs were involved in tumorigenesis. In vitro assays further demonstrated that the three lncRNAs promoted the migration and proliferation of ESCC cells. 29409459 2018 A three-lncRNA signature predicts overall survival and disease-free survival in patients with esophageal squamous cell carcinoma. AC103563.9 AC103563.9 NA NA NA GRCh38_2:95051395-95053176 esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues down-regulated Based on the fold change, significance, and number of transcripts, three upregulated lncRNAs (RP11-334E6.12, DNM3OS, and RP11-150O12.6) and three downregulated lncRNAs (AC103563.9, RP11-7K24.3, and RP11-351J23.1) with only one transcript were chosen as candidates for further validation. The results of qRT-PCR were consistent with the RNA sequencing data. 27449043 2016 Transcriptome profiling of lncRNA and co-expression networks in esophageal squamous cell carcinoma by RNA sequencing. AC104699.1 AC104699.1 NA ENSG00000224220 NA GRCh38_2:25421117-25427643 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues up-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. AC138128.1 NA NA NA NA NA gastric cancer C16 NA qPCR etc. gastric cancer tissues, cell lines (AGS, SGC-7901, BGC-823, HG27) down-regulated The results showed that the expression level of AC138128.1 in GC was significantly decreased compared to that in NAT. Levels of AC138128.1 in the GC cell lines, AGS BGC-823, HG27, and SGC-7901 were lower than those in the human normal gastric epithelial cell line GES-1. lncRNA AC138128.1 might be a novel biomarker for predicting GC. 25260808 2014 The novel long noncoding RNA AC138128.1 may be a predictive biomarker in gastric cancer. ADAMTS9-AS2 lncADAMTS9-AS2 100507098 ENSG00000241684 NR_038264 GRCh38_3:64684909-65011468 non small cell lung cancer C34 M8046/3 microarray, qPCR etc. NSCLC tissues down-regulated The expression level of ADAMTS9-AS2, C1401f132 and LINC00312 in NSCLC tumors were indeed significantly down-regulated when compared with those in normal lung tissues, while LINC00673 was significantly up-regulated in NSCLC tumors compared with normal lung tissues. These lncRNAs could be further exploited for the development of useful biomarkers in diagnosis, prognosis and treatment of NSCLC. 25590602 2015 Identification and Validation of Long non-coding RNA Biomarkers in Human Non-Small Cell Lung Carcinomas. ADAMTS9-AS2 lncADAMTS9-AS2 100507098 ENSG00000241684 NR_038264 GRCh38_3:64684909-65011468 glioma NA M9380/3 qPCR, RNAi, Western blot etc. glioma tumor tissues, cell lines (T98G, A172, SNB-19 etc.) down-regulated The results showed that the ADAMTS9-AS2 expression was significantly downregulated in tumor tissues compared with normal tissues and reversely associated with tumor grade and prognosis. We also found that ADAMTS9-AS2 expression was negatively correlated with DNA methyltransferase-1 (DNMT1). In addition, DNMT1 knockdown led to remarkable enhancement of ADAMTS9-AS2 expression. Overexpression of ADAMTS9-AS2 resulted in significant inhibition of cell migration in glioma, whereas knockdown of ADAMTS9-AS2 showed the opposite effetc. 24833086 2014 A new tumor suppressor LncRNA ADAMTS9-AS2 is regulated by DNMT1 and inhibits migration of glioma cells. ADAMTS9-AS2 lncADAMTS9-AS2 100507098 ENSG00000241684 NR_038264 GRCh38_3:64684909-65011468 clear cell renal cell carcinoma C64.9 M8005/0 Microarray, qRT-PCR ccRCC tissues, RCC cell lines (786-O) down-regulated the expression of three LncRNA (ENSG00000241684, ENSG00000231721 and NEAT1) were significantly downregulated in advanced ccRCC.LncRNA ENSG00000241684 had significant hazard ratios for predicting clinical outcome. LncRNA ENSG00000241684 expression was negatively correlated with pTNM stage. Overexpression of ENSG00000241684 significantly impaired cell proliferation and reduced the invasion ability in 786-O and ACHN cells. 29433989 2018 Downregulation of long non-coding RNA ENSG00000241684 is associated with poor prognosis in advanced clear cell renal cell carcinoma. ADAMTS9-AS2 lncADAMTS9-AS2 100507098 ENSG00000241684 NR_038264 GRCh38_3:64684909-65011468 lung cancer C34 NA Microarray, qPCR, Western blot etc lung cancer tissues, cell lines (A549, SPC-A1, H23 and NCI-H520) down-regulated lncADAMTS9-AS2 was lowly expressed in lung cancer tissues.High expression of ADAMTS9-AS2 in lung cancer cells significantly reduced proliferation ability and inhibited migration, as well as elevating their apoptosis rate.In vivo assay found that ADAMTS9-AS2 suppressed the lung tumor growth. Bioinformatics predicted that miR-223-3p bound directly to the ADAMTS9-AS2 and TGFBR3, which was later confirmed by luciferase reporter system.ADAMTS9-AS2 transfection increased TGFBR3 mRNA and protein expressions in lung cancer cells, but miR-223-3p transfection significantly decreased them. Besides,miR-223-3p induced cellular apoptosis while TGFBR3 group showed the complete opposite effect. It was proved that ADAMTS9-AS2 and TGFBR3 were the direct genes of miR-223-3p. MiR-223-3p promotes proliferation, migration and invasion of lung cancer cells by targeting TGFBR3. 29707897 2018 Upregulated lncRNA ADAMTS9-AS2 suppresses progression of lung cancer through inhibition of miR-223-3p and promotion of TGFBR3. AF070632 NA NA NA NA GRCh38_1:111770675-111772033 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues down-regulated We noted that LINC01419 was characterized by a significant increase in transcript expression from dysplasia to early HCC. The lncRNA AK021443 was also up-regulated in advanced HCC samples when compared with early HCC. Moreover, expression of LINC01419 and AK021443 was up-regulated in HCC tissues when compared with non-tumor liver tissue. AF070632 expression was down-regulated in HCC and was decreased in advanced HCC when compared with early HCC. These results suggest that LINC01419 may be related to the initiation of HCC, whereas AK021443 and AF070632 may be associated with the progression of HCC. 26540467 2015 Long non-coding RNA expression profiles of hepatitis C virus-related dysplasia and hepatocellular carcinoma. AF075041 NA NA NA NA GRCh38_5:14773382-14774024 pancreatic cancer C25 NA qPCR etc. pancreatic cancer tissues, cell lines (Sw1990, PANC-1, BXPC-3 etc.) up-regulated We further confirmed the selected 6 up-regulation of LncRNAs in PC tissues and PC cell lines through qPCR. Comparing to 293T cells, the expression of LncRNA AF339813 was significantly increased about 10-fold in PANC-1 cells, 8-fold in SW1990 cells and 8.9-fold in BxCP-3 cells. The other 5 LncRNAs have a certain degree of up-regulation in PC cell lines. 26045769 2015 Downregulation of NUF2 inhibits tumor growth and induces apoptosis by regulating lncRNA AF339813. AF086415 NA NA NA NA GRCh38_19:6372857-6373024 nasopharyngeal cancer C11 NA microarray, qPCR, RNAi etc. nasopharyngeal carcinoma tissues, cell lines (CNE-2 etc.) down-regulated qPCR results were consistent with the microarray analysis results of six lncRNAs (AF086415, AK095147, RP1-179N16.3, MUDENG, AK056098, and AK294004) in terms of regulation direction and significance. 24379026 2014 Curcumin enhances the radiosensitivity in nasopharyngeal carcinoma cells involving the reversal of differentially expressed long non-coding RNAs. AF088004 NA NA NA NA GRCh38_3:53813100-53813725 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow down-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. AF268386 DDR2, MIG20a, NTRKR3, TKT, TYRO10, uc001gch.1 NA NA NA GRCh38_1:162785489-162786465 lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. lung adenocarcinoma tissues down-regulated The remaining 10 lncRNAs, showed significantly different expression in the tumor samples. For 9 of these, expression was altered in the same direction as had been detected by microarray analysis. Differentially expressed lncRNAs in early stage lung adenocarcinoma and suggest that lncRNAs may be novel candidate biomarkers for the early detection of this disease. 25758555 2015 Identification of biomarkers for the detection of early stage lung adenocarcinoma by microarray profiling of long noncoding RNAs. AF339813 NA NA NA NA GRCh38_13:93293507-93295109 pancreatic cancer C25 NA qPCR, RNAi, Western blot etc. pancreatic cancer tissues, cell lines (Sw1990, PANC-1, BXPC-4 etc.) up-regulated We found LncRNA AF339813 was positively regulated by NUF2. We further demonstrated that knockdown of AF339813 by siRNA in PC cells significantly reduced cell proliferation and promoted apoptosis.We further demonstrated that knockdown of AF339813 by siRNA in PC cells significantly reduced cell proliferation and promoted apoptosis. Thus, we conclude that NUF2 is consistently overexpressed in human PC and NUF2 is closely linked with human PC progression through the meditator LncRNA AF339813. 26045769 2015 Downregulation of NUF2 inhibits tumor growth and induces apoptosis by regulating lncRNA AF339813. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 thyroid cancer C73.9 NA qPCR, Western blot, in vitro knockdown etc cell lines (Nthy-ori3-1 K-1, TPC-1, SW579, FTC133,XTC-1), FTC tumor tissues up-regulated Expression of AFAP1-AS1 was increased in thyroid cancer tissues. Down-regulation of AFAP1-AS1 could suppress growth of thyroid cancer cells. Knockdown of AFAP1-AS1 induced apoptosis in thyroid cancer. Decreased cell migration in thyroid cancer as a result of down-regulation of AFAP1-AS1. 29331858 2018 Down-regulation of long non-coding RNA AFAP1-AS1 inhibits tumor growth, promotes apoptosis and decreases metastasis in thyroid cancer. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 retinoblastoma C69.2 M9510/3 qPCR etc. retinoblastoma tissues, cell lines (Weri-Rb1, Y79, ARPE-19 and HRMECs) up-regulated In our results, AFAP1-AS1 expression was elevated in retinoblastoma tissues and cell lines, and associated with tumor size, choroidal invasion, and optic nerve invasion. Moreover, high expression of AFAP1-AS1 was an independent unfavorable prognostic factor in retinoblastoma patients. The experiment in vitro suggested down-regulation of AFAP1-AS1 inhibited retinoblastoma cell proliferation, migration and invasion, and blocked cell cycle. In conclusion, AFAP1-AS1 functions as an oncogenic lncRNA in retinoblastoma. 29654169 2018 LncRNA AFAP1-AS1 is a prognostic biomarker and serves as oncogenic role in retinoblastoma. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 tongue squamous cell carcinoma C02 M8070/3 qPCR, Western blot, in vitro knockdown TSCC tissues, TSCC cell lines (SCC-15, Tca8113, SCC-4, SCC-9 and CAL-27) up-regulated lncRNA AFAP1-AS1 was increased in TSCC tissues and that patients with high AFAP1-AS1 expression had a shorter overall survival.Furthermore, AFAP1-AS1 silencing partly inhibited cell migration and invasion. Inhibition of AFAP1-AS1 decreased the activity of the Wnt/B-catenin pathway and suppressed the expression of EMT-related genes (SLUG, SNAIL1, VIM, CADN, ZEB1, ZEB2, SMAD2 and TWIST1) in TSCC cells. 29310682 2018 Upregulation of the long non-coding RNA AFAP1-AS1 affects the proliferation, invasion and survival of tongue squamous cell carcinoma via the Wnt/B-catenin signaling pathway. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 cholangiocarcinoma NA M810/3 qPCR, Western blot cholangiocarcinoma tumor tissues up-regulated We found that lncRNA AFAP1-AS1 was increased in CCA tissues and patients with high AFAP1-AS1 expression had a shorter overall survival. 28535506 2017 Long Noncoding RNA AFAP1-AS1 Promoted Tumor Growth and Invasion in Cholangiocarcinoma AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 gallbladder cancer C23.9 NA qPCR, RNAi, Western blot etc. GBC tissues, cell lines (NOZ, H69 ,GBC-SD and SGC-996) up-regulated The expression levels of lncRNA AFAP1-AS1 were significantly elevated in GBC tissues and GBC cell lines. In addition, the expression level of lncRNA AFAP1-AS1 was significantly associated with tumor sizes and the higher expression of lncRNA AFAP1-AS1 was correlated with poor prognosis in GBC patients. Knockdown of LncRNA AFAP1-AS1 suppressed cell growth and invasion in NOZ and GBC-SD cells. Furthermore, we found that knockdown of LncRNA AFAP1-AS1 in GBC cells inhibited EMT by down-regulating the transcription factor Twist1 and Vimentin and up-regulated the E-cadherin. 27810781 2016 Overexpression of LncRNA AFAP1-AS1 predicts poor prognosis and promotes cells proliferation and invasion in gallbladder cancer. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 lung squamous cell carcinoma C34 M8070/3 qPCR, RNAi, Cell proliferation assay etc. lung cancer tissues, cell line (SK-MES-1) up-regulated We detected 6 lncRNAs including 3 that were up-regulated (LINC00511, AFAP1-AS1, CASC9) and 3 down-regulated (LINC00968, TINCR, LINC00035) in 20 paired LUAD and LUSC and normal tissues to evaluate the analysis results. The results of qPCR showed that all the chosen lncRNA expressions were increased or decreased in LUAD or LUSC tissues compared with those in the normal tissues, which is consistent with the bioinformatic analysis results. Knockdown of LINC00511, AFAP1-AS1, and PVT1 impaired LUAD or LUSC cell proliferation. 27797003 2016 Transcriptome analysis of distinct long non-coding RNA transcriptional fingerprints in lung adenocarcinoma and squamous cell carcinoma. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR etc. blood, cell lines (Panc1, MIAPaCa-2, Capan2, SW1990 etc.) up-regulated Microarray analysis revealed that up-regulation of AFAP1-AS1 expression in PDAC tissues compared with normal adjacent tissues, which was confirmed by RT-qPCR in 69/90 cases (76.7%). Its overexpression was associated with lymph node metastasis, perineural invasion, and poor survival. AFAP1-AS1 is a potential novel prognostic marker to predict the clinical outcome of PDAC patients after surgery and may be a rational target for therapy. 25925763 2015 High expression of AFAP1-AS1 is associated with poor survival and short-term recurrence in pancreatic ductal adenocarcinoma. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 esophageal adenocarcinoma C15 M8140/3 qPCR etc. EAC tissues, cell lines (OE-33, SK-GT-4, FLO-1, HEEpiC etc.) up-regulated Using quantitative reverse-transcription PCR, we assessed expression levels of AFAP1-AS1 in 20 matched pairs of human EAC and adjacent NE as well as in 12 matched pairs of human benign BE and adjacent NE. AFAP1-AS1 expression was elevated relative to NE in the majority of EACs (15/20) and BEs (11/12). These data suggest that AFAP1-AS1 expression is up-regulated in both EAC cell lines and primary EAC tissues, consistent with the DNA hypomethylation observed in these same samples. BE and EAC exhibit reduced methylation that includes non-coding regions. Methylation of the long noncoding RNA AFAP1-AS1 is reduced in BE and EAC, and its expression inhibits cancer-related biologic functions of EAC cells. 23333711 2013 Hypomethylation of noncoding DNA regions and overexpression of the long noncoding RNA, AFAP1-AS1, in Barrett's esophagus and esophageal adenocarcinoma. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 lung adenocarcinoma C34 M8140/3 qPCR etc. lung adenocarcinoma tissues up-regulated AFAP1-AS1 was overexpressed in lung adenocarcinoma and associated with survival time. The low expression of AFAP1-AS1 was an independent predictor for disease-free survival in patients with lung adenocarcinoma.AFAP1-AS1 down-regulation exerts growth suppression and apoptosis induction in lung adenocarcinoma cells, suggested it may participate in turmorigenesis and be a therapeutic target for treating lung adenocarcinoma in future. 28670387 2017 Down-regulation of long non-coding RNA AFAP1-AS1 inhibits tumor cell growth and invasion in lung adenocarcinoma AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Among them, AFAP1-AS1, BCAR4, H19, HOXA-AS2, MALAT1 and PVT1 were significantly up-regulated, and ADAMTS9-AS2 was significantly down-regulated in cancer tissue samples. 27596298 2016 Differentially expressed long non-coding RNAs and the prognostic potential in colorectal cancer. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 lung adenocarcinoma C34 M8140/3 RNA-seq, qPCR etc. LUAD tissues up-regulated The results showed that CHIAP2, LINC00472, LINC00961 and MGC27382 were downregulated in LUAD tumor tissues when compared with adjacent non-tumor lung tissues, while AFAP1-AS1, CHIAP2 and FER1L4 were upregulated in LUAD tumor tissues. 27826625 2016 Integrated analysis of long non-coding RNA-associated ceRNA network reveals potential lncRNA biomarkers in human lung adenocarcinoma. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 gastric cancer C16 NA qPCR, Western blot, etc. gastric cancer tissues, cell lines (AGS, BGC-823, MGC-803, SGC-7901) up-regulated We found that lncRNA AFAP1-AS1 was upregulated in GC and play as an important biomarker of prognosis in GC patients. Therefore, lncRNA AFAP1-AS1 may be a biomarker for prognosis and a therapeutic target of GC. 28975981 2017 Increased lncRNA AFAP1-AS1 expression predicts poor prognosis and promotes malignant phenotypes in gastric cancer AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 lung cancer C34 NA qPCR, Western blot lung cancer tissues, cell lines (A549, H1299 ,H460) up-regulated In the current study, we found that AFAP1-AS1 was substantially over expressed in lung cancer tissues and cell lines. In addition, AFAP1-AS1 expression level was proven to be associated with the malignant features of lung cancer. Knockdown of AFAP1-AS1 significantly suppressed cell proliferation by increasing cell apoptosis and G0/G1 phase retardation of cell cycle in lung cancer cells. Furthermore, AFAP1-AS1 knockdown could suppress tumor growth of lung cancer in BALB/c nude mice. We also identified that AFAP1-AS1 silencing could influence the expression of AFAP1 and KRT1 on mRNA and protein level by cis and trans regulatory mechanism. Moreover, the oncogenic activities of AFAP1-AS1 on cell proliferation are partially mediated by KRT1.With only 10-15 % of 5-year overall survival, lung cancer accounts for more than one quarter of all cancer deaths. The most important factor for survival of lung cancer patients is the stage of the disease at diagnosis. 29212176 2017 Silencing of lncRNA AFAP1-AS1 suppressed lung cancer development by regulatory mechanism in cis and trans. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 gastric cancer C16 NA qPCR, Western blot etc. GC tissues, cell lines (AGS, MGC-803, SGC-7901, and BGC-823) up-regulated A small interfering RNA (siRNA) that targeted AFAP1-AS1 was transfected into cells to inhibit the expression of AFAP1-AS1. AFAP1-AS1 was up-regulated in GC tissues and GC cells. AFAP1-AS1 knockdown suppressed cell viability of SGC7901 transfected with si-AFAP1-AS1. AFAP1-AS1 was up-regulated in GC cells and regulated the gastric cancer cell proliferation and apoptosis via PTEN/p-AKT pathway. AFAP1-AS1 was found to be associated with increased risk of developing lymph node metastasis, poor overall survival, and short recurrence-free survival. 28451917 2017 Long Noncoding RNA AFAP1-AS1 Promotes Cell Proliferation and Apoptosis of Gastric Cancer Cells via PTEN/p-AKT Pathway. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR, Cell proliferation assay etc. PDAC tissues, cell lines (AsPC-1, BxPC-3, Capan-2, CFPAC-1, HPAC, MIA PaCa-2, PANC-1 and SW1990) up-regulated The qRT-PCR results showed that CRNDE, NR_036488, ENSG00000244649, AFAP1-AS and UCA1 expression was significantly increased and ENSG00000218510 expression was remarkably decreased in PDAC tissues compared with paired normal pancreatic tissues. Consistent with the findings in PDAC tissues, CRNDE, NR_036488, ENSG00000244649, AFAP1-AS1 and UCA1 expression was dramatically enhanced and ENSG00000218510 reduced in all or most of 8 PDAC cell lines in relative to the nonmalignant HPDE6-C7 cells or hTERT-HPNE cells at the RNA level. 27628540 2016 Analysis of long non-coding RNA expression profiles in pancreatic ductal adenocarcinoma. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Cell proliferation assay etc. HCC tissues, cell lines (SMMC-7721, Bel-7402, MHCC-97 L, MHCC-97H) up-regulated AFAP1-AS1 was found to be increased in HCC tissues, and high AFAP1-AS1 expression was associated with tumor size, TNM stage, vascular invasion, and poor prognosis. Silencing of AFAP1-AS1 significantly reduced cell proliferation, clonal growth, cell migration, and invasion and increased apoptosis in vitro. Furthermore, AFAP1-AS1 silencing markedly reduced tumor growth in a murine allograft model in vivo. 26803513 2016 Critical role for the long non-coding RNA AFAP1-AS1 in the proliferation and metastasis of hepatocellular carcinoma. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 nasopharyngeal cancer C11 NA microarray, qPCR, RNAi, Western blot, ISH etc. NPC tissues, cell lines (5-8F, HNE2, HK-1) up-regulated AFAP1-AS1 expression was upregulated in NPC and associated with NPC metastasis and poor prognosis. In vitro experiments demonstrated that AFAP1-AS1 knockdown significantly inhibited the NPC cell migration and invasive capability. AFAP1-AS1 knockdown also increased AFAP1 protein expression. Proteomic and bioinformatics analyses suggested that AFAP1-AS1 affected the expression of several small GTPase family members and molecules in the actin cytokeratin signaling pathway. AFAP1-AS1 promoted cancer cell metastasis via regulation of actin filament integrity. 26246469 2015 Upregulated long non-coding RNA AFAP1-AS1 expression is associated with progression and poor prognosis of nasopharyngeal carcinoma. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 colorectal cancer C19.9 NA qPCR, RNAi etc. CRC tissues, cell lines (HCT116 and SW480) up-regulated In this study, we found that AFAP1-AS1 was aberrantly over-expressed in CRC tissues and closely correlated with tumor size, TNM stage and distant metastasis. Moreover, AFAP1-AS1 depletion resulted in the inhibition of CRC cell proliferation and colony formation. In addition, AFAP1-AS1 knockdown induced G0/G1 cell cycle arrest in CRC cells. 27261589 2016 Overexpression of lncRNA AFAP1-AS1 correlates with poor prognosis and promotes tumorigenesis in colorectal cancer. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Cell proliferation assay etc. lung cancer tissues, cell line (A549) up-regulated We detected 6 lncRNAs including 3 that were up-regulated (LINC00511, AFAP1-AS1, CASC9) and 3 down-regulated (LINC00968, TINCR, LINC00035) in 20 paired LUAD and LUSC and normal tissues to evaluate the analysis results. The results of qPCR showed that all the chosen lncRNA expressions were increased or decreased in LUAD or LUSC tissues compared with those in the normal tissues, which is consistent with the bioinformatic analysis results. Knockdown of LINC00511, AFAP1-AS1, and PVT1 impaired LUAD or LUSC cell proliferation. 27797003 2016 Transcriptome analysis of distinct long non-coding RNA transcriptional fingerprints in lung adenocarcinoma and squamous cell carcinoma. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 non small cell lung cancer C34 M8046/3 qPCR, Western blot, RIP etc. non small cell lung cancer tissues, Cell lines (16HBE, A549, SPC-A1 and H1299) up-regulated AFAP1-AS1 expression was increased in NSCLC tissues and was correlated with clinical outcomes of NSCLC. Over-expression of AFAP1-AS1 level reveals a poor overall survival time (OS) of patients with NSCLC and could be regarded AS an independent predictor for OS 29793547 2018 Long noncoding RNA AFAP1-AS1 predicts a poor prognosis and regulates non-small cell lung cancer cell proliferation by epigenetically repressing p21 expression AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissues, cell lines (GES-1, AGS, BGC-823, MKN-45 and SGC-7901) up-regulated The expression of AFAP1-AS1 was significantly increased in the primary tumor tissues of GC patients with lymph node metastasis or tumor node metastasis stage. The overexpression of AFAP1-AS1 was positively associated with the poor survival rates of GC patients. 29805596 2018 Long non-coding RNA AFAP1-antisense RNA 1 promotes the proliferation, migration and invasion of gastric cancer cells and is associated with poor patient survival AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 breast cancer C50 NA qPCR,etc. The normal human mammary epithelial cell line (MCF-10A). 4 breast cancer cell lines (MCF-7,SK-RB-3,MDA-MB231,MDA-MB-468). A total of 160 paired breast cancer tissue,adjacent normal tissue. up-regulated Up-regulated lncRNA AFAP1-AS1 indicates a poor prognosis in breast cancer patients and regulated the breast cancer cells proliferation, apoptosis and metastasis. AFAP1-AS1 knockdown can inhibit the proliferation,metastasis and promote apoptosis of MCF-7. However,the AFAP1 expression and actin filament integrity was not affected after AFAP1-AS1 knockdown.The Kaplan–Meier method was used to estimate survival curves,the log-rank test wasused to compare between groups. 29974352 2018 Up-regulated lncRNA AFAP1-AS1 indicates a poor prognosis and promotes carcinogenesis of breast cancer. AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 colorectal cancer C19.9 NA qPCR, ChIP, RIP, Western blot, etc. Cell lines (LOVO, SW1116, SW480, HCT116, SW620, HT29). 80 colorectal carcinoma tissues, 10 normal colon tissues. up-regulated Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.Kaplan-Meier survival analysis revealed a statistically significant worse prognosis for colorectal cancer patients with high AFAP1-AS1 mRNA levels compared with those with low. 29888110 2018 Long noncoding RNA AFAP1-AS1 facilitates tumor growth through enhancer of zeste homolog 2 in colorectal cancer. AGAP2-AS1 AGAP2-AS1, PUNISHER 100130776 ENSG00000255737 NR_027032 GRCh38_12:57726271-57728356 glioma NA M9380/3 microarray, qPCR, RNAi, Flow cytometry assay, Cell proliferation assay etc. glioma tissues, cell lines (LN229 and U87MG) up-regulated The expression of four lncRNAs in different grades showed that AGAP2-AS1, LINC01198 and MIR155HG were increased with tumor grade, while TPT1-AS1 was decreased. Knockdown of AGAP2-AS1 can inhibit the cell proliferation, migration and invasion, while increase the apoptosis cell rates in vitro. 27764782 2016 LncRNA profile study reveals four-lncRNA signature associated with the prognosis of patients with anaplastic gliomas. AGAP2-AS1 AGAP2-AS1, PUNISHER 100130776 ENSG00000255737 NR_027032 GRCh38_12:57726271-57728356 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, ChIP, Luciferase reporter assay, Cell proliferation assay, Cell migration and invasion assay etc. gastric cancer tissues, cell lines (BGC823, SGC7901, AGS, MGC803, and MKN45) up-regulated AGAP2-AS1 was highly expressed in the GC tissues and cell lines. Knockdown of AGAP2-AS1 significantly inhibited GC cell proliferation, migration, and invasion in vitro and tumor growth in vivo. AGAP2-AS1 overexpression promoted cell growth and invasion. In addition, the transcription factor SP1 activated AGAP2-AS1 expression in the GC cells. AGAP2-AS1 functions as an oncogenic lncRNA by interacting with LSD1 and EZH2 and suppressing CDKN1A (P21) and E-cadherin transcription. 28209205 2017 Long noncoding AGAP2-AS1 is activated by SP1 and promotes cell proliferation and invasion in gastric cancer. AGAP2-AS1 AGAP2-AS1, PUNISHER 100130776 ENSG00000255737 NR_027032 GRCh38_12:57726271-57728356 non small cell lung cancer C34 M8046/3 qPCR non-small cell lung cancer tissues up-regulated Expression of AGAP2-AS1 was up-regulated in the NSCLC tissues compared with the adjacent normal tissues (p < 0.01). Kaplan-Meier analysis demonstrated patients with higher AGAP2-AS1 expression had a shorter overall survival time than those with lower AGAP2-AS1 expression (p < 0.0001). 28617550 2017 Prognostic and diagnostic significance of long non-coding RNA AGAP2-AS1 levels in patients with non-small cell lung cancer AGAP2-AS1 AGAP2-AS1, PUNISHER 100130776 ENSG00000255737 NR_027032 GRCh38_12:57726271-57728356 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. NSCLC tissues, cell lines (A549, PC9, SPCA1, H1975 and H1299, H520, SK-MES-1 and H1703) up-regulated The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vitro loss- and gain-of-function assays revealed that AGAP2-AS1 knockdown inhibited cell proliferation, migration and invasion, and induced cell apoptosis. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription. Taken together, our findings indicate that AGAP2-AS1 may act as an oncogene by repressing tumor-suppressor LATS2 and KLF2 transcription. 27195672 2016 Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells. AI364715 NA NA NA NA NA gastric cancer C16 NA qPCR etc. gastric cancer tissues down-regulated The expression level of AI364715 in gastric cancer tissues was downregulated. Meanwhile, its expression level was closely associated with tumor size and differentiation. 25971582 2015 Reduced expression of the long non-coding RNA AI364715 in gastric cancer and its clinical significance. AK001796 MIR4435-2HG, AGD2, AK001796, LINC00978, MIR4435-1HG, MIR4435-2HG 541471 ENSG00000172965 NR_015395 GRCh38_2:111036776-111523376 esophageal squamous cell cancer NA NA qPCR, Western blot, in vitro knockdown etc cell lines (Eca-109,TE-1), ESCC tissues up-regulated lncRNA AK001796 was significantly upregulated in ESCC tumor tissues.lncRNA AK001796 regulates cell proliferation and cell cycle via modulating MDM2/p53 signaling in ESCC, which provides a new insight into the treatment targets for ESCC. 29568233 2018 The long non-coding RNA AK001796 contributes to tumor growth via regulating expression of p53 in esophageal squamous cell carcinoma. AK001796 MIR4435-2HG, AGD2, AK001796, LINC00978, MIR4435-1HG, MIR4435-2HG 541471 ENSG00000172965 NR_015395 GRCh38_2:111036776-111523376 lung cancer C34 NA microarray, qPCR, RNAi, Cell proliferation assay etc. lung cancer tissues, cell lines (BEAS-2B, A549 and H446) up-regulated AK001796, the lncRNA with the most clearly altered expression, was overexpressed in lung cancer tissues and cell lines, but its expression was downregulated in resveratrol-treated lung cancer cells. By monitoring cell proliferation and growth in vitro and tumor growth in vivo, we observed a significant reduction in cell viability in lung cancer cells and a slow growth in the tumorigenesis following AK001796 knockdown. We also found that AK001796 knockdown caused a cell-cycle arrest, with significant increases in the percentage of cells in G0/G1 in lung cancer cells. By using cell cycle pathway-specific PCR arrays, we detected changes in a number of cell cycle-related genes related to lncRNA AK001796 knockdown. 25888808 2015 A novel long noncoding RNA AK001796 acts as an oncogene and is involved in cell growth inhibition by resveratrol in lung cancer. AK001796 MIR4435-2HG, AGD2, AK001796, LINC00978, MIR4435-1HG, MIR4435-2HG 541471 ENSG00000172965 NR_015395 GRCh38_2:111036776-111523376 breast cancer C50 NA qPCR etc. breast cancer tissues, cell lines (MCF10A, MDA-MB-231, ZR751, ZR7530, MCF-7, SKBR3, BCAP37 etc.) up-regulated Here, we identify a lncRNA, LINC00978, which is upregulated in breast cancer cell lines and tissues compared with corresponding controls. Furthermore, LINC00978 expression is negatively associated with hormone receptor (HR) status in 195 breast cancer patients studied. 27897214 2016 LINC00978 predicts poor prognosis in breast cancer patients. AK001796 MIR4435-2HG, AGD2, AK001796, LINC00978, MIR4435-1HG, MIR4435-2HG 541471 ENSG00000172965 NR_015395 GRCh38_2:111036776-111523376 lung cancer C34 NA qPCR, RIP, Western blot etc. lung cancer tissues, cell line (6HBE, A549, H1770, H596, H1975, H1650 and H1299) up-regulated The lncRNA MIR4435-2HG was highly expressed in lung cancer tissues and correlated with histological grades and lymph node metastasis. Phenotypic analysis indicated that MIR4435-2HG knockdown inhibited lung cancer cell proliferation and invasion in vitro and in vivo. Notably, MIR4435-2HG knockdown suppressed the EMT (epithelial-mesenchymal transition) process and cancer stem cell traits of lung cancer cells. Mechanistically, MIR4435-2HG knockdown decreased the transactivation of B-catenin. MIR4435-2HG interacted with B-catenin and thus prevented its degradation by the proteasome system. High expression of lncRNA MIR4435-2HG correlates with lung cancer progression MIR4435-2HG promotes lung cancer cells proliferation and invasion MIR4435-2HG knockdown suppresses the EMT process and cancer stem cell traits MIR4435-2HG knockdown inhibits the B-catenin signalling. Kaplan-Meier analysis of the 52 patients with lung cancer revealed that high MIR4435-2HG expression in lung cancer tissues was significantly correlated with a reduction in overall survival. 29872866 2018 The lncRNA MIR4435-2HG promotes lung cancer progression by activating β-catenin signalling. AK021443 HELLS, ICF4, LSH, Nbla10143, PASG, SMARCA6 NA ENSG00000119969 NA GRCh38_10:94501434-94613905 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues up-regulated We noted that LINC01419 was characterized by a significant increase in transcript expression from dysplasia to early HCC. The lncRNA AK021443 was also up-regulated in advanced HCC samples when compared with early HCC. Moreover, expression of LINC01419 and AK021443 was up-regulated in HCC tissues when compared with non-tumor liver tissue. AF070632 expression was down-regulated in HCC and was decreased in advanced HCC when compared with early HCC. These results suggest that LINC01419 may be related to the initiation of HCC, whereas AK021443 and AF070632 may be associated with the progression of HCC. 26540467 2015 Long non-coding RNA expression profiles of hepatitis C virus-related dysplasia and hepatocellular carcinoma. AK022029 NA NA NA NA GRCh38_6:75121877-75124164 pancreatic cancer C25 NA qPCR etc. pancreatic cancer tissues, cell lines (Sw1990, PANC-1, BXPC-5 etc.) up-regulated We further confirmed the selected 6 up-regulation of LncRNAs in PC tissues and PC cell lines through qPCR. Comparing to 293T cells, the expression of LncRNA AF339813 was significantly increased about 10-fold in PANC-1 cells, 8-fold in SW1990 cells and 8.9-fold in BxCP-3 cells. The other 5 LncRNAs have a certain degree of up-regulation in PC cell lines. 26045769 2015 Downregulation of NUF2 inhibits tumor growth and induces apoptosis by regulating lncRNA AF339813. AK022159 NA NA NA NA GRCh38_3:23438674-23440786 pancreatic cancer C25 NA qPCR etc. pancreatic cancer tissues, cell lines (Sw1990, PANC-1, BXPC-6 etc.) up-regulated We further confirmed the selected 6 up-regulation of LncRNAs in PC tissues and PC cell lines through qPCR. Comparing to 293T cells, the expression of LncRNA AF339813 was significantly increased about 10-fold in PANC-1 cells, 8-fold in SW1990 cells and 8.9-fold in BxCP-3 cells. The other 5 LncRNAs have a certain degree of up-regulation in PC cell lines. 26045769 2015 Downregulation of NUF2 inhibits tumor growth and induces apoptosis by regulating lncRNA AF339813. AK022971 SLCO5A1, OATP-J, OATP-RP4, OATP5A1, OATPJ, OATPRP4, SLC21A15 81796 ENSG00000137571 NA GRCh38_8:69667047-69835064 gastric cancer C16 NA microarray, qPCR etc. primary gastric adenocarcinoma tissues up-regulated For the lncRNAs, the results demonstrated that uc003iqu, uc003tfx, AK022971 and uc.341 were upregulated and that HIV1230, BC011663, AK057054 and M14574 were downregulated in the GC tissues relative to their matched counterparts. 24819045 2014 Integrated analysis of long non-coding RNAs and mRNA expression profiles reveals the potential role of lncRNAs in gastric cancer pathogenesis. AK023391 NA NA NA NA GRCh_8:123500153-123501863 gastric cancer C16 NA qPCR, microarray, western blot gastric cancer tissues, cell lines(HGC-27, AGS, SGC-7901,BGC-823, and MGC-803,GES-1) up-regulated Expression of lncRNA AK023391 was significantly upregulated in gastric cancer samples and cell lines in comparison to adjacent normal tissues, and was positively correlated with poor survival in patients with gastric cancer.AK023391 expression acted as an independent prognostic factor for survival in patients with gastric cancer. Knockdown of AK023391 inhibited cell growth and invasion both in vitro and in vivo, and induced apoptosis and cell cycle arrest in gastric cancer cells,whereas its overexpression reversed these effects. PI3K/Akt signaling mediated the NF-kB, FOXO3a, and p53 pathways. Moreover,downstream transcription factors, such as c-myb, cyclinB1/G2, and BCL-6 might be involved in AK023391-induced tumorigenesis in gastric cancer. 29282102 2017 LncRNA AK023391 promotes tumorigenesis and invasion of gastric cancer through activation of the PI3K/Akt signaling pathway. AK023948 PTCSC1, NCRNA00197, PTCSC 100302522 NA NR_146773 GRCh38_8:133054959-133057767 hepatocellular carcinoma C22.0 M8170/3 qPCR, microarray, Western blot etc. cell lines (HepG2, Hep3B, SNU182, SNU449, MHCC-97H, CL-48) up-regulated In current study, we have unraveled a novel function of AK023948 in HCC. We found that AK023948 was substantially upregulated in tumor tissues. Meanwhile, higher AK023948 expression correlated with poor survival. Upregulation of AK023948 expression can promote HepG2 and Hep3B proliferation and invasion in in vitro experiments. Furthermore, AK023948 also decreased tumor growth in vivo. The tumorigenic role of AK023948 was partially ascribed to PI3K/Akt/mTOR signaling and AK023948 knockdown decreased pathway activation and tumor growth. These data collectively suggest an oncogenic role for AK023948 and may provide potential insight into therapeutic intervention. 29042961 2017 The long non-coding RNA AK023948 enhances tumor progression in hepatocellular carcinoma AK024584 NA NA NA NA GRCh38_14:52286459-52287957 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow down-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. AK027145 NA NA NA NA GRCh38_21:38273476-38275519 gastric cancer C16 NA microarray, qPCR etc. cell lines (SGC-7901, SGC-7901, AGS) down-regulated To confirm the microarray results, we randomly selected two up-regulated lncRNAs (XLOC_000983, XLOC_005104) and six down-regulated lncRNAs (M18204.1, ENST00000548900.1, XLOC_006324, ENST00000420902.1, AK027145, HIX0023999) with log foldchanges > 2 to perform real-time PCR. The results of real-time PCR indicated a consistency of 87.5% between the real-time PCR results and the microarray results in SGC-7901 cells, these also showed a same result between PCR and microarray in AGS cells. 28043146 2017 Microarray analysis of long non-coding RNAs related to microRNA-148b in gastric cancer. AK027193 NA NA NA NA GRCh38_6:89939848-89941740 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow down-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. AK057054 NA NA NA NA GRCh38_9:38142493-38142631 gastric cancer C16 NA microarray, qPCR etc. primary gastric adenocarcinoma tissues down-regulated For the lncRNAs, the results demonstrated that uc003iqu, uc003tfx, AK022971 and uc.341 were upregulated and that HIV1230, BC011663, AK057054 and M14574 were downregulated in the GC tissues relative to their matched counterparts. 24819045 2014 Integrated analysis of long non-coding RNAs and mRNA expression profiles reveals the potential role of lncRNAs in gastric cancer pathogenesis. AK093543 NA NA NA NA GRCh38_2:101018542-101019779 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues down-regulated To validate the microarray analysis results, five lncRNAs were randomly selected from the differential lncRNAs and their expressions were analyzed using qPCR in 29 pairs of HCC and matched NT tissues. Our data indicated that the expressions of TCONS_00018278, AK093543, D16366 and ENST00000501583 were significantly downregulated in HCC, whereas the expression of NR_002819 showed no significant difference. 24876753 2014 LncRNAs expression signatures of hepatocellular carcinoma revealed by microarray. AK09398 NA NA NA NA NA small cell lung cancer C56.9 M8441/3 qPCR etc. SCLC tissues up-regulated The expression of LncRNA AK09398 in lung cancer tissues was (7.813±0.373). This value was significantly increased in paracarcinoma tissues (1.782±0.116) and normal lung tissues (1.209±0.200). 27866518 2016 Expression of LncRNA AK09398 and Relationship with Prognosis in Patients with Small Cell Lung Cancer. AK094982 NA NA NA NA GRCh38_15:31475404-31478502 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow down-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML. 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. AK095147 NA NA NA NA GRCh38_13:36843533-36845846 nasopharyngeal cancer C11 NA microarray, qPCR, RNAi etc. nasopharyngeal carcinoma tissues, cell lines (CNE-2 etc.) down-regulated qPCR results were consistent with the microarray analysis results of six lncRNAs (AF086415, AK095147, RP1-179N16.3, MUDENG, AK056098, and AK294004) in terms of regulation direction and significance. 24379026 2014 Curcumin enhances the radiosensitivity in nasopharyngeal carcinoma cells involving the reversal of differentially expressed long non-coding RNAs. AK096174 NA NA NA NA GRCh38_12:121794810-121797029 gastric cancer C16 NA Microarray, qPCR, Western blot etc. gastric cancer tissues, cell lines (GES-1, SGC-7901, MGC-803, MKN-28, AGS and BGC-823) up-regulated We identified a novel lncRNA, AK096174, which was upregulated and associated with tumorigenesis, tumor size, metastasis, and poor prognosis in gastric cancer. Our data showed that AK096174 was highly expressed in the gastric cancer tissues and cell lines (SGC-7901, AGS, BGC-823, MGC-803), and patients with higher AK096174 expression had a poorer prognosis and shorter overall survival. AK096174 knockdown inhibited the proliferation, migration and invasiveness in SGC-7901 and BGC-823 cells, whereas AK096174 overexpression had the promoting effects. Furthermore, mechanistic investigation showed that AK096174 positively correlated with the expression of WD repeat-containing protein 66 (WDR66) gene at the translational level. Knockdown of WRD66 attenuated the positive impact of AK096174 in gastric cancer cells. 29717028 2018 Long non-coding RNA AK096174 promotes cell proliferation and invasion in gastric cancer by regulating WDR66 expression. AK123657 NA NA NA NA GRCh38_11:17381406-17383531 colorectal cancer C19.9 NA microarray, qPCR, RNAi etc. cell lines (HCT116 ,SW1116) down-regulated Functional experiments demonstrated three dysregulated lncRNAs, AK123657, BX648207 and BX649059 were required for efficient invasion and proliferation suppression in CRC cell lines. 24809982 2014 A long non-coding RNA signature to improve prognosis prediction of colorectal cancer. AK123765 TTF2, HuF2, ZGRF6 8458 ENSG00000116830 NA GRCh38_1:117060303-117107453 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow up-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML/ 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. AK123790 NA NA NA NA GRCh38_1:226697684-226700465 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RIP, RNA pull-down assay etc. HCC tissues down-regulated AY129027, uc002pyc and DQ786243 were over-expressed in HCC, whereas the expression of AK055007 and AK123790 was decreased. 21769904 2011 Long noncoding RNA high expression in hepatocellular carcinoma facilitates tumor growth through enhancer of zeste homolog 2 in humans. AK124454 LOC105372310 NA NA NA GRCh38_19:20220597-20222169 breast cancer C50 NA microarray, qPCR, RNAi, Cell proliferation assay, Cell invasion assay etc. breast cancer tissues, cell lines (MDA-MB-231, BT549, Hs578T and 293T) up-regulated lncRNAs HIF1A-AS2 and AK124454 could promote cell proliferation and invasion, and attenuate G2-M arrest, which might contribute to paclitaxel resistance in TNBC cells. 26921339 2016 Transcriptome Analysis of Triple-Negative Breast Cancer Reveals an Integrated mRNA-lncRNA Signature with Predictive and Prognostic Value. AK124936 FAM47E NA ENSG00000189157 NA GRCh38_4:76214040-76283780 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow up-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. AK124939 NA NA NA NA GRCh38_15:80198797-80200629 glioblastoma NA M9440/3 qPCR etc. GNS cell lines differential expression In addition, we detected 28 differentially expressed long non-coding RNAs 23046790 2012 Digital transcriptome profiling of normal and glioblastoma-derived neural stem cells identifies genes associated with patient survival AK126698 NA NA NA NA NA non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. NSCLC tissues, cell lines (A549, NCI-H520, and H1299) down-regulated Our results showed that lncRNA AK126698 was significantly downregulated in NSCLC tissues, compared with paired adjacent nontumor tissue samples. Furthermore, lower AK126698 expression was associated with larger tumor size and advanced tumor stage. Ectopic AK126698 expression inhibited cell proliferation and migration and induced apoptosis. Conversely, decreased AK126698 expression promoted cell proliferation and migration and inhibited cell apoptosis. Importantly, we demonstrated that Frizzled-8, a receptor of Wnt/B-catenin pathway, was a target of AK126698. Furthermore, AK126698 could inhibit the activation of Wnt/B-catenin pathway, which was demonstrated by measuring the expression levels of Axin1, B-catenin, c-myc, cyclin D1, and E-cadherin. 27445486 2016 Long noncoding RNA AK126698 inhibits proliferation and migration of non-small cell lung cancer cells by targeting Frizzled-8 and suppressing Wnt/B-catenin signaling pathway. AK130275 PAX8-AS1 654433 ENSG00000189223 NR_015377 GRCh38_2:113211522-113276581 thyroid cancer C73.9 NA qPCR, Western blot, etc. cell lines (BHT101, BCPAP) up-regulated whereas thyroid cancer patients with higher PAX8-AS1 or lower CRYM-AS1 expression levels had shorter RFS time 29923329 2018 Identification of differential expressed lncRNAs in human thyroid cancer by a genome-wide analyses. AK294004 ORAOV1, TAOS1 220064 ENSG00000149716 NA GRCh38_11:69653076-69675416 nasopharyngeal cancer C11 NA microarray, qPCR, RNAi etc. nasopharyngeal carcinoma tissues, cell lines (CNE-2 etc.) up-regulated qPCR results were consistent with the microarray analysis results of six lncRNAs (AF086415, AK095147, RP1-179N16.3, MUDENG, AK056098, and AK294004) in terms of regulation direction and significance. 24379026 2014 Curcumin enhances the radiosensitivity in nasopharyngeal carcinoma cells involving the reversal of differentially expressed long non-coding RNAs. AKR7L AKR7L, AFAR3, AFB1-AR 3, AFB1-AR3, AKR7A4 246181 ENSG00000211454 NA GRCh38_1:19265982-19274194 gastric cancer C16 NA microarray, qPCR, RNAi etc. gastric cancer tissues down-regulated LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC. 25765901 2015 Reciprocal repression between TUSC7 and miR-23b in gastric cancer. AL359062 COL8A1, C3orf7 1295 ENSG00000144810 NA GRCh38_3:99638475-99799226 nasopharyngeal cancer C11 NA microarray, qPCR etc. NPC tissues up-regulated All four lncRNAs (LOC84740, ENST00000498296, AL359062, and ENST00000438550) were differentially expressed in the metastatic and primary NPC tumors based on microarray analysis, which was validated via QPCR using the same tissues. The validation results of the four lncRNAs indicated that the microarray data strongly correlated with the QPCR results. These lncRNAs displayed higher expression levels in NPC primary tumors with progression than in those without progression. 26448942 2015 Long Noncoding RNA Expression Signatures of Metastatic Nasopharyngeal Carcinoma and Their Prognostic Value. AL389956 NA NA NA NA GRCh38_8:123523808-123525468 pancreatic cancer C25 NA qPCR etc. pancreatic cancer tissues, cell lines (Sw1990, PANC-1, BXPC-7 etc.) up-regulated We further confirmed the selected 6 up-regulation of LncRNAs in PC tissues and PC cell lines through qPCR. Comparing to 293T cells, the expression of LncRNA AF339813 was significantly increased about 10-fold in PANC-1 cells, 8-fold in SW1990 cells and 8.9-fold in BxCP-3 cells. The other 5 LncRNAs have a certain degree of up-regulation in PC cell lines. 26045769 2015 Downregulation of NUF2 inhibits tumor growth and induces apoptosis by regulating lncRNA AF339813. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 pancreatic cancer C25 NA qPCR, Cell transfection, Western blot, Cell migration and invasion assay etc. cell lines (PANC1, Miapaca II, HPDE6-C7) up-regulated ANRIL expression in the PC cells was higher than in normal pancreatic duct epithelial cells. By inhibiting the ATM-E2F1 signaling pathway in PC cells, E-cadherin expression increased but N-cadherin and Vimentin expressions decreased. After ANRIL was silenced or the ATM-E2F1 signaling pathway inhibited, PC cell migration and invasion abilities were decreased. 28344092 2017 The over expression of long non-coding RNA ANRIL promotes epithelial-mesenchymal transition by activating the ATM-E2F1 signaling pathway in pancreatic cancer: An in vivo and in vitro study. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 ovarian cancer C56.9 NA qPCR, Western blot etc. cell lines (SKOV3, OVCAR3, A2780, Hey, OVCA429 and OVCA433) up-regulated we evaluated ANRIL expression in epithelial ovarian cancer (EOC) and defined its clinical implications and biological functions. ANRIL was overexpressed in EOC tissues relative to normal controls. Overexpression correlated with advanced International Federation of Gynecologists and Obstetricians stage and high histological grade. Multivariate analysis indicated that ANRIL is an independent prognostic factor for overall survival in EOC. Gain- and loss-of-function experiments demonstrated that ANRIL promotes EOC cell proliferation both in vitro and in vivo. The proliferative effect was linked to the promotion of cell cycle progression and inhibition of apoptosis and senescence. Down-regulation of P15INK4B and up-regulation of Bcl-2 by ANRIL may partially explain ANRIL-induced EOC cell proliferation 27095571 2016 The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 lung cancer C34 NA qPCR, RNAi, Western blot, Cell apoptosis assay etc. cell lines (H460, H1975, HCT116, BEAS2B) up-regulated The expression level of ANRIL was increased up to 13.6-fold by PLD inhibition in H460 human lung cancer cells. Moreover, knockdown of ANRIL using its specific small-interfering RNA significantly suppressed PLD inhibition-induced apoptosis. Collectively, our findings showed that ANRIL is an lncRNA responsible in anti-tumorigenesis caused by PLD inhibition and combined incorporation of ANRIL into PLD inhibition-induced anti-tumorigenic signaling network could be a new effective therapeutic approach for controlling lung cancer. 25964559 2015 Down-regulation of Phospholipase D Stimulates Death of Lung Cancer Cells Involving Up-regulation of the Long ncRNA ANRIL. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 triple negative breast cancer C50 NA qPCR, Luciferase reporter assay, RIP. triple-negative breast cancer tissues, cell lines (MDA-MB-231, MDA-MB-468, MDA-MB-453,TB-549,MCF-7 and TD-47) up-regulated Expression level of ANRIL was up-regulated in TNBC tumor tissue and cell lines compared to noncancerous tissue and non-TNBC cells.the up-regulated ANRIL expression was closely correlated to poor prognosis.ANRIL knockdown interfered by interference oligonucleotide could markedly suppress TNBC cells proliferation and enhance apoptosis. ANRIL overexpression modulated TNBC tumorigenesis through acting as molecular 'sponge' for miR-199a. 28961506 2017 Long non-coding RNA ANRIL promotes carcinogenesis via sponging miR-199a in triple-negative breast cancer. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 renal cell carcinoma C64.9 NA qPCR, RNAi, Western blot, Cell migration and invasion assay, CCK-8 assay etc. RCC tissues, cell lines (786-O, A498, caki-1 and caki-2, and HEK-293T) up-regulated ANRIL was highly expressed in RCC tissues and RCC cell lines. ANRIL significantly promoted cell proliferation, migration, invasion and EMT but inhibited cell apoptosis. Additionally, the expression levels of B-catenin, Ki-67, glycogen synthase kinase 3B (GSK-3B), phosphorylated GSK-3B, T cell transcription factor 4 (TCF-4) and leukemia enhancer factor 1 (LEF-1) were all markedly up-regulated by ANRIL. 28251886 2017 Highly Expressed Antisense Non-coding RNA in the INK4 Locus Promotes 5 Growth and Invasion of Renal Clear Carcinoma Cells Via the B-catenin Pathway. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 gallbladder cancer C23.9 NA qPCR, Western blot etc. GBC tissues, GBC cell lines (GBC-SD and QBC940) down-regulated The effects of MEG3 and ANRIL were also verified in mice. Compared with normal tissues, the expression of MEG3 was significantly lower in GBC tissues, whereas the expression of ANRIL was significantly higher. The overexpression of MEG3 and underexpression of ANRIL were significantly associated with GBC prognosis. The expressions of MEG3 and ANRIL were higher in pcDNA-MEG3 and pcDNA-ANRIL-transfected cells than in empty vector-transfected cells in vitro. Most of the pcDNA-MEG3-transfected cells were in the G0-G1 phase, which showed reduced cell activity and clone counts and increased p53 and decreased cyclin D1, whereas the pcDNA-ANRIL-transfected cells were mostly in the S phase and showed contrasting behavior. Mice injected with pcDNA-MEG3-transfected cells had smaller and lighter tumors, decreased ki-67 levels, and increased caspase 3 levels, whereas those injected with pcDNA-ANRIL showed contrasting results. MEG3 can inhibit the proliferation of GBC cells and promote apoptosis, whereas ANRIL can improve the proliferation of gallbladder cells and inhibit apoptosis 26812694 2016 Expression and mechanisms of long non-coding RNA genes MEG3 and ANRIL in gallbladder cancer ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 thyroid cancer C73.9 NA qPCR, RNAi, Western blot etc. thyroid cancer tissues, cell lines (K1, TPC-1, SW579 and Nthy-ori 3-1) up-regulated The results of qRT-PCR showed significantly higher expression of ANRIL mRNA in the TC tissues relative to the adjacent normal tissues. ANRIL may reduce p15INK4B expression through inhibiting TGF-B/Smad signaling pathway, promoting invasion and metastasis of TC cells, and the silencing of ANRIL inhibits the invasion and metastasis of TPC-1 cells. 27507052 2016 Long non-coding RNA ANRIL promotes the invasion and metastasis of thyroid cancer cells through TGF-B/Smad signaling pathway. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 bladder cancer C67 NA qPCR, RNAi, Western blot etc. urine, cell lines (SV-HUC, 5637, TCC-SUP, T24, UMUC3, HT1376, J82, and RT4) up-regulated In comparison to the level of expression of these selected lncRNA and mRNA in the control SV-40 immortalized non-tumorigenic urothelial cell line SV-HUC, we found elevated expression of HOTAIR, HOXA-AS-2, ANRIL, and HOXA13 in T24 UBC cells. While in TCC-SUP UBC cell line we found HOTAIR, HOX-AS-2, linc-RoR, ANRIL and HOXA13 were elevated 26800519 2016 Expression of the Long Non-Coding RNA HOTAIR Correlates with Disease Progression in Bladder Cancer and Is Contained in Bladder Cancer Patient Urinary Exosomes. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 serous ovarian cancer C56.9 M8441/3 qPCR, RNAi, Western blot etc. SOC tissues, cell lines (SK-OV-3, HO8910) up-regulated We found that ANRIL levels were elevated in SOC tissues compared with normal controls and were highly correlated with advanced FIGO stage, high histological grade, lymph node metastasis, and poor prognosis. Functional studies suggest a critical role of ANRIL in the control of SOC cell migration/invasion at least in part through regulation of MET and MMP3. 25845387 2015 Long non-coding RNA ANRIL predicts poor prognosis and promotes invasion/metastasis in serous ovarian cancer. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 esophageal squamous cell cancer NA NA qPCR, RNAi, Western blot etc. ESCC tissues, cell lines (TE1, ECA109) up-regulated Compared with matched adjacent non-tumor tissues, the expression levels of ANRIL in ESCC tissues were significantly increased. Furthermore, inhibition of ANRIL was found to increase the expression of p15(INK4b) and TGFB1 and depletion of ANRIL in ESCC cell lines may inhibit cellular proliferation. 24747824 2014 ANRIL inhibits p15(INK4b) through the TGFB1 signaling pathway in human esophageal squamous cell carcinoma. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Northern blot etc. cell lines (HT29, SW480, HCT116 and LoVo) up-regulated ANRIL was overexpressed in colorectal cancer. By statistical analysis, increased ANRIL was found to be in close association with TNM staging, Duke staging and lymphatic metastasis and poor prognosis. Through down-regulation of the overexpressed ANRIL, lymphangiogenesis may be suppressed and therefore lymphatic metastasis may be inhibited. 27286457 2016 Downregulation of long non-coding RNA ANRIL suppresses lymphangiogenesis and lymphatic metastasis in colorectal cancer. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 nasopharyngeal cancer C11 NA RT-qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP NPC cell lines (C666-1, SUNE-1, CNE1, CNE2 and HNE-1) up-regulated Mechanistically, SOX2 binds with ANRIL and increases its RNA level, which upregulates B-catenin signalling, resulting in enhanced nasopharyngealcarcinoma tumourigenesis. Expression levels of ANRIL are positively correlated with SOX2 and B-catenin in clinical nasopharyngeal carcinoma samples.The transcription factor SOX2 is widely recognized for its pivotal roles during mammalian embryogenesis. 29463902 2018 Upregulation of SOX2-activated lncRNA ANRIL promotes nasopharyngeal carcinoma cell growth. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP etc. gastric cancer tissues, cell lines (SGC7901, BGC823, MGC803) up-regulated Higher expression of ANRIL was significantly correlated with a higher TNM stage and tumor size. Further experiments revealed that ANRIL knockdown significantly repressed the proliferation both in vitro and in vivo. We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation. 24810364 2014 Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 colorectal cancer C19.9 NA qPCR, RNAi etc. CRC tissues, cell lines (HT29 and RKO) up-regulated The CRC tissues were revealed to express higher levels of ANRIL lncRNA compared with the adjacent non-neoplastic tissues. Furthermore, high ANRIL expression was significantly associated with reduced survival rate. ANRIL gene expression was successfully silenced in human CRC cells. ANRIL knockdown decreased proliferation, inhibited migration and invasion, and reduced the colony-forming ability of the cells. 27314206 2016 ANRIL is associated with the survival rate of patients with colorectal cancer, and affects cell migration and invasion in vitro. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 gastric cancer C16 NA qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. gastric cancer tissues, cell lines (MGC803, AGS, and MKN-28) up-regulated Here, we found that lncRNA-ANRIL was upregulated in human gastric cancer tissues. We demonstrate that TET2 inhibits the proliferation and colony formation of human gastric cancer cells. Overexpression of TET2 induces apoptosis in human gastric cancer cells. The mechanism study shows that TET2 binds to the promoter region of the oncogenic long noncoding RNA (lncRNA-ANRIL) and regulates the expression of ANRIL and its downstream genes (INK4a, INK4b, and ARF). Finally, we demonstrate that ANRIL knockdown blocks the effects of TET2 on gastric cancer cell proliferation and colony formation 27027260 2016 TET2 regulates LncRNA-ANRIL expression and inhibits the growth of human gastric cancer cells. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 osteosarcoma NA M9180/3 qRT-PCR, Western blot, in vitro knockdown The tumor tissues, Human OS cell lines (MNNG/HOS and U2 OS) up-regulated The expression level of ANRIL was significantly increased in OS tissues than in the adjacent normal tissues. 33 patients were included in the high expression group and the other 24 patients were included in the normal expression group. ANRIL expression was significantly associated with tumor size (5.7cm±2.4cm vs. 4.3cm±1.7cm, p=0.02) and the 5-year survival rate (51.5% vs. 79.1%, p=0.03). Knockdown of ANRIL could significantly induce cell apoptosis and inhibit cell proliferation and invasion. Moreover, knockdown of ANRIL could significantly decrease the expression level of phosphorylated PI3K and AKT in OS cells. 29520337 2018 Long non-coding RNA ANRIL is associated with a poor prognosis of osteosarcoma and promotes tumorigenesis via PI3K/Akt pathway. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 cervical cancer C53 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. cervical cancer tissues, cell lines (HeLa, CaSki, SiHa, ME-180) up-regulated The expression of lncRNA ANRIL was significantly increased both in cervical cancer tissues and cell lines. Patients with high ANRIL expression had advanced FIGO stage, lymph node metastasis and poor overall survival than those with low ANRIL expression. Loss-of-function experiments showed that decreased expression of ANRIL inhibited cell proliferation, migration and invasion of cervical cancer. Finally, western blot indicated that the PI3K/Akt pathway was found to be inactivated in cervical cancer cells after ANRIL inhibition. 27899255 2017 Long non-coding RNA ANRIL indicates a poor prognosis of cervical cancer and promotes carcinogenesis via PI3K/Akt pathways. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 nasopharyngeal cancer C11 NA qPCR, RNAi, Western blot, MTT assay etc. NPC tissues, cell lines (NP69 and N5-Tert) up-regulated In this study, we report that LncRNA ANRIL generally up-regulated in nasopharyngeal carcinoma. ANRIL was highly expressed in advanced-stage cancer. Further investigation showed that knockdown of ANRIL significantly repressed NPC cell proliferation and transformation. We also found that ANRIL could induce the percentage of side population cells (SP cells) in NPC. 27557514 2016 LncRNA ANRIL is up-regulated in nasopharyngeal carcinoma and promotes the cancer progression via increasing proliferation, reprograming cell glucose metabolism and inducing side-population stem-like cancer cells. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. NSCLC tissues, cell lines (SK-MES-1, A549, SPC-A1, and NCI-H1975) up-regulated The high expression level of ANRIL was positively correlated with advanced tumor-node-metastasis stage and greater tumor diameter. Furthermore, chromatin immunoprecipitation assays confirmed the physical interaction between c-Myc and ANRIL. ANRIL silencing significantly inhibited NSCLC cell proliferation. 27307748 2016 Long noncoding RNA ANRIL could be transactivated by c-Myc and promote tumor progression of non-small-cell lung cancer. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Cell proliferation assay etc. NSCLC tissues, cell lines (A549, SPC-A1, NCI-H1650) up-regulated The expression level of lncRNA ANRIL was higher in NSCLC tissues and lung cancer cells than in adjacent non-tumor tissues and normal human bronchial epithelial cells. Higher expression of lncRNA ANRIL in NSCLC tissues was associated with higher TNM stage and advanced lymph node metastasis. Patients with high lncRNA ANRIL expression had poorer overall survival compared with low lncRNA ANRIL group. Moreover, knockdown of lncRNA ANRIL expression could inhibit lung cancer cell proliferation, migration and invasion in vitro. 25889788 2015 Increased expression of the long non-coding RNA ANRIL promotes lung cancer cell metastasis and correlates with poor prognosis. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. NSCLC tissues, cell lines (PC9, SPC-A1, NCI-H1975, H1299, H358) up-regulated In this study, we reported that ANRIL expression was increased in NSCLC tissues and Its expression level was significantly correlated with TNM stages and tumor size. Moreover, patients with high levels of ANRIL expression had a relatively poor prognosis. In addition, taking advantage of loss of function experiments in NSCLC cells, we found that knockdown of ANRIL expression could impair cell proliferation and induce cell apoptosis both in vitro and vivo. 25504755 2014 Long noncoding RNA ANRIL promotes non small cell lung cancer cells proliferation and inhibits apoptosis by silencing KLF2 and P21 expression. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. HCC tissues, cell lines (HepG2, Hep3B, MHCC-97H, L02) up-regulated ANRIL expression was up-regulated in HCC tissues, and the higher expression of ANRIL was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. clonogenic survival was significantly decreased following inhibition of ANRIL both in HepG2 and Hep3B cell lines. 29029488 2017 Erratum to: Long non-coding RNA ANRIL is upregulated in hepatocellular carcinoma and regulates cell proliferation by epigenetic silencing of KLF2. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi etc. HCC tissues, cell lines (HepG2 etc.) up-regulated LncRNA ANRIL expression in HCC tissues was significantly higher than in the adjacent non-tumor tissues. The expression of lncRNA ANRIL was remarkably associated with the histologic grade and TNM stage of HCC patients. In addition, HCC patients with higher lncRNA ANRIL expression had significantly poorer overall survival. Moreover, in vitro assays revealed that the decreased expression of lncRNA ANRIL could suppress the cell proliferation, migration and invasion HCC cells. 26045820 2015 High expression of long non-coding RNA ANRIL is associated with poor prognosis in hepatocellular carcinoma. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 glioblastoma NA M9440/3 qPCR etc. GNS cell lines up-regulated In addition, we detected 27 differentially expressed long non-coding RNAs 23046790 2012 Digital transcriptome profiling of normal and glioblastoma-derived neural stem cells identifies genes associated with patient survival AOC4P AOC4P, AOC4, UPAT 90586 ENSG00000260105 NA GRCh38_17:42865922-42874369 colon cancer C18 NA qPCR, RNAi, RIP, RNA pull-down assay etc. cell lines (HCT116, DLD-1, RKO, HAEC, HaCaT and 293FT) up-regulated Here we show that an lncRNA termed UPAT is required for the survival and tumorigenicity of colorectal cancer cells. UPAT expression was up-regulated in highly tumorigenic colon cancer cell lines compared with weakly tumorigenic colon cancer cell lines and normal cell lines. UPAT interacts with and stabilizes the epigenetic factor UHRF1 by interfering with its B-transducin repeat-containing protein (TrCP)-mediated ubiquitination. Furthermore, we demonstrate that UHRF1 up-regulates Stearoyl-CoA desaturase 1 and Sprouty 4, which are required for the survival of colon tumor cells. 26768845 2016 Long noncoding RNA UPAT promotes colon tumorigenesis by inhibiting degradation of UHRF1. AP000459 AP000459.7 NA NA NA GRCh38_21:23477641-23490724 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated To confirm the reliability and validity of the microarray data, we selected 14 differentially expressed key lncRNAs and analyzed their actual expression levels in 30 advanced GC samples and paired adjacent non-tumor tissue samples with qRT-PCR. Results showed that, RP5-919F19, CTD-2541M15 and UCA1 expression was significantly higher in carcinoma than in adjacent non-tumor tissues. AP000459, LOC101928316, RP11-167N4 and LINC01071 expression was significantly lower in carcinoma than in adjacent non-tumor tissues. 26718650 2016 Differential expression profiles of long non-coding RNAs reveal potential biomarkers for identification of human gastric cancer. AP001439.2 AP001439.2 NA ENSG00000224541 NA GRCh38_21:26158091-26175824 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. ARNILA NA NA NA NA NA triple negative breast cancer C50 NA Microarray, qPCR, Luciferase reporter assay, Western blot, ChIP etc. triple negative breast cancer tissues, cell line (MDA-MB-231 and Hs578T) up-regulated We performed experiments with or without DHT treatment in three TNBC cell lines, and we identified an AR negatively induced lncRNA (ARNILA), which correlated with poor progression-free survival (PFS) in TNBC patients and promoted epithelial-mesenchymal transition (EMT), invasion and metastasis in vitro and in vivo. Subsequently, we demonstrated that ARNILA functioned as a competing endogenous RNA (ceRNA) for miR-204 to facilitate expression of its target gene Sox4, which is known to induce EMT and contribute to breast cancer progression, thereby promoting EMT, invasion and metastasis of TNBC. High ARNILA expression was correlated with poor PFS(HR, 2.72; 95%CI, 1.26?5.70; P = 0.012) in TNBC. 29844570 2018 An androgen receptor negatively induced long non-coding RNA ARNILA binding to miR-204 promotes the invasion and metastasis of triple-negative breast cancer. ASAP1-IT1 ASAP1-IT1, ASAP1-IT, ASAP1IT, ASAP1IT1, DDEF1IT1, HSPC054, NCRNA00050 29065 NA NR_002765 NA epithelial ovarian cancer C56.9 NA qPCR etc. primary EOC tissues differential expression We observed high expression of ASAP1-IT1, FAM215A and LINC00472 more frequently in low grade tumors and early stage disease compared to high grade tumors and late stage disease, respectively. 27667152 2016 Long non-coding RNAs, ASAP1-IT1, FAM215A, and LINC00472, in epithelial ovarian cancer. ASAP1-IT1 ASAP1-IT1, ASAP1-IT, ASAP1IT, ASAP1IT1, DDEF1IT1, HSPC054, NCRNA00050 29065 NA NR_002765 NA cholangiocarcinoma NA M810/3 qPCR, Western blot etc. cholangiocarcinoma tissues, cell lines (HuH-28, QBC939, HuCCT1, CCLP1 and RBE) up-regulated The high expression level of ASAP1-IT1 was tested in Cholangiocarcinoma tissues and cells with qRT-PCR. Upregulation of ASAP1-IT predicted the unfavorable prognosis for Cholangiocarcinoma patients. Next, ASAP1-IT1 was knocked down in cancerous cells for loss-of function assay. MTT, colony formation and transwell and western bot assays were performed to demonstrate the specific impacts of ASAP1-IT1 on proliferation, migration and EMT progression of Cholangiocarcinoma Cells. As a results, the Cholangiocarcinoma progression was inhibited. Hedgehog signaling pathway has been discovered to be a treatment target in Cholangiocarcinoma. In this study, the interaction between ASAP1-IT1 and hedgehog pathway was specifically investigated. Smo and Gli1, two hedgehog-related proteins were examined in Cholangiocarcinoma cells. The results of qRT-PCR and western blot assay suggested that ASAP1-IT1 could positively modulate Smo and Gli1 in Cholangiocarcinoma. Finally, rescue assays were carried out to prove that ASAP1-IT1 could improve Cholangiocarcinoma progression and development via hedgehog signaling pathway. 29653361 2018 LncRNA ASAP1-IT1 positively modulates the development of cholangiocarcinoma via hedgehog signaling pathway. ASAP1-IT1 ASAP1-IT1, ASAP1-IT, ASAP1IT, ASAP1IT1, DDEF1IT1, HSPC054, NCRNA00050 29065 NA NR_002765 NA bladder cancer C67 NA qPCR, Western blot bladder cancer tissues, cell lines (T24, J82, UMUC3, RT4 and 5637) up-regulated In our study, we found that an uncharacterized lncRNA, ASAP1-IT1, was overexpressed in UBC tissues compared with adjacent non-malignant tissues. High ASAP1-IT1 expression levels in UBC specimens were correlated with advanced tumor stage, higher clinical stage, poor pathological differentiation and bad overall survival. 28895409 2017 Long noncoding RNA ASAP1-IT1 promotes cancer stemness and predicts a poor prognosis in patients with bladder cancer ASHGA5P014632 AL589743.1, PCAN-2 NA ENSG00000244306 NA GRCh38_14:19284653-19337730 breast cancer C50 NA qPCR, RNAi etc. breast cancer tissues, cell line (MCF-7) up-regulated The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines. 27322459 2016 Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis. ASO1937 NA NA NA NA NA astrocytoma NA M9400/3 qPCR etc. astrocytoma tissues down-regulated Our analysis ultimately generated a list of 7 lncRNAs that were differentially expressed in astrocytomas in comparison to the NAT samples. Among these lncRNAs, ENST00000244906, ENST00000545440, NR_002809 and ENST00000436616 were shown to be upregulated by a factor greater than twofold, whereas 3 lncRNAs, XLOC_010967, BC002811 and ASO1937, were shown to be downregulated by a factor greater than two-fold. 26252651 2016 The Use of Three Long Non-Coding RNAs as Potential Prognostic Indicators of Astrocytoma. AWPPH NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RIP, ChIP etc. HCC tissues, cell lines (QSG-7701, SMMC-7721, HCCLM3, Huh7, HepG2, QSG-7701 and SMMC-7721) up-regulated High AWPPH expression is an independent prognostic factor for poor recurrence-free and overall survival. AWPPH promotes HCC cell proliferation and migration in vitro, and tumor growth and metastasis in vivo. AWPPH interacts with YBX1, promotes YBX1-mediated activation of SNAIL1 translation, and upregulates SNAIL1 expression.To identify lncRNAs involved in the progression and prognosis of HCC, we analyzed online-available data sets, including GSE54238 (lncRNAs microarray data of 30 noncancerous hepatic tissues and 23 HCC tissues) and GSE40144 (lncRNAs microarray data of 59 HCC tissues with disease-free survival and overall survival information). 28428004 2017 Long noncoding RNA AWPPH promotes hepatocellular carcinoma progression through YBX1 and serves as a prognostic biomarker. AY129027 LINC01451, HCCAT4 401561 ENSG00000279141 NR_135288 GRCh38_9:136612024-136617181 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RIP, RNA pull-down assay etc. HCC tissues up-regulated AY129027, uc002pyc and DQ786243 were over-expressed in HCC, whereas the expression of AK055007 and AK123790 was decreased. 21769904 2011 Long noncoding RNA high expression in hepatocellular carcinoma facilitates tumor growth through enhancer of zeste homolog 2 in humans. BAIAP2-AS1 BAIAP2-AS1 NA ENSG00000226137 NA GRCh38_17:81029130-81034881 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RNAi etc. HCC tissues up-regulated To validate expression of the 6 HH-lncRNAs, qRT-PCR was performed in a cohort of 20 HCC patients, including 10 primary HCC and 10 HBV-related HCC. Expression of 6 HH-lncRNAs validated by qRT-PCR was consistent with microarray results. 27285756 2016 Comprehensive analysis of long non-coding RNA expression profiles in hepatitis B virus-related hepatocellular carcinoma. BALR-6 NA NA NA NA NA B-lymphoblastic leukemia NA M9811/3 qPCR, RNAi, Northern blot etc. cell lines (MV, Reh, 697, Nalm-6, 70Z/3, HEK 293) up-regulated Overexpression of BALR-6 in murine bone marrow transplantation experiments caused a significant increase in early hematopoietic progenitor populations, suggesting that its dysregulation may cause developmental changes. Notably, the knockdown of BALR-6 resulted in global dysregulation of gene expression. The gene set was enriched for leukemia-associated genes, as well as for the transcriptome regulated by Specificity Protein 1 (SP1). We confirmed changes in the expression of SP1, as well as its known interactor and downstream target CREB1. Luciferase reporter assays demonstrated an enhancement of SP1-mediated transcription in the presence of BALR-6. These data provide a putative mechanism for regulation by BALR-6 in B-ALL 26694754 2015 BALR-6 regulates cell growth and cell survival in B-lymphoblastic leukemia BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 gastric adenocarcinoma C16 M8140/3 qPCR, RNAi, Western blot, MTT assay etc. gastric adenocarcinoma tissues, cell lines (BGC823, SGC7901) up-regulated BANCR expression was significantly up-regulated in gastric tumor tissues and gastric cell lines. Down-regulation of BANCR inhibited gastric cancer cell growth and promoted cell apoptosis, and it also contributed to a significant decrease of NF-B1 (P50/105) expression and 3'UTR of NF-B1 activity. Overexpression of NF-B1 reversed the effect of BANCR on cancer cell growth and apoptosis. MiroRNA-9 (miR-9) targeted NF-B1, and miR-9 inhibitor also reversed the effects of BANCR on gastric cancer cell growth and apoptosis. 26248136 2015 BRAF activated non-coding RNA (BANCR) promoting gastric cancer cells proliferation via regulation of NF-B1. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 thyroid cancer C73.9 NA Western blot PTC tissues, adjacent normal tissues, thyroid cancer cell lines (WRO, CAL-62, BCPAP and FTC-133.) up-regulated Overexpression of BANCR promoted the migration and invasion of BCPAP cells. Additionally, BANCR mediated epithelial-mesenchymal transition (EMT) by regulating the expression of epithelial (E)-cadherin, vimentin and neuronal (N)-cadherin. Overexpression of BANCR in BCPAP cells decreased the expression of E-cadherin and increased the expression of vimentin, N-cadherin, phospho (p)-c-Raf, p-extracellular-signal-regulated kinase (ERK)/mitogen activated protein kinase (MEK)1/2 and p-ERK1/2. Administration of U0126 inhibitor inhibited the regulation of phosphorylation levels by MEK1/2 and ERK1/2. Additionally, U0126 upregulated the expression of E-cadherin and downregulated the expression of vimentin. BANCR induces EMT in PTC through the Raf/MEK/ERK signaling pathway. 29552216 2018 lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 esophageal squamous cell cancer NA NA qPCR etc. ESCC tissues, cell lines (KYSE-30, KYSE-70, KYSE-140, KYSE-150, KYSE-450, KYSE-510, TE-10 and TE-12) up-regulated BANCR levels in plasma were significantly higher in ESCC patients than in normal controls and correlated well with the presence of tumor status. Besides, BANCR expression increased significantly from low to high-grade intraepithelial neoplasia. Additionally, increased BANCR expression was associated with worse histologic grade, advanced TNM stage, more lymph node metastasis, and shorter survival of ESCC patients. The expression level of BANCR reverts to normal after the tumor has been resected, and the expression level of BANCR increased with the disease progression. 27470379 2016 Upregulation of the long non-coding RNA BANCR correlates with tumor progression and poor prognosis in esophageal squamous cell carcinoma. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 retinoblastoma C69.2 M9510/3 qPCR, RNAi etc. retinoblastoma tissues, cell lines (Weri-Rb1, Y79) up-regulated In our results, lncRNA BANCR is overexpressed in retinoblastoma tissues and cell lines and is associated with tumor size, choroidal invasion, and optic nerve invasion. lncRNA BANCR plays a significant role in retinoblastoma aggressiveness and prognosis and may act as a promising target for therapeutic strategy and prognostic prediction. 25894373 2015 Long non-coding RNA BANCR regulates growth and metastasis and is associated with poor prognosis in retinoblastoma. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 malignant melanoma NA M8720/3 qPCR, Western blot, in vitro knockdown etc. malignant melanoma tissues, cell lines (A-375, 1205Lu, UACC903, CHL-1 and sk-mel-5 etc.) up-regulated BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages. The linkage between BANCR and MAPK pathway may provide a novel interpretation for the mechanism of proliferation regulation in malignant melanoma 24967732 2014 Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot etc. NSCLC tissues, cell lines (A549, SPC-A1, NCI-H1975, SK-MES-1 etc.) down-regulated BANCR expression was significantly decreased in 113 NSCLC tumor tissues compared with normal tissues. Additionally, reduced BANCR expression was associated with larger tumor size, advanced pathological stage, metastasis distance, and shorter overall survival of NSCLC patients. Reduced BANCR expression was found to be an independent prognostic factor for NSCLC. Histone deacetylation was involved in the downregulation of BANCR in NSCLC cells. Ectopic expression of BANCR impaired cell viability and invasion, leading to the inhibition of metastasis in vitro and in vivo. Overexpression of BANCR was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression. 24655544 2014 Downregulation of BRAF activated non-coding RNA is associated with poor prognosis for non-small cell lung cancer and promotes metastasis by affecting epithelial-mesenchymal transition. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 breast cancer C50 NA qPCR,Western blot, in vitro knockdown etc. cell line (MCF-7, MDA-MB-231, SKBR3, BT-20), breast cancer tissue up-regulated LncRNA BANCR is highly expressed in breast cancer, which is significantly correlated with the prognosis of patients; moreover, it can promote the growth, invasion and metastasis of ovarian cancer cells. The down-regulation of BANCR can inhibit the proliferation, invasion and metastasis capacities of MCF-7 cells. 29565494 2018 Long non-coding RNA BANCR indicates poor prognosis for breast cancer and promotes cell proliferation and invasion. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 gastric cancer C16 NA RNA-seq, Microarray, RT-qPCR, Western blot, Luciferase reporter assay, in vitro knockdown GC cell lines (MNK-45, SGC-7901, HGC-27, BGC-23, and AGS) up-regulated We then conducted a series of in vivo and in vitro assays to explore the effect of LINC01410 on miR-532-5p-mediated GC malignancy and the underlying mechanism involved. MiR-532-5p overexpression inhibited GC metastasis and angiogenesis in vitro and in vivo,whereas miR-532-5p silencing had the opposite effect. Further study showed that miR-532-5p attenuated NF-kB signaling by directly inhibiting NCF2 expression, while miR-532-5p silencing in GC enhanced NF-kB activity. Furthermore,we demonstrated miR-532-5p down-regulation was caused by aberrantly high expression of LINC01410 in GC. Mechanistically, overexpression of LINC01410 promoted GC angiogenesis and metastasis by binding to and suppressing miR-532-5p, which resulted in up-regulation of NCF2 and sustained NF-kB pathway activation.Interestingly, NCF2 could in turn increase the promoter activity and expression of LINC01410 via NF-kB, thus forming a positive feedback loop that drives the malignant behavior of GC. For instance, lncRNA HCP5 up-regulates expression of Runt-related transcription factor 1 (RUNX1) in glioma cells, while overexpression of RUNX1 can also up-regulate HCP expression. 29483646 2018 LINC01410-miR-532-NCF2-NF-kB feedback loop promotes gastric cancer angiogenesis and metastasis. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 osteosarcoma NA M9180/3 qPCR etc. osteosarcoma tissues, cell lines (HOS, Saos-2, U2OS, and MG-63) down-regulated BANCR overexpression was observed in osteosarcoma cell lines and clinical specimens. Increased BANCR expression was significantly associated with large tumor size, positive distant metastasis, and advanced clinical stage. High BANCR expression in osteosarcoma was an independent predictor of poor survival. Downregulation of BANCR inhibited MG-63 cell proliferation and invasion and promoted cell apoptosis in vitro. 27051014 2016 Increased expression of the lncRNA BANCR and its prognostic significance in human osteosarcoma BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Upregulation of lncRNA BANCR may be associated with the lymph node metastasis and poor survival of CRC. LncRNA BANCR could be served as a novel and useful biomarker for CRC lymph node metastasis and prognosis. 28969673 2017 Upregulation of lncRNA BANCR associated with the lymph node metastasis and poor prognosis in colorectal cancer BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Flow cytometry assay, Cell proliferation assay etc. HCC tissues, cell lines (HuH-7, Hep3B, HepG2, and H2-M) up-regulated BANCR expression was remarkably increased in HCC tissues compared with adjacent noncancerous tissues. BANCR expression in four HCC cell lines was also significantly upregulated. Clinicopathologic analysis revealed that high BANCR expression correlated with high tumor grade, large tumor size, venous infiltration, advanced tumor, node, and metastasis (TNM) stage, and shorter overall survival. Moreover, BANCR downregulation in Hep3B cells impaired cell proliferation, promoted cell apoptosis, reduced cell invasion and migration, led to downregulated vimentin, and upregulated E-cadherin protein levels. 26758762 2016 Increased expression of LncRNA BANCR and its prognostic significance in human hepatocellular carcinoma. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 papillary thyroid cancer NA M8260/3 qPCR,Western blot, in vitro knockdown etc. cells lines(NPA, BCPAP,TPC1,Nthy-ori3-1),PTC tissues down-regulated BANCR was significantly correlated with lymph node metastasis.BANCR inhibited cancer cell proliferation and invasion, which was associated with the induction of cell-cycle G2/M phase arrest and increased apoptosis. BANCR-mediated PTC cell proliferation and migration. BANCR functions as a tumor suppressor during thyroid carcinogenesis. 29675113 2018 Downregulation of BANCR Promotes Aggressiveness in Papillary Thyroid Cancer via the MAPK and PI3K Pathways. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 breast cancer C50 NA qPCR etc. breast cancer tissues, cell lines (MDA-MB-468, MCF7 and HCC1569) up-regulated In conclusion, BANCR overexpression could promote the clinical progression, metastasis and proliferation of BC and indicate poor prognosis of patients with BC. 29805676 2018 Long non-coding RNA BRAF-regulated lncRNA 1 promotes lymph node invasion, metastasis and proliferation, and predicts poor prognosis in breast cancer BC002811 NA NA NA NA GRCh38_17:75165587-75167249 astrocytoma NA M9400/3 qPCR etc. astrocytoma tissues down-regulated Our analysis ultimately generated a list of 7 lncRNAs that were differentially expressed in astrocytomas in comparison to the NAT samples. Among these lncRNAs, ENST00000244906, ENST00000545440, NR_002809 and ENST00000436616 were shown to be upregulated by a factor greater than twofold, whereas 3 lncRNAs, XLOC_010967, BC002811 and ASO1937, were shown to be downregulated by a factor greater than twofold. 26252651 2016 The Use of Three Long Non-Coding RNAs as Potential Prognostic Indicators of Astrocytoma. BC005232 NMT2 NA ENSG00000152465 NA GRCh38_10:15102584-15168693 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow down-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. BC005927 NA NA NA NA GRCh38_7:101127135-101127845 gastric cancer C16 NA qPCR,Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (SGC7901,MKN45), GC tissues up-regulated lncRNA BC005927 can be induced by hypoxia in GC cells and mediates hypoxia-induced GC cell metastasis. Furthermore, BC005927 is frequently upregulated in GC samples and increased BC005927 expression was correlated with a higher tumor-node-metastasis stage. GC patients with higher BC005927 expression had poorer prognoses than those with lower expression. Additional experiments showed that BC005927 expression is induced by hypoxia inducible factor-1 alpha (HIF-1a); CThis lncRNA is a direct transcriptional target of HIF-1a. Next, we found that EPHB4, a metastasis-related gene, is regulated by BC005927 and that the expression of EPHB4 was positively correlated with that of BC005927 in the clinical GC samples assessed. Intriguingly, EPHB4 expression was also increased under hypoxia, and its upregulation by BC005927 resulted in hypoxia-induced GC cell metastasis. These results advance the current understanding of the role of BC005927 in the regulation of hypoxia signaling and offer new avenues for the development of therapeutic interventions against cancer progression. 29383777 2018 Long noncoding RNA BC005927 upregulates EPHB4 and promotes gastric cancer metastasis under hypoxia. BC008363 LINC00491 285708 ENSG00000250682 NR_103753 GRCh38_5:102609156-102671559 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues down-regulated We found that the expression level of lncRNA BC008363 was significantly lower (23-fold) in PDAC tissues compared to corresponding nontumor pancreatic tissues, and patients with high levels of lncRNA BC008363 expression had significantly better survival rates than those with low levels of lncRNA BC008363 expression. lncRNA BC008363 may be a novel biomarker for the prognosis of pancreatic cancer. 25200694 2014 Long non-coding RNAs expressed in pancreatic ductal adenocarcinoma and lncRNA BC008363 an independent prognostic factor in PDAC. BC011663 NA NA NA NA GRCh38_16:1437154-1439315 gastric cancer C16 NA microarray, qPCR etc. primary gastric adenocarcinoma tissues down-regulated For the lncRNAs, the results demonstrated that uc003iqu, uc003tfx, AK022971 and uc.341 were upregulated and that HIV1230, BC011663, AK057054 and M14574 were downregulated in the GC tissues relative to their matched counterparts. 24819045 2014 Integrated analysis of long non-coding RNAs and mRNA expression profiles reveals the potential role of lncRNAs in gastric cancer pathogenesis. BC014579 NA NA NA NA GRCh38_10:4973366-4973805 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues up-regulated We found that the expression of 7 lncRNAs in preneoplastic lesions and HCC was significantly different. 26540467 2015 Long non-coding RNA expression profiles of hepatitis C virus-related dysplasia and hepatocellular carcinoma. BC023629 NA NA NA NA GRCh38_5:177486968-177488049 pancreatic cancer C25 NA qPCR etc. pancreatic cancer tissues, cell lines (Sw1990, PANC-1, BXPC-8 etc.) up-regulated We further confirmed the selected 6 up-regulation of LncRNAs in PC tissues and PC cell lines through qPCR. Comparing to 293T cells, the expression of LncRNA AF339813 was significantly increased about 10-fold in PANC-1 cells, 8-fold in SW1990 cells and 8.9-fold in BxCP-3 cells. The other 5 LncRNAs have a certain degree of up-regulation in PC cell lines. 26045769 2015 Downregulation of NUF2 inhibits tumor growth and induces apoptosis by regulating lncRNA AF339813. BC031319 NA NA NA NA GRCh38_1:150544946-150545630 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow up-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. BC032469 CTD-3080P12.3 NA NA NA GRCh38_5:1173141-1178605 gastric cancer C16 NA microarray, qPCR, Western blot, Luciferase reporter assay etc. gastric cancer tissues, cell lines (KATO-III, SGC-7901, MKN28, AGS, MKN45) up-regulated Here, we report that BC032469, a novel lncRNA, expressed highly in gastric cancer tissues, and the upregulation was clinically associated with larger tumor size, poor differentiation and shorter survival of gastric cancer patients. Mechanistically, BC032469 could directly bind to miR-1207-5p and effectively functioned as a sponge for miR-1207-5p to modulate the derepression of hTERT. Thus, BC032469 may function as a ceRNA to impair miR-1207-5p-dependent hTERT downregulation, suggesting that it may be clinically valuable as a poor prognostic biomarker of gastric cancer. 26549025 2015 Long noncoding RNA BC032469, a novel competing endogenous RNA, upregulates hTERT expression by sponging miR-1207-5p and promotes proliferation in gastric cancer. BC032469 CTD-3080P12.3 NA NA NA GRCh38_5:1173141-1178605 esophageal squamous cell cancer NA NA qPCR, RNAi, Western blot, Cell proliferation assay etc. ESCC tissues, cell lines (ECA-109 and KYSE150) up-regulated The expression level of BC032469 in esophageal squamous cell carcinoma tissues was higher than that in the corresponding non-cancerous tissues. High BC032469 levels were correlated with lymph node metastasis, TNM stage, and tumor size and lower overall survival. Knockdown of BC032469 in TE13 and Eca109 cells inhibited cell proliferation, migration, and invasion; induced cell cycle arrest in the G0/G1 phase; and promoted apoptosis. Western blot analysis revealed that BC032469 regulated the expression of human telomerase reverse transcriptase (hTERT), which is important for cell proliferation and metastasis. 27726103 2016 Upregulated long non-coding RNA BC032469 enhances carcinogenesis and metastasis of esophageal squamous cell carcinoma through regulating hTERT expression. BC040587 LINC00901, LSAMP-AS4, TCONS_00005428 100506724 ENSG00000242385 NR_121607 GRCh38_3:116921431-116932238 gastric cancer C16 NA microarray, qPCR, RNAi etc. gastric cancer tissues down-regulated LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC. 25765901 2015 Reciprocal repression between TUSC7 and miR-23b in gastric cancer. BC040587 LINC00901, LSAMP-AS4, TCONS_00005428 100506724 ENSG00000242385 NR_121607 GRCh38_3:116921431-116932238 breast cancer C50 NA qPCR etc. breast cancer tissues, cell lines (ZR-75-30, MCF-7, SKBR-3, T47D cells) down-regulated It showed that BC040587 expression was down regulated both in BC samples and in BC cell lines compared with corresponding normal control. BC040587 expression was correlated with menopausal status and tumor differentiation. Furthermore, expression of BC040587 was significantly associated with worse prognosis and was shown to be an independent prognostic marker breast cancer. 25435812 2014 Role of BC040587 as a predictor of poor outcome in breast cancer. BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 esophageal squamous cell cancer NA NA qPCR etc. ESCC tissues up-regulated We found that the relative expression of BC200 was significantly higher in ESCC tissues compared with adjacent normal tissue samples. But the expression of BC200 were not related to clinical-pathological features, such as age, TNM stages, and histological grade. Kaplan-Meier analysis showed that high expression levels of BC200 were correlated with poor prognosis in ESCC patients. Patients with a high level of BC200 had a shorter disease-free survival and overall survival than those with low BC200 expression. On multivariate analysis, the hazard ratio (HR) of BC200 expression was 2.17 for disease-free survival and 2.24 for overall survival 27143917 2016 BC200 LncRNA a potential predictive marker of poor prognosis in esophageal squamous cell carcinoma patients BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 colon cancer C18 NA qPCR, Western blot etc. cell lines (HCT-116,HT29), colon cancer tissues up-regulated The BC200 level was positively correlated with advanced TNM stage. Knockdown of BC200 inhibited proliferation of HCT-116 and HT29 colon cancer cell lines and reduce the expression of cell proliferation markers, such as Ki-67 and PCNA. In addition, silencing of BC200 could induce obvious G0/G1 arrest and cause apoptosis in HCT-116 and HT29 cells and reduced the expression of cyclin D1, cyclin E, and c-Myc through inhibiting the expression of B-catenin. Importantly, we found that knockdown of BC200 reduced invasion of HCT-116 and HT29 cells and epithelial-mesenchymal transition (EMT) by reducing the expression of MMP-2 and MMP-9. Mechanistically, silencing of BC200 significantly reduced the phosphorylation of STAT3. Overall, the findings presented here suggest that lncRNA BC200 may serve as a novel oncogene and a new therapeutic target for colon cancer. 29625226 2018 Long noncoding RNA BC200 regulates cell growth and invasion in colon cancer. BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 lung cancer C34 NA qPCR etc. cell lines (HEK293T, MCF-7, MDA-MB-231, SK-BR-3, T47D, A549, SK-OV-3, IMR-90, MCF-11A) up-regulated BC201 expression was substantially upregulated in brain and elevated expression was also observed in testes, small intestine and ovary. Expression in cultured tumour cells was dramatically higher than corresponding normal tissue; however, expression in cultured primary cells was similar to that in immortalized and cancer cell lines. BC200 knockdown resulted in a dramatic loss of viability through growth arrest and induction of apoptosis that could be partially rescued by overexpression of wild-type BC200 but not an siRNA-resistant sequence mutant. Upon release from cell cycle arrest, BC200 expression was recovered as cells entered S-phase, but did not follow a periodic expression pattern during synchronized progression through the cell cycle. This elevated expression was critical for the survival of proliferating cancerous and non-cancerous cells, but is dispensable upon senescence or cell cycle arrest. Our knock-down assays challenge reports that BC200 knockdown confers a survival advantage, as we clearly demonstrate growth arrest and induction of apoptosis in a broad spectrum of both cancer and normal primary cells. For the first time, we show that BC200 expression is greatly reduced in senescent and arrested cells and is elevated upon resumption of the cell cycle, suggesting the possibility of a distinct role for this long non-coding RNA outside of the nervous system. 28651607 2017 The long non-coding RNA BC200 (BCYRN2) is critical for cancer cell survival and proliferation. BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 glioma NA M9380/3 qPCR etc. cell lines (HEK293T, MCF-7, MDA-MB-231, SK-BR-3, T47D, A549, SK-OV-3, IMR-90, MCF-12A) up-regulated BC202 expression was substantially upregulated in brain and elevated expression was also observed in testes, small intestine and ovary. Expression in cultured tumour cells was dramatically higher than corresponding normal tissue; however, expression in cultured primary cells was similar to that in immortalized and cancer cell lines. BC200 knockdown resulted in a dramatic loss of viability through growth arrest and induction of apoptosis that could be partially rescued by overexpression of wild-type BC200 but not an siRNA-resistant sequence mutant. Upon release from cell cycle arrest, BC200 expression was recovered as cells entered S-phase, but did not follow a periodic expression pattern during synchronized progression through the cell cycle. This elevated expression was critical for the survival of proliferating cancerous and non-cancerous cells, but is dispensable upon senescence or cell cycle arrest. Our knock-down assays challenge reports that BC200 knockdown confers a survival advantage, as we clearly demonstrate growth arrest and induction of apoptosis in a broad spectrum of both cancer and normal primary cells. For the first time, we show that BC200 expression is greatly reduced in senescent and arrested cells and is elevated upon resumption of the cell cycle, suggesting the possibility of a distinct role for this long non-coding RNA outside of the nervous system. 28651607 2017 The long non-coding RNA BC200 (BCYRN3) is critical for cancer cell survival and proliferation. BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 breast cancer C50 NA qPCR etc. cell lines (HEK293T, MCF-7, MDA-MB-231, SK-BR-3, T47D, A549, SK-OV-3, IMR-90, MCF-10A) up-regulated BC200 expression was substantially upregulated in brain and elevated expression was also observed in testes, small intestine and ovary. Expression in cultured tumour cells was dramatically higher than corresponding normal tissue; however, expression in cultured primary cells was similar to that in immortalized and cancer cell lines. BC200 knockdown resulted in a dramatic loss of viability through growth arrest and induction of apoptosis that could be partially rescued by overexpression of wild-type BC200 but not an siRNA-resistant sequence mutant. Upon release from cell cycle arrest, BC200 expression was recovered as cells entered S-phase, but did not follow a periodic expression pattern during synchronized progression through the cell cycle. This elevated expression was critical for the survival of proliferating cancerous and non-cancerous cells, but is dispensable upon senescence or cell cycle arrest. Our knock-down assays challenge reports that BC200 knockdown confers a survival advantage, as we clearly demonstrate growth arrest and induction of apoptosis in a broad spectrum of both cancer and normal primary cells. For the first time, we show that BC200 expression is greatly reduced in senescent and arrested cells and is elevated upon resumption of the cell cycle, suggesting the possibility of a distinct role for this long non-coding RNA outside of the nervous system. 28651607 2017 The long non-coding RNA BC200 (BCYRN1) is critical for cancer cell survival and proliferation. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 gastric cancer C16 NA Western Blot Sgastric cancer7901, drug-resistant cell lines. up-regulated In this research, we investigated whether lncRNAs have relations with drug resistance in gastric cancer to find new potential targets for therapy, which can increase the survival time of the drug-resistant gastric patient.Gastric cancer is a common malignancy with increasing worldwide incidence, and chemotherapeutic drugs for gastric cancer are not effective. Long non-coding RNA (lncRNA) has been proved to be important in different cancer progression. In this research, we investigated whether lncRNAs have relations with drug resistance in gastric cancer to find new potential targets for therapy, which can increase the survival. 29028095 2017 BCAR4 increase cisplatin resistance and predicted poor survival in gastric cancer patients. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Among them, AFAP1-AS1, BCAR4, H19, HOXA-AS2, MALAT1 and PVT1 were significantly up-regulated, and ADAMTS9-AS2 was significantly down-regulated in cancer tissue samples. 27596298 2016 Differentially expressed long non-coding RNAs and the prognostic potential in colorectal cancer. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 osteosarcoma NA M9180/3 qPCR, RNAi, Luciferase reporter assay, Cell proliferation assay etc. osteosarcoma tissues, cell lines (hFOB 1.19, MG63 and U2-OS) up-regulated In this study, we found that BCAR4 was significantly upregulated in osteosarcoma tissues. Increased expression of BCAR4 was significantly correlated with large tumor size, advanced Enneking stage, lung metastasis, and poor prognosis. Functional experiments demonstrated that knockdown of BCAR4 inhibits the proliferation and migration of osteosarcoma cell in vitro. Consistently, knockdown of BCAR4 inhibits osteosarcoma tumorigenesis and lung metastasis in vivo. 27460090 2016 Long noncoding RNA BCAR4 promotes osteosarcoma progression through activating GLI2-dependent gene transcription. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 osteosarcoma NA M9180/3 qPCR, Cell proliferation assay, Cell migration and invasion assay etc. osteosarcoma tissues, cell lines (hFOB, MG-63, U2OS and SW1353) up-regulated We found that BCAR4 expression was higher in osteosarcoma tissues and cell lines than that in normal controls. The BCAR4 levels were significantly correlated with clinical stage and distant metastasis. Furthermore, decreased expression of BCAR4 markedly inhibited osteosarcoma cell proliferation, migration, and invasion. 27874956 2016 Up-regulation of long non-coding RNA BCAR4 predicts a poor prognosis in patients with osteosarcoma, and promotes cell invasion and metastasis. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues, cell lines (L78, A549, H1229, H358, and H1650) up-regulated The expression level of lncRNA BCAR4 was significantly higher in NSCLC tissues compared to their matched non-tumor tissues. Moreover, BCAR4 expression was significantly upregulated in NSCLC cell lines, when compared to the normal human bronchial epithelial cell line BEAS-2B. In addition, the BCAR4 expression was associated with the lymph node metastasis, distant metastasis and clinical stage. 28077810 2017 Increased Expression of Long Non-Coding RNA BCAR4 Is Predictive of Poor Prognosis in Patients with Non-Small Cell Lung Cancer. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. breast cancer tissues, cell lines (MDA-MB-453, MDA-MB-231, MCF-7 and T47D) up-regulated Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly. 26550436 2015 Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5. BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 cervical cancer C53 NA qPCR, Western blot, etc. cervical cancer tissues, cell lines (HeLa, SiHa, Caski, C4-1, C-33A) up-regulated patients with high BCAR4 expression showed worse survival outcomes and overexpression of BCAR4 might be an independent prognostic factor in cervical cancer. 29937186 2018 Up-regulated BCAR4 contributes to proliferation and migration of cervical cancer cells.overexpression of BCAR4 promoted epithelial-mesenchymal transition (EMT) process and silencing BCAR4 suppressed EMT process in cervical cancer cells. BDNF-AS BDNF-AS, ANTI-BDNF, BDNF, BDNF-AS1, BDNFAS, BDNFOS, NCRNA00049 497258 ENSG00000245573 NR_002832 GRCh38_11:27506838-27698174 prostate cancer C61.9 NA qPCR, in vitro knockdown etc. prostate cancer tissues down-regulated BDNF-AS was downregulated in human CaP tumors. Low BDNF-AS expression was correlated with CaP patients' poor prognosis and shorter overall survival. BDNF-AS was also found to be lowly expressed in CaP cell lines. In LNCaP and PC-3 cells, lentivirus-driven BDNF-AS overexpression exerted significantly tumor-suppressing effects on hindering cancer cell proliferation and invasion in vitro, and explant growth in vivo. 29710528 2018 Long noncoding RNA BDNF-AS is associated with clinical outcomes and has functional role in human prostate cancer. BDNF-AS BDNF-AS, ANTI-BDNF, BDNF, BDNF-AS1, BDNFAS, BDNFOS, NCRNA00049 497258 ENSG00000245573 NR_002832 GRCh38_11:27506838-27698174 retinoblastoma C69.2 M9510/3 qPCR, Cell proliferation assay, Cell cycle assay etc. RB tissues, cell lines (ARPE-19, hTERT-RPE1, Y79, WERI-Rb-1, Rb116, Rb143, SO-RB50 and HXO-RB44) down-regulated BDNF-AS is downregulated in RB tumors and cell lines. Low BDNF-AS expression in RB tumors is correlated with patients' advanced clinical stage and tumor differentiation status. Low BDNF-AS expression is associated with shorter overall survival and may be acting as an independent marker in RB. In Y79 and WERI-Rb-1 cells, forced overexpression of BDNF-AS inhibited cancer proliferation and migration. It also induced cell-cycle arrest at G0/G1 phase by downregulating CDC42, Cyclin E and BDNF. 28131827 2017 Long noncoding RNA BDNF-AS is a potential biomarker and regulates cancer development in human retinoblastoma. BDNF-AS BDNF-AS, ANTI-BDNF, BDNF, BDNF-AS1, BDNFAS, BDNFOS, NCRNA00049 497258 ENSG00000245573 NR_002832 GRCh38_11:27506838-27698174 oesophageal cancer NA M8070/3 qPCR, Luciferase reporter assay, Western blot, etc. Normal oesophageal epithelial cell line (SHEE), eight EC cell lines (OE19, KYSE-70, KYSE-170, KYSE-180, OE33, Eca-109, TE-1, TE-13). EC tissues. down-regulated Overexpression of BDNF-AS was found to suppress cell proliferation, invasion and metastasis in vitro and suppress the EMT in EC cells. Further analysis demonstrated BDNF-AS functioned as a miR-214 sponge to positively regulate cell proliferation, metastasis and the EMT. 2 Advances in chemoradiotherapy and surgery could prolong the survival time of patients with EC. 29896888 2018 LncRNA BDNF-AS inhibits proliferation, migration, invasion and EMT in oesophageal cancer cells by targeting miR-214. BF2-AS1 NA NA NA NA NA esophageal squamous cell cancer NA NA in vitro knockdown, qPCR, Western blot, Luciferase reporter assay cell lines (HEsEpiC), ESCC tissues up-regulated SBF2-AS1 was also silenced using small interfering RNA. Cell proliferative and invasive ability were significantly inhibited (P<0.05) following SBF2-AS1 silencing, the cell cycle was arrested in the G2 phase; however, there was no significant difference in the proportion of apoptotic cells. Gene Set Enrichment Analysis revealed that genes associated with cell cycle biological processes, including the cancer suppressor gene cyclin-dependent kinase 1A (CDKN1A), were significantly associated with SBF2-AS1 in ESCC tissues. CDKN1A expression levels were increased in ECA-109 cells following SBF2-AS1 silencing. SBF2-AS1 is significantly upregulated in ESCC, and that silencing of SBF2-AS1 inhibits the proliferative and invasive ability of ESCC cells. SBF2-AS1 may be a novel biomarker and therefore a potential therapeutic target for ESCC. 29552140 2018 Upregulated long non-coding RNA SBF2-AS1 promotes proliferation in esophageal squamous cell carcinoma. BISPR lncBST2 105221694 ENSG00000282851 NR_130765 GRCh38_19:17405686-17419324 papillary thyroid cancer NA M8260/3 Microarray, qPCR, Western blot etc. papillary thyroid cancer tissues, cell line (BHT101 and Hth83) up-regulated BISPR in TPC tissues was over-expressed. BISPR knockdown restrained the propagation and invasiveness and enhanced the iodine uptake of TPC cells. The tumor-forming rate reduced after BISPR knockdown. In addition, miR-21-5p was lowly expressed in cancer tissues. BISPR promoted the development of TPC cells by inhibiting miR-21-5p expression. Bcl-2 was suppressed by miR-21-5p and sh-BISPR. BISPR, which was over-expressed in TPC, improved TPC cell viability, propagation, and invasiveness. MiR-21-5p was lowly expressed in TPC which inhibited Bcl-2 expression. BISPR stimulated propagation and invasiveness of TPC cells by depressing miR-21-5p. Patients with low expression of BISPR had higher fraction survival compared with patients with high BISPR expression. 29856242 2018 LncRNA BISPR promotes the progression of thyroid papillary carcinoma by regulating miR-21-5p. BLACAT1 BLACAT1, LINC00912, UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 cervical cancer C53 NA qPCR, Western blot, in vitro knockdown cervical cancer tissues, Cervical cancer cell lines (Siha,CaSki, Hela, ME180 and C33A) up-regulated BLACAT1 was highly expressed in human cervical cancer tissues and cell lines. The knockdown of BLACAT1 with specific short hairpin RNA reduced colony formation rates in ME180 and C33A cells. Cell cycle and cell proliferation assays revealed that depletion of BLACAT1 in ME180, and C33A cells arrested the cell cycle at the G0/G1 phase and inhibited cell proliferation. Transwell assays demonstrated that the knockdown of BLACAT1 inhibited cell migration and invasion in ME180,and C33A cells. Moreover, wound-healing assays supportedthe aformentioned observations. Western blot analysis showed that the knockdown of BLACAT1 in ME180 and C33A cells decreased the protein levels of cyclin B1, cell division cycle 25C, and N-cadherin, while increasing the protein level of E-cadherin. 29456724 2018 Long noncoding RNA BLACAT1 promotes cell proliferation and invasion in human cervical cancer. BLACAT1 BLACAT1, LINC00912, UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, RIP, ChIP, Flow cytometry assay, Cell proliferation assay etc. CRC tissues, cell lines (HCT116, SW480) up-regulated Our experiments showed that increased BLACAT1 was an independent unfavorable prognostic indicator for colorectal cancer, and revealed that BLACAT1 knockdown significantly repressed proliferation, both in vitro and in vivo. Mechanistic investigations demonstrated that BLACAT1 had a key role in G1/G0 arrest, and showed that BLACAT1 can repress p15 expression by binding to EZH2, thus contributing to the regulation of CRC cell cycle and proliferation. 28277544 2017 Long noncoding RNA BLACAT1 indicates a poor prognosis of colorectal cancer and affects cell proliferation by epigenetically silencing of p15. BLACAT1 BLACAT1, LINC00912, UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay etc. NSCLC cancer tissue, cell lines (A549, SK-MES-1, H1299, Calu-3) up-regulated In NSCLC cells, BLACAT1 expression was also upregulated. Both in vivo and in vitro, BLACAT1 silencing transfected with si-BLACAT1 could suppress proliferation, migration, and invasion, and induce G0/G1 phase arrest. Furthermore, combining experiments of miR-144 and BLACAT1 indicated that miR-144 could reverse the function of BLACAT1 on NSCLC cells' phenotype. Overall, this study reveals the overexpression of BLACAT1 in NSCLC tissue and cells, and discovers the oncogenic role of BLACAT1 in NSCLC genesis through sponging miR-144, providing a potential biomarker for early detection and prognosis prediction of NSCLC. 28885863 2017 Long Noncoding RNA Bladder Cancer Associated Transcript 1 Promotes the Proliferation, Migration, and Invasion of Nonsmall Cell Lung Cancer Through Sponging miR-144 BLACAT1 BLACAT1, LINC00912, UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 cervical cancer C54 NA qPCR, RNAi, Western blot etc. cervical cancer tissues, cell line (HeLa, CaSki, SiHa, ME-180 and H8) up-regulated We found that BLACAT1 expression was significantly increased in CC tissues and cells lines. In addition, the expression level of BLACAT1 was positively correlated with distant metastasis (p=0.001), FIGO stage (p=0.010), and histological grade (p=0.012). Moreover, patients with high BLACAT12 expression had shorter overall survival and progression-free survival time than those with low BLACAT1 expression, with the data provided by multivariate analysis suggesting that BLACAT1 expression could serve as an independent prognostic factor in CC patients. Functionally, in vitro assay indicated that down-regulation of BLACAT1 significantly suppressed CC cells proliferation, migration, and invasion. Mechanistically, the results of Western blot showed that the expression of B-catenin and MMP-7 was significantly down-regulated in CC cells transfected with si-BLACAT1. 29863244 2018 Long non-coding RNA BLACAT1 promotes cell proliferation, migration and invasion in cervical cancer through activation of Wnt/β-catenin signaling pathway. BLACAT1 BLACAT1, LINC00912, linc-UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Flow cytometry assay etc. NSCLC tissues, cell lines (A549 and NCI-H1299) up-regulated We found the lung cancer associated lncRNA 6 (LCAL6) was significantly unregulated and predicted survival in LUAD. Silence of LCAL6 inhibited LUAD tumor cell growth both in vitro and in vivo. 26918601 2016 Comprehensive analysis of lncRNA expression profiles and identification of functional lncRNAs in lung adenocarcinoma. BLACAT1 BLACAT1, LINC00912, linc-UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. CRC tissues, cell lines (SW480, HCT116, HT29, and SW620) up-regulated linc-UBC1 was significantly overexpressed in CRC tissues and the majority of CRC cell lines compared with the matched non-tumor mucosa and normal intestinal epithelial cells. The results also revealed that reducing the expression of linc-UBC1 led to the inhibition of migration, invasion, and proliferation of CRC cells in vitro. 28260919 2017 Overexpression of the long non-coding RNA, linc-UBC1, is associated with poor prognosis and facilitates cell proliferation, migration, and invasion in colorectal cancer. BLACAT1 BLACAT1, LINC00912, linc-UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 gastric cancer C16 NA qPCR, RNAi etc. gastric cancer tissues, cell lines (BGC-823, SGC-7901, AGS, MKN-45, HGC-27 etc.) up-regulated We found that linc-UBC1 was significantly upregulated in gastric cancer tissues compared to adjacent normal tissues. Furthermore, high linc-UBC1 expression was associated with lymph-node metastasis, tumor size, TNM stage and poorer prognosis. Inhibition of linc-UBC1 suppressed the proliferation, motility and invasion of gastric cancer cells.Inhibition of linc-UBC1 suppressed the proliferation, motility and invasion of gastric cancer cells. 25755750 2015 Long noncoding RNA linc-UBC1 is negative prognostic factor and exhibits tumor pro-oncogenic activity in gastric cancer. BLACAT1 BLACAT1, LINC00912, linc-UBC1, onco-lncRNA-30 101669762 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 bladder cancer C67 NA microarray, qPCR, RNAi, ISH etc. bladder cancer tissues, cell lines (J82, UMUC-3, HT-1376, T24, 5637 etc.) up-regulated qPCR confirmed that linc-UBC1 expression is up-regulated in 60 cases (58.8%) in bladder cancer tissues compared with normal adjacent tissues, and its overexpression correlates with lymph node metastasis and poor survival. Further functional analysis demonstrated that knockdown of linc-UBC1 attenuates bladder cancer cell proliferation, motility, invasion, colony formation ability, tumorigenicity and metastatic potential. RIP and ChIP assay confirmed that linc-UBC1 physically associates with PRC2 complex and regulates histone modification status of target genes. 23688781 2013 linc-UBC1 physically associates with polycomb repressive complex 2 (PRC2) and acts as a negative prognostic factor for lymph node metastasis and survival in bladder cancer. BM742401 GATA6-AS1, BM742401, locus5689 100128893 ENSG00000266010 NR_102763 GRCh38_18:22166898-22168968 chronic lymphocytic leukemia NA M9823/3 qPCR, MSP-PCR, Western blot, in vitro knockdown etc. bone marrow, cell lines (MEC1 and CLL-AAT) up-regulated The promoter of BM742401 was unmethylated in normal controls including three each of normal bone marrow, peripheral blood buffy coats, and CD19-sorted peripheral B-cells, but methylated in four (57.1%) CLL cell lines. Functionally, stable overexpression of BM742401 resulted in inhibition of cellular proliferation and enhanced apoptosis through caspase-9-dependent intrinsic but not caspase-8-dependent extrinsic apoptosis pathway, suggesting a tumor suppressor role of BM742401 in CLL. In primary CLL samples, methylation of BM742401 was detected in 43/98 (43.9%) of patients. 27689399 2016 Epigenetic silencing of tumor suppressor long non-coding RNA BM742401 in chronic lymphocytic leukemia. BM742401 GATA6-AS1, BM742401, locus5689 100128893 ENSG00000266010 NR_102763 GRCh38_18:22166898-22168968 gastric cancer C16 NA RNA-seq, qPCR, in vitro knockdown etc. gastric cancer tissues, cell line (B16F1) down-regulated BM742401 was downregulated in cancer, and its downregulation was associated with poor survival in gastric cancer patients. Ectopic overexpression of BM742401 inhibited metastasis-related phenotypes and decreased the concentration of extracellular MMP9. 23846333 2013 A known expressed sequence tag, BM742401, is a potent lincRNA inhibiting cancer metastasis. BOKAS BOK-AS1, BOK-AS, BOKAS, NAToB, NCRNA00151 NA NA NA NA testicular cancer C62 NA qPCR etc. cell line (Hela) up-regulated The mRNA expression of BOKAS was only detected in testis and certain cancer tissues but not in other normal adult tissues examined. Overexpression of BOKAS alone exhibited no significant anti- or pro-apoptotic activity but it was able to inhibit Bok-induced apoptosis in HeLa cells. Our results suggest that BOKAS may function specifically in the human testis, where it serves as an antisense molecule to regulate Bok-induced apoptosis. 19287972 2009 A natural antisense transcript, BOKAS, regulates the pro-apoptotic activity of human Bok. BX648207 NA NA NA NA GRCh38_12:43718993-43724000 colorectal cancer C19.9 NA microarray, qPCR, RNAi etc. cell lines (HCT116 ,SW1116) down-regulated Functional experiments demonstrated three dysregulated lncRNAs, AK123657, BX648207 and BX649059 were required for efficient invasion and proliferation suppression in CRC cell lines. 24809982 2014 A long non-coding RNA signature to improve prognosis prediction of colorectal cancer. BX648695 POT1-AS1 401398 ENSG00000224897 NR_125718 GRCh38_7:124929873-125179315 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). BX649059 GAS2L3, G2L3 NA NA NA GRCh38_12:100623715-100626864 colorectal cancer C19.9 NA microarray, qPCR, RNAi etc. cell lines (HCT116 ,SW1116) down-regulated Functional experiments demonstrated three dysregulated lncRNAs, AK123657, BX648207 and BX649059 were required for efficient invasion and proliferation suppression in CRC cell lines. 24809982 2014 A long non-coding RNA signature to improve prognosis prediction of colorectal cancer. C12orf47 MAPKAPK5-AS1, C12orf47 51275 ENSG00000234608 NA GRCh38_12:111839764-111842902 glioblastoma multiforme NA M9440/3 qPCR, Cell transfection, MTT assay etc. cell line (U87) differential expression The viability of U87 cells transfected with C12orf47 was reduced. Overexpression of C12orf47 induced substantial apoptosis in U87 cells. 28168356 2017 Identifying survival-associated modules from the dysregulated triplet network in glioblastoma multiforme. C20orf200 C20orf166-AS1, C20orf200, NCRNA00335 NA NA NA GRCh38_20:62544343-62551526 colon cancer C18 NA microarray, qPCR, RNA pull-down assay etc. cell line (HCT-122) down-regulated Quantitative RT-PCR analyses confirmed transcriptional silencing in HCT-116 cells and demethylation-associated reactivation in DKO cells for seven (70%) of the lncRNAs: TP53TG1, NCRNA00028, LOC157627, MIR155HG, WT1AS, C20orf200, and MYCNOS. 27821766 2016 Epigenetic inactivation of the p53-induced long noncoding RNA TP53 target 1 in human cancer. C5orf66-AS1 C5orf66-AS1, CTC-276P9.1, Epist 101927953 ENSG00000249082 NR_105049 GRCh38_5:135038831-135040047 gastric cardia cancer C16.0 M8140/3 qPCR, Luciferase reporter assay etc. cell lines (MGC-803, BGC-823, HGC-27, SGC-7901, NCI-N87), gastric cardia tissues down-regulated Downregulation and aberrant hypermethylation of C5orf66-AS1 have been detected in a limited several tumors. C5orf66-AS1 was significantly downregulated in GCA tissues and cell lines, and the expression level was associated with TNM stage, pathological differentiation, lymph node metastasis, and distant metastasis or recurrence. The expression level of C5orf66-AS1 was significantly increased in cancer cells after treated with 5-Aza-dC. Aberrant hypermethylation of the regions around the transcription start site of C5orf66-AS1 was more tumor specific and was associated with its expression. Sp1 may upregulate C5orf66-AS1 expression and CpG sites hypermethylation within the binding sites may abrogate Sp1 binding. In addition, C5orf66-AS1 inhibited gastric cancer cell proliferation and invasion, and the dysregulation and hypermethylation of the regions around the transcription start site of C5orf66-AS1 were associated with poorer GCA patients'survival. 29566283 2018 Aberrant methylation-mediated downregulation of long noncoding RNA C5orf66-AS1 promotes the development of gastric cardia adenocarcinoma. C5orf66-AS1 C5orf66-AS1, CTC-276P9.1, Epist 101927953 ENSG00000249082 NR_105049 GRCh38_5:135038831-135040047 esophageal squamous cell cancer NA NA Microarray, qRT-PCR, Western blot, Luciferase reporter assay Primary ESCC tissues, esophageal cancer cell lines (TE1, TE13, T.Tn, YES2, Eca109, and Kyse170) down-regulated Significant downregulation of CTC-276P9.1 was detected in esophageal cancer cells and ESCC tissues, and the expression of CTC-276P9.1 in ESCC tissues was associated with TNM stage, pathological differentiation, lymph node metastasis, and distant metastasis or recurrence.The aberrant hypermethylation of the regions around the transcription start site was more tumor specific and associated with the expression levels of CTC-276P9.1.histone modification may also participate in the regulation of CTC-276P9.1. Furthermore, over-expression of CTC-276P9.1 inhibited esophageal cancer cells proliferation and invasion in vitro, decreased the expression of proliferative markers and inhibited esophageal cancer cells invasion probably by regulating EMT. In addition, the dysregulation and hypermethylation of the regions around the transcription start site of CTC-276P9.1 were associated with poorer ESCC patients' survival. 29524086 2018 Aberrant methylation-mediated silencing of lncRNA CTC-276P9.1 is associated with malignant progression of esophageal squamous cell carcinoma. C5orf66-AS1 C5orf66-AS1, CTC-276P9.1, Epist 101927953 ENSG00000249082 NR_105049 GRCh38_5:135038831-135040047 esophageal squamous cell cancer NA NA microarray, qPCR etc. cell lines (KYSE510, KYSE450, KYSE150, KYSE30, EC109, TE-1) down-regulated We identified a novel nuclear-retained lncRNA, named Epist, which is generally highly expressed in esophagus, and which is down-regulated during ESCC progression. Epist over-expression and knockdown studies further suggest that Epist inhibits the metastasis, acting as a tumor suppressor in ESCC. Collectively 26158411 2015 Transcriptome profiling of esophageal squamous cell carcinoma reveals a long noncoding RNA acting as a tumor suppressor CACNA1C-AS3 CACNA1C-AS3 106478964 ENSG00000256769 NA GRCh38_12:2603350-2607440 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues up-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. CADM1-AS1 NA NA NA NA NA clear cell renal cell carcinoma C64.9 M8005/0 qPCR, RNAi etc. renal cancer tissues, cell lines (786-O, ACHN etc.) down-regulated The results showed that CADM1-AS1 expression was down-regulated in tumor tissues in 64 patients with ccRCC compared with adjacent non-tumor tissues. Furthermore, the expression of CADM1-AS1 was positively correlated with the expression of mRNA CADM1 in ccRCC specimens. Decreased CADM1-AS1 expression was correlated with the progression of AJCC stage and worse survival of ccRCC patients. Also, multivariate analysis identified low CADM1-AS1 expression as an independent prognostic factor for ccRCC.CADM1-AS1 is a new tumor suppressor in ccRCC which regulates cell proliferation, apoptosis and migration via the expression pattern of CADM1-AS1/CADM1 mRNA gene pairs. 25031695 2014 Decreased expression of a novel lncRNA CADM1-AS1 is associated with poor prognosis in patients with clear cell renal cell carcinomas. CAI2 NA NA NA NA NA neuroblastoma NA M9500/3 qPCR etc. neuroblastoma tissues, cell line (NMB7) up-regulated Concordant expression of CAI2 with p16 and ARF in normal tissue along with the ability of CAI2 to induce p16 expression suggested that CAI2 may regulate p16 and/or ARF. In neuroblastoma cells transformed by serial passage in vitro, leading to more rapid proliferation, CAI2, p16, and ARF expression all increased dramatically. Consistent with its association with high-risk disease, CAI2 expression was also significantly associated with poor clinical outcomes, although this effect was reduced when adjusted for MYCN amplification. 25028366 2014 High expression of CAI2, a 9p21-embedded long noncoding RNA, contributes to advanced-stage neuroblastoma. CASC15 CASC15, LINC00340, lnc-SOX4-1 401237 ENSG00000272168 NR_015410 GRCh38_6:21664772-22368328 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, in vitro knockdown hepatocellular carcinoma tissues, cell lines (SMMC7721, Hep-G2,Huh-7, HCCLM3, Hep3B, QSG-7701) up-regulated CASC15 was overexpressed in HCC tissues compared with corresponding adjacent normal tissues, and the CASC15 expression level was significantly correlated with metastasis,tumor size,and TNM stage.high CASC15 expression was associated with poor prognosis in HCC patients.CASC15 significantly impaired HCC cell proliferation, migration, and invasion.CASC15 knockdown also induced cell apoptosis in vitro and impaired tumor growth in vivo. 29075788 2017 Long non-coding RNA CASC15 is upregulated in hepatocellular carcinoma and facilitates hepatocarcinogenesis. CASC15 CASC15, LINC00340, lnc-SOX4-1 401237 ENSG00000272168 NR_015410 GRCh38_6:21664772-22368328 gastric cancer C16 NA qPCR, microarray cell lines (MKN453, AGS, MKN28, GES-1) up-regulated We extracted total RNA from clinical samples of 42 normal gastric epithelial tissues and 60 gastric cancer tissues. The results of quantitative reverse transcriptase- polymerase chain reaction (qRT-PCR) were consistent with those of TCGA analysis. Clinical data analysis showed that the expression of LncRNA CASC15 was correlated with the total survival, tumor size and TMN staging in clinical patients. Clinical data analysis showed that the expression level of CASC15 was correlated with tumor size and TNM stage in clinical patients. Compared with the negative control group, the proliferation and cell cloning ability of MKN28 cells overexpressing LncRNA CASC15 significantly increased,indicating that overexpression of LncRNA CASC15 promoted the proliferation of MKN28 cells. 29272000 2017 High expression of LncRNA CASC15 is a risk factor for gastric cancer prognosis and promote the proliferation of gastric cancer. CASC15 CASC15, LINC00340, lnc-SOX4-1 401237 ENSG00000272168 NR_015410 GRCh38_6:21664772-22368328 gastric cancer C16 NA RNA-seq, RT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP gastric cancer tissues, GC cell lines (BGC-823, AGS, SGC-7901, NCI-N87, MKN-45 and MKN-28) up-regulated The Kaplan-Meier method was used to demonstrate that high expression of CASC15 is linked to a poor prognosis for patients suffering from GC. Additionally, functional experiments proved that the down- or up-regulation of CASC15 inhibited or facilitated cell proliferation via the induction of cell cycle arrest and apoptosis, and also suppressed or accelerated cell migration and invasion by affecting the progression of the epithelial-to-mesenchymal transition (EMT). In vivo experiments showed that the knockdown of CASC15 lessened the tumor volume and weight and influenced the EMT process. This was confirmed by western blot assays and immunohistochemistry, indicating impaired metastatic ability in nude mice. CASC15 involvement in the tumorigenesis of GC occurs when CASC15 interacts with EZH2 and WDR5 to modulate CDKN1A in nucleus. Additionally, the knockdown of CASC15 triggered the silencing of ZEB1 in cytoplasm, which was shown to be associated with the competitive binding of CASC15 to miR-33a-5p. 29489064 2018 Long non-coding RNA CASC15 regulates gastric cancer cell proliferation, migration and epithelial mesenchymal transition by targeting CDKN1A and ZEB1. CASC15 CASC15, LINC00340, lnc-SOX4-1 401237 ENSG00000272168 NR_015410 GRCh38_6:21664772-22368328 neuroblastoma NA M9500/3 RNA-seq, qPCR, RNAi, Luciferase reporter assay, RNA-FISH etc. neuroblastoma cell lines down-regulated Here we report that the most highly significant single-nucleotide polymorphism (SNP) associations reside within CASC15, a long noncoding RNA that we define as a tumor suppressor at 6p22. Low-level expression of a short CASC15 isoform (CASC15-S) associated highly with advanced neuroblastoma and poor patient survival. 26100672 2015 CASC15-S Is a Tumor Suppressor lncRNA at the 6p22 Neuroblastoma Susceptibility Locus. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 esophageal cancer C15 NA qPCR, Luciferase reporter assay, Western blot esophageal carcinoma tissues, cell lines (Het-1A,EC,EC9706, Eca109, EC-1, KYSE30, and KYSE150) down-regulated the expression of CASC2 to be significantly downregulated in EC tissues and EC cell lines;low expression of CACS2 was associated with advanced TNM stage and lymph node metastases.upregulation of CASC2 significantly inhibited the proliferation of EC cells.CASC2, acting as a competing endogenous RNAs (ceRNAs) of miR-18a-5p, exerts its biological effects by modulating the expression of PTEN.The expression level of PTEN is related to a patient's clinicopathologic characteristic and overall survival 28964779 2017 The long noncoding RNA CASC2 inhibits tumorigenesis through modulating the expression of PTEN by targeting miR-18a-5p in esophageal carcinoma. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 lung adenocarcinoma C34 M8140/3 qPCR, Western blot etc. LAC tissues, cell line (A549, SPCA1, H1975, PC-9, 16 HBE) down-regulated In our study, CASC2 expression level was lower in LAC tissues than that in corresponding tissues. CASC2 expression was associated with lymph node metastasis, clinical stage and survival time of these patients. Moreover, overexpression of CASC2 inhibited migrated and invaded ability of LAC cells. Then, epithelial to mesenchymal transition (EMT) process of LAC cells and SOX4 expression was suppressed by upregulating CASC2. 29131257 2017 Long noncoding RNA CASC2 inhibits metastasis and epithelial to mesenchymal transition of lung adenocarcinoma via suppressing SOX4 CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 osteosarcoma NA M9180/3 qPCR cell lines (143B, U.2 OS, KHOS.240S, D22, Saos.2, HOS and MG.63,hFOB) down-regulated CASC2 transduction may decrease proliferation, migration and invasion of osteosarcoma cell lines whereas knockdown of CASC2 displayed opposing effects.Patients with low CASC2 levels were predicted to have a poor survival. 29257211 2017 The long noncoding RNA cancer susceptibility candidate 2 inhibits tumor progression in osteosarcoma. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 bladder cancer C67 NA qPCR, Cell transfection, Western blot, Flow cytometry assay, Cell proliferation assay, Cell migration and invasion assay etc. bladder cancer tissues, cell lines (T24, 5637, SW780, J82 and UMUC3) down-regulated CASC2 was significantly down-regulated in bladder cancer tissues and cell lines. Moreover, overexpression of lncRNA CASC2 remarkably reduced the cell growth, migration and invasion, as well as promoted early apoptosis of bladder cancer cell in vitro. Furthermore, we illustrated that lncRNA CASC2 inhibited Wnt/B-catenin signal pathway activity by decrasing the B-catenin expression and reversing the downstream target gene expression of Wnt signaling pathway. 28199978 2017 Down-regulation of lncRNA CASC2 promotes cell proliferation and metastasis of bladder cancer by activation of the Wnt/B-catenin signaling pathway. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 pancreatic cancer C25 NA qPCR, Western blot,Luciferase reporter assay ,ChIP etc. pancreatic cancer tissues,cell line (HPDE,SW1990,BxPC-3, AsPC-1, CFPAC-1 and PANC-1) down-regulated a lower CASC2 expression in PC was related with a poorer prognosis. CASC2 gene possessed a HNF1A-responsive element (CASC2-HNF1A RE); HNF1A could promote CASC2 expression through direct binding to CASC2-HNF1A RE. 28865121 2017 HNF1A/CASC2 regulates pancreatic cancer cell proliferation through PTEN/Akt signaling. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 non small cell lung cancer C34 M8046/3 qPCR, Cell transfection, Flow cytometry assay etc. NSCLC tissues, cell lines (A549, PC-9, and NCI-H1299) down-regulated CASC2 expression was significantly downregulated in 92.1 % cancerous tissues compared with normal counterparts. The lower expression of CASC2 was remarkably correlated with advanced TNM stage and tumor size. Multivariate analyses found that CASC2 expression served as an independent predictor for overall survival of NSCLC. Moreover, overexpression of CASC2 significantly inhibited NSCLC cell proliferation both in vitro and in vivo. 26790438 2016 Low expression of long noncoding RNA CASC2 indicates a poor prognosis and regulates cell proliferation in non-small cell lung cancer. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 gastric cancer C16 NA qPCR etc. GC tissue, cell lines (MKN-1, SGC7901, BGC823, MGC803) down-regulated It was found that the expression level of lncRNA CASC2 was decreased, which correlated with TNM stages, vessel invasion, metastasis, and overall survival of patients with GC. Furthermore, overexpression of CASC2 inhibited the invasion and angiogenesis of GC cells. Thus, the present study indicated the important roles and underlying molecular mechanisms of lncRNA CASC2 on GC, and indicated that lncRNA CASC2 may present as a potential therapeutic target for the treatment of GC. 28849111 2017 Overexpression of long non-coding RNA cancer susceptibility 2 inhibits cell invasion and angiogenesis in gastric cancer CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 glioma NA M9380/3 qPCR, Western blot, Luciferase report assay etc. glioma tissues, cell lines (U251 and U87) down-regulated CASC2 expression was significantly downregulated in glioma tissues and cell lines (U87 and U251) compared to adjacent normal brain tissues or normal human astrocytes. CASC2 may potentially serve as a valuable diagnostic and prognostic biomarker and a therapeutic target for glioma patients.CASC2 could be considered as an independent risk factor for poor prognosis. CASC2 overexpression remarkably suppressed glioma cell proliferation, migration, and invasion through suppressing Wnt/B-catenin signaling pathway. 28744130 2017 Long noncoding RNA CASC2 predicts the prognosis of glioma patients and functions as a suppressor for gliomas by suppressing Wnt/B-catenin signaling pathway. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown HCC tissues, hepatoma cell lines (HepG2, SMMC-7721, Hep3B, and Huh-7) down-regulated CASC2 is downregulated in human HCC tissues and HCC cell lines as compared to adjacent non-tumor tissues (NTTs) and a liver cell line, respectively.we determined that CASC2 regulates HCC cell activity by targeting miR-362-5p and thus inhibiting the NF-kB pathway. 29319182 2018 Long noncoding RNA CASC2 regulates hepatocellular carcinoma cell oncogenesis through miR-362-5p/Nf-kB axis. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 urothelial cancer NA M8120/3 RNA-seq, qPCR Tumor tissues down-regulated CASC2a was down-regulated in UCB tissues, and was highly negatively correlated with the pT, pN, tumor size, and lymphovascular invasion (LVI). 29358570 2018 Long Non-Coding RNA Cancer Susceptibility Candidate 2a (CASC2a) Is a Marker of Early Recurrence After Radical Cystectomy in Patients with Urothelial Carcinoma of the Bladder. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 astrocytoma NA M9400/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell migration and invasion assay, ISH etc. astrocytoma tissues, cell lines (U251 and U87) up-regulated High CASC2c was positively correlated with astrocytoma progression, and an unfavorable prognosis factor for patients. Knockdown CASC2c inhibited proliferation and tumorgenesis. Overexpression of CASC2c promotes the malignant characteristic of astrocytoma cells.CASC2c directly bound miR-101 and mediated pre-miR-101 processing into mature miR-101, and functions as a competitor of miR-101 target genes such as CPEB1. 28252647 2017 CASC2c as an unfavorable prognosis factor interacts with miR-101 to mediate astrocytoma tumorigenesis. CASC9 CASC9, ESCCAL-1, ESSCAL1, LINC00981 101805492 ENSG00000249395 NR_103848 GRCh38_8:75223404-75324741 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR, RNAi, MTT assay etc. cell lines (SW1990, BxPC etc.) up-regulated We selected two upregulated lncRNAs (LINC00152 and CASC9) that were reported to be upregulated in other cancers, and two mostly downregulated lncRNAs (LINC00226 and F11-AS1) for further validation in PDAC cell lines and the normal cell line HPDE. CASC9 and LINC00152 were overexpressed in most of the PDAC cell lines compared with HPDE cells. Knockdown of LINC00152 and CASC9 impaired PDAC cells proliferation and invasion. 28220683 2017 Analysis of distinct long noncoding RNA transcriptional fingerprints in pancreatic ductal adenocarcinoma. CASC9 CASC9, ESCCAL-1, ESSCAL1, LINC00981 101805492 ENSG00000249395 NR_103848 GRCh38_8:75223404-75324741 nasopharyngeal cancer C11 NA qPCR, Western blot nasopharyngeal carcinoma tissues up-regulated In this study, we identified that lncRNA cancer susceptibility candidate 9 (CASC9) is highly expressed in NPC tissues, which facilitates cell growth and is correlated with a poor prognosis of cancer patients. 28398871 2017 The Long Noncoding RNA Cancer Susceptibility Candidate 9 Promotes Nasopharyngeal Carcinogenesis via Stabilizing HIF1a CASC9 CASC9, ESCCAL-1, ESSCAL1, LINC00981 101805492 ENSG00000249395 NR_103848 GRCh38_8:75223404-75324741 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Cell proliferation assay etc. lung cancer tissues, cell line (A549) up-regulated We detected 6 lncRNAs including 3 that were up-regulated (LINC00511, AFAP1-AS1, CASC9) and 3 down-regulated (LINC00968, TINCR, LINC00035) in 20 paired LUAD and LUSC and normal tissues to evaluate the analysis results. The results of qPCR showed that all the chosen lncRNA expressions were increased or decreased in LUAD or LUSC tissues compared with those in the normal tissues, which is consistent with the bioinformatic analysis results. Knockdown of LINC00511, AFAP1-AS1, and PVT1 impaired LUAD or LUSC cell proliferation. 27797003 2016 Transcriptome analysis of distinct long non-coding RNA transcriptional fingerprints in lung adenocarcinoma and squamous cell carcinoma. CASC9 CASC9, ESCCAL-1, ESSCAL1, LINC00981 101805492 ENSG00000249395 NR_103848 GRCh38_8:75223404-75324741 lung squamous cell carcinoma C34 M8070/3 qPCR, RNAi, Cell proliferation assay etc. lung cancer tissues, cell line (SK-MES-1) up-regulated We detected 6 lncRNAs including 3 that were up-regulated (LINC00511, AFAP1-AS1, CASC9) and 3 down-regulated (LINC00968, TINCR, LINC00035) in 20 paired LUAD and LUSC and normal tissues to evaluate the analysis results. The results of qPCR showed that all the chosen lncRNA expressions were increased or decreased in LUAD or LUSC tissues compared with those in the normal tissues, which is consistent with the bioinformatic analysis results. Knockdown of LINC00511, AFAP1-AS1, and PVT1 impaired LUAD or LUSC cell proliferation. 27797003 2016 Transcriptome analysis of distinct long non-coding RNA transcriptional fingerprints in lung adenocarcinoma and squamous cell carcinoma. CASC9 CASC9, ESCCAL-1, ESSCAL1, LINC00981 101805492 ENSG00000249395 NR_103848 GRCh38_8:75223404-75324741 esophageal squamous cell cancer NA NA qPCR, Western blot esophageal squamous cell carcinoma tissues, cell lines (KYSE30,KYSE150, TE-1, Eca-109,HEEpiC) up-regulated CASC9 expression is independent Multivariate analysis showed prognostic indicators of overall survival and disease-free survival.inhibition of CASC9 can inhibit the proliferation, migration and invasion of ESCC. Abnormal CASC9 expression can regulate the expression level of markers EMT. 29424900 2018 LncRNA CASC9 promotes tumorigenesis by affecting EMT and predicts poor prognosis in esophageal squamous cell cancer. CASC9 CASC9, ESCCAL-1, ESSCAL1, LINC00981 101805492 ENSG00000249395 NR_103848 GRCh38_8:75223404-75324741 esophageal squamous cell cancer NA NA microarray, RIP, in vitro knockdown, luciferase reporter assay, Western blot etc. cell line (Het-1A,EC109, KYSE150, KYSE450), FFPE tissue up-regulated CASC9 preferentially affected gene expression linked to ECM-integrin interactions, including LAMC2, an upstream inducer of the integrin pathway. CASC9 and LAMC2 depletion reduced the phosphorylation of FAK, PI3K, and Akt, which are downstream effectors of the integrin pathway. Moreover, the reduction in phosphorylation caused by CASC9 depletion was rescued by LAMC2 overexpression, further confirming that CASC9 exerts a pro-metastatic role through LAMC2.CASC9 could bind with the transcriptional coactivator CREB-binding protein (CBP) in the nucleus.CASC9 increased the enrichment of CBP and H3K27 acetylation in the LAMC2 promoter, thereby upregulating LAMC2 expression. 29511340 2018 LncRNA CASC9 promotes esophageal squamous cell carcinoma metastasis through upregulating LAMC2 expression by interacting with the CREB-binding protein. CASC9 CASC9, ESCCAL-1, ESSCAL1, LINC00981 101805492 ENSG00000249395 NR_103848 GRCh38_8:75223404-75324741 esophageal squamous cell cancer NA NA Western blot esophageal squamous cell carcinoma tissues down-regulated ESCCAL_1 knockdown significantly inhibited EC9706 cell growth in nude mice.reduced expression of ESCCAL_1 resulted in distinct alterations of relative phosphorylation level of kinases (p-p38a, p-JNK, p-FAK and p-Src), and significant changes of the expression level of apoptosis-related proteins (p53,BAX, Bcl-2 and Caspase-3).Over-expression of ESCCAL_1 activates survival pathway and decrease apoptosis. 29416654 2017 Down-regulation of long non-coding RNA ESCCAL_1 inhibits tumor growth of esophageal squamous cell carcinoma in a xenograft mouse model. CASC9.5 NA NA NA NA NA lung adenocarcinoma C34 M8140/3 qPCR, Western blot, in vitro knockdown, RNAi, RIP lung adenocarcinoma tissue, lung adenocarcinomar cell lines (A549 and SPC-A1) up-regulated CASC9.5 expression levels were significantly higher in lung cancer tissues and cells compared with normal lung tissues.CASC9.5 promoted lung adenocarcinoma cell proliferation and metabolism by regulating the expression levels of cyclin D1, E-cadherin, N-cadherin and B-catenin. 29311567 2018 Long noncoding RNA CASC9.5 promotes the proliferation and metastasis of lung adenocarcinoma. CAT1297 NA NA NA NA NA bladder cancer C67 NA qPCR bladder cancer tissues, cell lines (SW780, SW800) up-regulated Up-regulation of three lncRNAs CAT266, CAT1297, and CAT1647 in bladder cancer, in comparison to normal urothelium, was confirmed in an independent series of normal, non-muscle invasive (NMIBC) and MIBC tissue samples. Furthermore, expression levels of CAT1297 were found to be correlated with disease-free and overall survival in MIBC. 28415801 2017 Identification of long non-coding RNAs that stimulate cell survival in bladder cancer Cat2184.4 NA NA NA NA NA prostate cancer C61.9 NA qPCR etc. prostate cancer tissues, cell line (PC5) down-regulated The expression of Cat2184.4 showed a significant down-regulation in tumor samples (P<0.0001), compared to BPH ones. 29671889 2018 Two long non-coding RNAs, Prcat17.3 and Prcat40, could efficiently discriminate benign prostate hyperplasia from prostate cancer. CCAL NA NA NA NA NA papillary thyroid cancer NA M8260/3 RT-qPCR, Western blot, in vitro knockdown Human thyroid epithelium cell lines (BCPAP, FTC133, 8505C, TPC-1 and HTH-83) up-regulated In mechanism, we found that knockdown of CCAL dramatically decreased the expression of NOTCH1 and suppressed the activation of NOTCH1 signaling pathway. Furthermore, Overexpression of NOTCH1 rescued the proliferation, migration and invasion in papillary thyroid cancer cells. Taken together, our data indicated that CCAL promoted papillary thyroid cancer development and progression by activation of NOTCH1 pathway, which provided a new insight on the design of therapeutic targets. 29471887 2018 Long non-coding RNA CCAL promotes papillary thyroid cancer progression by activation of NOTCH1 pathway. CCAL NA NA NA NA NA gastric cancer C16 NA RT-PCR, Western blot GC tumor tissue, GC cell lines (BGC-823, MKN-45, AGS, SGC-7901, MGC-803) up-regulated CCAL was upregulated in gastric cancer cell lines. Patients whose tumors had high CCAL expression had a shorter overall survival than patients whose tumors had low CCAL expression Overexpression CCAL promoted the proliferation, migration and invasion of GC by regulating the expression of myc. 29441950 2018 Long noncoding RNA CCAL promotes gastric cancer cell proliferation and migration in a Myc dependent way. CCAL NA NA NA NA NA osteosarcoma NA M9180/3 qPCR, Cell proliferation assay, Cell migration and invasion assay etc. osteosarcoma tissues, cell lines (MG-63, HOS, U2OS) up-regulated We showed that CCAL was significantly up-regulated in OS tissues compared with adjacent nontumor tissues. Increased expression of CCAL was correlated with advanced TNM stage and metastasis. 28009431 2017 Up-regulation of long noncoding RNA CCAL predicts poor patient prognosis and promotes tumor metastasis in osteosarcoma. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 endometrial cancer NA M8380/3 qPCR etc. EC tissues up-regulated CARLo-5 expression was significantly higher in EC tissues than in NETs and significantly associated with FIGO stage and lymph node metastasis. Patients with high CARLo-5 expression had significantly shorter overall survival than those with low CARLo-5 expression. The rs6983267 genotype was significantly correlated with CARLo-5 expression. 27432114 2016 The rs6983267 SNP and long non-coding RNA CARLo-5 are associated with endometrial carcinoma. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RIP, ChIP etc. HCC tissues, cells lines (MHCC-97H, SMCC-7721 MHCC97L, L02) up-regulated CARLo-5 expression was significantly higher in HCC tissues and upregulated CARLo-5 expression was closely correlated with tumor size and advanced tumor stage. higher CARLo-5 expression predicted a poor prognosis for HCC patients and was an independent risk factor for OS in HCC patients. CARLo-5 inhibited the miR-200b expression via EZH2. CARLo-5 represented a novel tumor biomarker and therapeutic target for HCC. 29050269 2017 Long non-coding RNA CARLo-5 promotes tumor progression in hepatocellular carcinoma via suppressing miR-200b expression. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 melanoma NA M8720/3 qPCR, Luciferase reporter assay, in vitro knockdown cell lines (M21, B16F10, melanoma200, MEL-RM, A375, A2058) up-regulated Expression of CCAT1 was significantly upregulated in melanoma tissue and cell lines. CCAT1 knockdown observably suppressed the proliferation, migration, and invasion abilities. CCAT1 acts as an oncogenic factor in the genesis of melanoma and exerts tumor-promoting roles via sponging miR-33a, providing a novel insight for competing endogenous RNA (ceRNA) in the tumorigenesis of melanoma. 28409554 2017 The lncRNA CCAT1 Upregulates Proliferation and Invasion in Melanoma Cells via Suppressing miR-33a. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 acute myeloid leukemia NA M9861/3 qPCR, Western blot, Luciferase reporter assay, Flow cytometry assay etc. blood, cell line (HL-60) up-regulated the aberrant upregulation of CCAT1 was detected in French-American-British M4 and M5 subtypes of adult AML patients. By gain- and loss-of-function analysis, we determined that CCAT1 repressed monocytic differentiation and promoted cell growth of HL-60 by sequestering tumor suppressive miR-155. Accordingly, a significant decrease in miR-155 level was detected in AML patients. Re-introduction of miR-155 into HL-60 cells restored monocytic maturation and repressed cell proliferation. Furthermore, CCAT1 could up-regulated c-Myc via its competing endogenous RNA (ceRNA) activity on miR-155. In conclusion, these results revealed new mechanism of lncRNA CCAT1 in AML development, and suggested that the manipulation of CCAT1 expression could serve as a potential strategy in AML therapy. 26923190 2016 Long Non-Coding RNA CCAT1 Acts as a Competing Endogenous RNA to Regulate Cell Growth and Differentiation in Acute Myeloid Leukemia CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 cervical cancer C53 NA qPCR etc. cervical cancer tissues up-regulated The effects of lncRNA CCAT1 expression on HeLa cell viability, and migration and invasion were also analyzed by MTT and Transwell assays. The results demonstrated that lncRNA CCAT1 was highly expressed in the cervical cancer tissue compared with the adjacent normal tissue. High expression of lncRNA CCAT1 was positively associated with tumor size, and there was correlation between high lncRNA CCAT1 expression and a poor survival rate of cervical cancer. The cell viability, and migratory and invasive abilities were suppressed by silencing CCAT1. The results of the present study indicate that lncRNA CCAT1 was highly expressed in cervical cancer, and may serve important roles in promoting the progression and metastasis of cervical cancer. 28849215 2017 Long noncoding RNA colon cancer associated transcript-1 promotes the proliferation, migration and invasion of cervical cancer CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 cholangiocarcinoma NA M810/3 qPCR cholangiocarcinoma tissues up-regulated The CCAT1 expression was significantly upregulated in CCA tumor tissues compared with adjacent normal tissues. The overall survival of CCA patients with high CCAT1 expression was worse. 28387907 2017 LncRNA CCAT1 as the unfavorable prognostic biomarker for cholangiocarcinoma CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 esophageal squamous cell cancer NA NA qPCR, RNAi, Western blot, Cell proliferation assay etc. ESCC tissues, cell lines (Eca-109 and TE-1) up-regulated We found that lncRNA CCAT1, whose expression is significantly increased and is correlated with outcomes in Esophageal Squamous Cell Carcinoma.Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo. In cytoplasm, CCAT1 regulates HOXB13 as a molecular decoy for miR-7, a microRNA that targets both CCAT1 and HOXB13, thus facilitating cell growth and migration. 27956498 2017 H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 breast cancer C50 NA qPCR etc. breast cancer tissues up-regulated Expression levels of lncRNA CCAT1 in BC tissues were significantly higher than those in adjacent normal tissues. High expression of lncRNA CCAT1 was associated with differentiation grade, TNM stage, and lymph node metastases. Kaplan-Meier analysis with the log-rank test indicated that high expression of lncRNA CCAT1 had a decreased overall survival and progression-free survival. Multivariable analysis was further identified high expression of lncRNA CCAT1 as an independent prognosis factor for overall survival and progression-free survival. 26464701 2015 Overexpression of long non-coding RNA CCAT1 is a novel biomarker of poor prognosis in patients with breast cancer CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 breast cancer C50 NA qPCR, Luciferase reporter assay, RIP Breast cancer tissues, human breast cancer cell lines (MCF-7 and MDA-MB-231) up-regulated CCAT1 was up-regulated and miR-148b was down-regulated in radioresistant breast cancer tissues compared with radiosensitive breast cancer tissues.CCAT1 down-regulation reduced colony formation rates and caspase3 activity in breast cancer cells under irradiation. Moreover, CCAT1 could negatively regulate miR-148b expression. Furthermore, overexpression of miR-148b suppressed colony survival fraction and caspase3 expression under irradiation in breast cancer cells, which was exacerbated by CCAT1 knockdown. 29024383 2017 Down-regulation of LncRNA CCAT1 enhances radiosensitivity via regulating miR-148b in breast cancer. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot etc. NSCLC tissues, cell lines (A549, SPC-A1, NCI-H1975) up-regulated In the present study, a great upregulation of CARLo-5 was observed in cancer tissues compared to their adjacent normal tissues. Meanwhile, patients with high CARLo-5 expression have significantly poorer prognosis than those with low expression. Inhibition of CARLo-5 by siRNA suppressed the proliferation, migration, and invasion in NSCLC cell lines in vitro. In addition, silencing of CARLo-5 reversed the epithelial-mesenchymal transition in NSCLC cell line. 25129441 2014 Long non-coding RNA CARLo-5 is a negative prognostic factor and exhibits tumor pro-oncogenic activity in non-small cell lung cancer. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 gastric cancer C16 NA qPCR, Western blot, in vitro knockdown etc. gastric cancer tissues up-regulated In the present study, a great upregulation of CARLo-5 was observed in gastric cancer compared to paired adjacent normal tissues. Knockdown of CARLo-5 in gastric cancer cell lines significantly inhibited the cell proliferation via inducing G0/G1 cell-cycle arrest and apoptosis. 25674211 2015 Enhanced expression of long noncoding RNA CARLo-5 is associated with the development of gastric cancer. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. cell lines (HepG2, Hep3B, SK-HEP1, SMMC7721, MHCC97-L, MHCC97-H, PLC/PRF/5, HCCLM3) up-regulated The results showed that CARLo-5 levels were significantly overexpressed in HCC tissues compared to ANLT. Besides, high expression of CARLo-5 was associated with liver cirrhosis, tumor number, vascular invasion, capsular formation and Edmondson-Steiner grade, which proved that CARLo-5 was an independent risk factor for overall survival and disease-free survival. In addition, in highly metastatic HCC cell lines (HCCLM3 and MHCC97-L), CARLo-5 was up-regulated, but in lowly metastatic HCC cell lines (HepG2, SNU387), it showed down-regulated. Besides, by using gain and loss of function experiments in HCC cell lines (HCCLM3 and HepG2), the results showed that CARLo-5 overexpression significantly enhanced cell proliferation, migration and invasion in vitro. Our study also revealed that CARLo-5 was prominently up-regulated in HCC specimens and its high expression was associated with poor prognosis of HCC patients 26433964 2015 Long non-coding RNA CARLo-5 expression is associated with disease progression and predicts outcome in hepatocellular carcinoma patients CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 ovarian cancer C56.9 NA qPCR ovarian cancer tissues, cell lines (OVCAR-8 and SKOV-3, OMC685, IOSE386) up-regulated the expression of lncRNA CCAT1 was closely related to prognosis, tumor size, and lymph node metastasis. lncRNA CCAT1 could sponge miR-1290 in ovarian cancer.high expression of lncRNA CCAT1 could be used as an indicator of the survival time of OC patients. 29424889 2018 LncRNA colon cancer-associated transcript 1 (CCAT1) promotes proliferation and metastasis of ovarian cancer via miR-1290. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 ovarian cancer C56.9 NA qPCR, Western blot, Luciferase reporter assay etc. EOC tissue, cell lines (HO8910, HO8910PM, OVCAR3, SKOV3) up-regulated CCAT1 was an independent prognostic indicator. While CCAT1 downregulation inhibited EOC cell epithelial-mesenchymal transition(EMT), migration and invasion, CCAT1 upregulation promoted EOC cell EMT, migration and invasion. We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b, respectively, and could be regulated by CCAT1 in EOC cells. Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion. Taken together, our study first revealed a critical role of CCAT1-miR-152/miR-130b-ADAM17/WNT1/STAT3/ZEB1 regulatory network in EOC cell metastasis. These findings provide great insights into EOC initiation and progression, and novel potential therapeutic targets and biomarkers for diagnosis and prognosis for EOC. 28754469 2017 Long non-coding RNA CCAT1 promotes metastasis and poor prognosis inepithelial ovarian cancer CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 colorectal cancer C19.9 NA qPCR, RNAi etc. primary prostate cancer tissues up-regulated CARLo-5 is highly expressed in CRC-derived cell lines compared with normal colon-derived fibroblasts and CRC primary tissues compared with their matched normal adjacent tissues (NATs). In addition, CARLo-5 is highly expressed in prostate cancer (PC) tissues compared with their NATs. CARLo-5 is significantly correlated with the rs6983267 allele associated with increased cancer susceptibility. We also found the MYC enhancer region physically interacts with the active regulatory region of the CARLo-5 promoter, suggesting long-range interaction of MYC enhancer with the CARLo-5 promoter regulates CARLo-5 expression. 24594601 2014 Long-range interaction and correlation between MYC enhancer and oncogenic long noncoding RNA CARLo-5. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot etc. HCC tissues, cell lines (HepG2 and 97H) differential expression c-Myc directly binds to the E-box element in the promoter region of CCAT, and when ectopically expressed increases promoter activity and expression of CCAT1. Moreover, Kaplan-Meier analysis demonstrated that the patients with low expression of CCAT1 demonstrated better overall and relapse-free survival compared with the high expression group. Cox proportional hazards analyses showed that CCAT1 expression was an independent prognostic factor for HCC patients 26225650 2016 Aberrant Expression of CCAT1 Regulated by c-Myc Predicts the Prognosis of Hepatocellular Carcinoma CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell lines (L-02, HepG2, SNU423, SMMC-7721, Hep3B) up-regulated The results indicated that the expression of CCAT1 was significantly increased in HCC tissues and cells compared with controls. We also found that the abnormally expressed CCAT1 could promote cell proliferation, migration and invasion. Taken together, our findings demonstrated that the aberrant expression of CCAT1 promotes hepatocellular carcinoma in vitro 26191246 2015 CCAT1 promotes hepatocellular carcinoma cell proliferation and invasion CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RIP, Flow cytometry assay, Cell proliferation assay etc. HCC tissues, cell lines (LO2, QSG-7701, SMMC-7721, Hep3B, Huh7, and HepG2) up-regulated CCAT1 levels are markedly increased in HCC tissues compared with pair-matched noncancerous hepatic tissues. Up-regulation of CCAT1 is correlated with tumor size, microvascular invasion, AFP and poor prognosis. CCAT1 promotes the proliferation and migration of HCC cells. CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. 25884472 2015 Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 cervical cancer C53 NA qPCR, Western blot etc. cervical cancer tissues, cell lines (HeLa, CaSki) up-regulated the expression of CCAT-1 in cervical cancer tissue was significantly upregulated.Kaplan-Meier survival analysis showed that recurrence-free survival of the low-CCAT-1 group was significantly higher than that of the high-CCAT-1 group. 28978096 2017 CCAT-1 promotes proliferation and inhibits apoptosis of cervical cancer cells via the Wnt signaling pathway. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 cervical squamous cell carcinoma C53 M8070/3 qPCR etc. cervical cancer tissues up-regulated We found that lncRNA CCAT2 was up-regulated in cervical squamous cell cancer tissues compared to the adjacent non-tumor tissues. In addition, the high lncRNA CCAT2 expression was significantly associated with the FIGO stage, lymph node metastasis and depth of cervical invasion. 26722527 2015 Up-regulation of long non-coding RNA CCAT2 correlates with tumor metastasis and poor prognosis in cervical squamous cell cancer patients. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 endometrial cancer NA M8380/3 qPCR, Luciferase reporter assay, Western blot endometrial cancer tissues, cell lines (HEC-1-A and RL95-2) up-regulated Knockdown of CCAT2 inhibited HEC-1-A and RL95-2 cells viability, migration, invasion, but induced apoptosis. CCAT2 was an endogenous sponge by competing for miR-216b, and miR-216b suppression alleviated CCAT2 silence-diminished cell growth and metastasis. miR-216b negatively regulated Bcl-2 and Bcl-2 could further active PTEN/PI3K/AKT and mTOR signaling pathways.patients with elevated expression of CCAT2 are prone to developing distant metastasis, and have poorer over all survival and progression-free survival. 29036788 2017 Knockdown of lncRNA CCAT2 inhibits endometrial cancer cells growth and metastasis via sponging miR-216b. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 cholangiocarcinoma NA M810/3 qPCR, Western blot, in vitro knockdown etc. cell lines (RBE, HCCC-9810, QBC939, CCLP-1, Huh-28, HuCCT1, KMBC, HIBEC), CCA tissue up-regulated The potential effects of CCAT2 in CCA cells was evaluated in vitro including cell proliferation, colony-forming ability, apoptosis, migration, invasion and epithelial-to-mesenchymal transition (EMT). CCAT2 was aberrantly overexpressed in CCA tissue samples and cells, and this upregulation was correlated with tumor size, lymph node invasion, TNM stage and postoperative recurrence in CCA patients. Overexpression of CCAT2 was a dismal prognostic indicator for patients with CCA. Furthermore, CCAT2 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion, inducing cell apoptosis and reversing the EMT process in HuCCT1 and CCLP1 cells. 29329034 2018 Long non-coding RNA CCAT2 promotes cholangiocarcinoma cells migration and invasion by induction of epithelial-to-mesenchymal transition. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, Western blot, Luciferase reporter assay etc. clear cell renal cell carcinoma tissues, cell lines (HK-2, 786-O and ACHN) up-regulated CCAT2 expression was markedly higher in ccRCC cell lines and tissues, being positively associated with tumor size and tumor stage in ccRCC patients. Patients with higher CCAT2 expression had a markedly poorer overall survival than did patients with low CCAT2 expression. Knocking down CCAT2 expression led to reduced cell proliferation and increased apoptosis of ccRCC cells in vitro as well as the activation of Wnt/B-catenin signaling pathway, and CCAT2 overexpression remarkably enhanced these oncogenic properties. In vivo mice xenograft model also showed that knocking CCAT2 expression inhibited the growth of ccRCC xenografts. In conclusion, these results indicated that CCAT2 may play a critical role in ccRCC progression and will be further considered as a biomarker for predicting the survival of ccRCC patients and a potential therapeutic target for ccRCC intervention. 28718366 2018 Long non-coding RNA CCAT2 promotes cell proliferation and invasion through regulating Wnt/B-catenin signaling pathway in clear cell renal cell carcinoma. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 pituitary adenoma C75.1 M8272/0 RT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP pituitary adenomas tissues, cell line (HP75) up-regulated CCAT2 was significantly upregulated in pituitary adenomas tissues. Elevated CCAT2 expression was correlated with poor prognosis in patients with pituitary adenomas. Moreover, CCAT2 expression was activated by E2F1. Loss-of-function and gain-of-function assays showed that CCAT2 positively regulated pituitary adenoma cell proliferation, migration, and invasion. Further investigation demonstrated that CCAT2 interacted with PTTG1, and promoted its stability. Furthermore, CCAT2 affected the expression of downstream genes regulated by PTTG1, including SOX2, DLK1, MMP2, and MMP13. 29511595 2018 Long noncoding RNA CCAT2 is activated by E2F1 and exerts oncogenic properties by interacting with PTTG1 in pituitary adenomas. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 pancreatic ductal adenocarcinoma C25.3 M8500/3 qRT-PCR, Western blot, Luciferase reporter assay PDAC tissues, pancreatic cancer cell line (PANC-1, SW1990, PC-3) up-regulated CCAT2 was up-regulated in PDAC cell lines, as compared with normal pancreatic cells. Silencing of CCAT2 inhibited cell proliferation and invasion in PANC-1 cells in vitro, and attenuated tumorigenesis of PANC-1 xenograft in vivo. Furthermore, CCAT2 was regulated by KRAS through MEK/ERK signaling pathway. 29298720 2018 CCAT2 is an oncogenic long non-coding RNA in pancreatic ductal adenocarcinoma. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 prostate cancer C61.9 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. prostate cancer tissues, cell lines (DU-145, 22RV1, WPMY-1) up-regulated We found that the expression level of CCAT2 was higher in PCa tissues and cells compared to adjacent non-tumor tissues and normal prostate stromal immortalized cells WPMY-1. We also found that knockdown of CCAT2 could inhibit cell growth, migration, and invasion in vitro. In addition, knockdown of CCAT2 stimulated epithelial-mesenchymal transition (EMT) through abrogating N-cadherin, vimentin expression and intensifing the expression levels of E-cadherin. 27558961 2016 The up-regulation of long non-coding RNA CCAT2 indicates a poor prognosis for prostate cancer and promotes metastasis by affecting epithelial-mesenchymal transition. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 small cell lung cancer C56.9 M8441/3 qPCR, Cell proliferation assay, Cell migration and invasion assay etc. SCLC tissues, cell lines (DMS-53, H446, 16HBE) up-regulated CCAT2 expression was elevated in SCLC tissues and cell lines, and correlated with malignant status and poor prognosis of SCLC patients. Furthermore, knockdown of CCAT2 expression effectively suppressed SCLC cell growth and metastasis in vitro. 27470400 2016 LncRNA CCAT2 predicts poor prognosis and regulates growth and metastasis in small cell lung cancer. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 esophageal squamous cell cancer NA NA qPCR etc. ESCC tissues up-regulated CCAT2 was upregulated in ESCC tissues, especially in cases with lymph node metastasis (LNM), advanced TNM stages, and MYC amplification. Furthermore, the level of CCAT2 was positively correlated with TNM stages, LNM, and the number of positive lymph nodes. High CCAT2 expression and MYC amplification were significantly associated with TNM stages and LNM. CCAT2 may have great potential prognostic value for assessing postoperative ESCC patients. 25919911 2015 Elevated expression of CCAT2 is associated with poor prognosis in esophageal squamous cell carcinoma. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 oral squamous cell carcinoma C06.9 M8070/3 qPCR, Western blot, Luciferase reporter assay etc. oral squamous cell carcinoma tissues, cell lines (OSCC Tca8113, Cal27 and hNOK) up-regulated Our results showed that CCAT2 functioning as a potential oncogene was upregulated in oral squamous cell carcinoma. CCAT2 with high expression level was correlated with poor differentiation, higher T stage, and clinical stage, which made CCAT2 to be a prognostic biomarker in oral squamous cell carcinoma. LiCl-activated Wnt/B-catenin signaling pathway could partly restore the CCAT2-mediated malignant biological behaviors of oral squamous cell carcinoma cells by suppressing B-catenin, CCND1, and MYC and activating glycogen synthase kinase 3 beta expression. However, CCAT2 expression was not associated with other parameters such as gender ( p = 0.5057), age ( p = 0.8907), smoking ( p = 0.2778), drinking ( p = 0.5626), position ( p = 0.1337), and N stage ( p = 0.1138) in OSCC (Table 1). These findings pro- vided initial evidence that CCAT2 may play an important role in the OSCC progression. Furthermore, Kaplan–Meier survival analysis revealed that patients with high CCAT2 expression level had a significantly poorer overall survival than those with low expression level. 28671055 2017 Silencing of long non-coding RNA CCAT2 depressed malignancy of oral squamous cell carcinoma via Wnt/B-catenin pathway. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colon cancer C18 NA qPCR etc. colon tumor tissues down-regulated Here, we show that the long ncRNA CCAT2, located at the 8q24 amplicon on cancer risk-associated rs6983267 SNP, regulates cancer metabolism in vitro and in vivo in an allele-specific manner by binding the Cleavage Factor I (CFIm) complex with distinct affinities for the two subunits (CFIm25 and CFIm68).Moreover, when we assessed the proliferation of HCT116 control and CCAT2-overexpressing cells treated with the GLS inhibitor 968, we found that cells overexpressing CCAT2 were more sensitive to GLS (GAC in this case) inhibition, implying that cells with high CCAT2 expression are dependent on GAC for survival. 28934601 2016 Allele-Specific Reprogramming of Cancer Metabolism by the Long Non-coding RNA CCAT2 CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colon cancer C18 NA qPCR etc. colon cancer tissues up-regulated Our results revealed that CCAT1 was significantly overexpressed in colon cancer tissues when compared with normal tissues, and its increased expression was correlated with patients' clinical stage, lymph nodes metastasis, and survival time after surgery. Moreover, c-Myc could promote CCAT1 transcription by diretcly binding to its promoter region, and upregulation of CCAT1 expression in colon cancer cells promoted cell proliferation and invasion. 25185650 2014 C-Myc-activated long noncoding RNA CCAT1 promotes colon cancer cell proliferation and invasion. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 gastric cancer C16 NA qPCR, Western blot etc. cell lines (BGC-823) up-regulated CCAT2 was able to positively regulate the expression of POU5F1B gene. Furthermore, silencing of CCAT2 gene inhibited the proliferation of BGC-823 cells, as well as induced apoptosis and autophagy in BGC-823 cells, by suppression of the PI3K/mTOR signaling pathways.Recent studies confirmed that the lncRNA CCAT2, located at the 8q24 amplicon of the cancer risk-associated rs6983267 SNP, regulated the cancer metabolism in vitro and in vivo by directly interacting in an allele-specific manner with a protein complex. The chromosomal region 8q24 emerged as an important region for genetic susceptibility in various cancer types, thus DNA methylation or SNPs at this locus may contribute to cancer risk. RT-qPCR results revealed that CCAT2 gene expression was effectively suppressed by the transfection, while POU domain class 5 transcription factor 1B (POU5F1B) gene expression was significantly decreased. 29435046 2017 Effect of silencing colon cancer-associated transcript 2 on the proliferation,apoptosis and autophagy of gastric cancer BGC-823 cells. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 breast cancer C50 NA qPCR breast cancer tissues down-regulated significant inverse correlations were found between CCAT2 expression and stage, as well as lymph node involvement. Besides, a significant inverse correlation was found between the relative MYC expression in tumor tissues compared with their corresponding ANCTs and disease stage.CCAT2 expression level was suggested as a predictor of metastasis and poor survival for a particular subgroup of breast cancer patients. 28480695 2017 Expression Study and Clinical Correlations of MYC and CCAT2 in Breast Cancer Patients CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. cell lines (HCT116, KM12SM and COLO320DM) differential expression Here, we show that the long ncRNA CCAT2, located at the 8q24 amplicon on cancer risk-associated rs6983267 SNP, regulates cancer metabolism in vitro and in vivo in an allele-specific manner by binding the Cleavage Factor I (CFIm) complex with distinct affinities for the two subunits (CFIm25 and CFIm68). 26853146 2016 Allele-Specific Reprogramming of Cancer Metabolism by the Long Non-coding RNA CCAT2. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 ovarian cancer C56.9 NA Western blot, Luciferase reporter assay, in vitro knockdown cell lines (SKOV3, OMC685, A2780 and HO8910,OSE386), EOC tissue up-regulated CCAT2 acts as competing endogenous RNA (ceRNA) or sponge via negatively targeting miR-424, providing a novel diagnostic marker and therapeutic target for EOC. 28550684 2017 Long Noncoding RNA CCAT2 Knockdown Suppresses Tumorous Progression by Sponging miR-424 in Epithelial Ovarian Cancer. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase report assay, RIP, ChIP etc. HCC tissues, cell lines (SMMC-7721, PLC/PRF/5, Huh7, SK-Hep-1, and Hep3B) up-regulated a significant upregulation of CCAT2 in HCC tissues as compared to non-tumor tissues. CCAT2 functions as a competitive endogenous RNA (ceRNA) of FOXM1 through competitive interaction with miR-34a. a positive correlation between the tumorous CCAT2 expression and a significantly reduced overall survival (OS) (P<0.001). 28744394 2017 A positive feedback loop of long noncoding RNA CCAT2 and FOXM0 promotes hepatocellular carcinoma growth. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Cell migration and invasion assay etc. HCC tissues, cell lines (HepG2, SMMC772, MHCC97H and MIHA) up-regulated CCAT2 was upregulated in HCC cell lines and cancerous tissues. The level of CCAT2 was positively associated with tumor-node-metastasis stages and vessel invasion. Moreover, we also found that knockdown of CCAT2 expression reduced cell migration and invasion in vitro. We further demonstrated that CCAT2 played a key role in enhancing the epithelial-mesenchymal transition (EMT) through the regulation of vimentin, E-cadherin and transcription factor snail2 expression. 28280353 2017 Long non-coding RNA CCAT2 is associated with poor prognosis in hepatocellular carcinoma and promotes tumor metastasis by regulating Snail2-mediated epithelial-mesenchymal transition. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 glioma NA M9380/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. glioma tissues, cell lines (U87, U251, A172 and SHG44) up-regulated lncRNA CCAT2 was overexpressed in glioma tissues and cell lines and associated with tumor grade and tumor size. Furthermore, patients with high levels of lncRNA CCAT2 had poorer survival than those with lower levels of lncRNA CCAT2. Knocking down lncRNA CCAT2 expression significantly suppressed the glioma cell growth, migration and invasion, as well as induced early apoptosis of glioma cell in vitro. Moreover, lncRNA CCAT2 regulated epithelial-mesenchymal transition (EMT)-associated gene expression. 27938499 2016 Knockdown of long noncoding RNA CCAT2 inhibits cellular proliferation, invasion, and EMT in glioma cells. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 ovarian cancer C56.9 NA qPCR, RNAi, MTT assay etc. ovarian cancer tissues, cell lines (SKOV3, IGROV1, A2780, OVCAR3 etc.) up-regulated Expression levels of the lncRNA CCAT2 in ovarian cancer tissues and cell lines were significantly higher compared with values obtained for adjacent non-tumor tissues and normal ovarian epithelial cells. 27283598 2016 The long non-coding RNA CCAT2 is up-regulated in ovarian cancer and associated with poor prognosis. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colon cancer C18 NA qPCR, Western blot etc. colon cancer tissues, cell lines (SOSP-9607, MG-63, U2OS and SAOS-2) up-regulated We indicated that CCAT2 expression was up-regulated in osteosarcoma tissues and cell lines (SOSP-9607, MG-63, U2OS and SAOS-2). In addition, osteosarcoma cases with higher CCAT2 expression had a poorer disease-free survival and shorter the overall survival time compared to those with lower expression. Overexpression of CCAT2 promoted osteosarcoma cell proliferation, invasion and cell cycle. Furthermore, ectopic expression of CCAT2 increased the expression of mesenchymal markers N-cadherin, vimentin and snail and reduced the expression of N-cadherin marker E-cadherin. CCAT2 overexpression promoted the LATS2 and c-Myc expression in osteosarcoma cell. These data indicated that CCAT2 served as an oncogene in osteosarcoma and promoted osteosarcoma cell proliferation, cell cycle and invasion. 29502343 2018 LncRNA CCAT2 promoted osteosarcoma cell proliferation and invasion. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 breast cancer C50 NA qPCR, Western blot, RIP, ChIP etc. breast tissues, cell lines (MCF-7, MDA-MB-231, MCF10A) up-regulated Moreover, when CCAT2 silencing, the cell cycle relative protein CyclinD1, CyclinE1 and CDK4 expression were downregulated, but p15 was up-regulated in MCF7 and MDA-MB-231 cells.CCAT2 expression levels in tumor tissues were markedly increased than that in adjacent normal tissues. higher CCAT2 expression was closely correlated with shorter over survival (OS) time in patients. CCAT2 suppressed the p15 expression level via interacting with EZH2 in breast cancer cells. In vivo, the tumor growth was inhibited after knockdown of CCAT2. 28531944 2017 Upregulation of CCAT2 promotes cell proliferation by repressing the P15 in breast cancer. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. gastric cancer tissues, cell lines (GES-1, SGC7901, MKN45, BGC-823 and MKN-28) up-regulated The expression levels of CCAT2 were significantly up-regulated in 108 cases GC tissues compared with adjacent non-tumor tissues by qRT-PCR analysis. Higher CCAT2 expression was correlated with tumor size, lymph node metastasis and TNM stage in GC patients. Further function analysis demonstrated that knockdown of CCAT2 inhibited the cell migration and invasion, whereas, the overexpression of CCAT2 showed the opposite results in GC cells. Our results also demonstrated that CCAT2 promoted the GC cells EMT by downregulated the E-cadherin expression and upregulated the ZEB2, Vimentin and N-cadherin expression. 27904778 2016 Long non-coding RNA CCAT2 promotes gastric cancer proliferation and invasion by regulating the E-cadherin and LATS2. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 gastric cancer C16 NA qPCR, RNAi etc. gastric cancer tissues, cell lines (BGC-823, SGC-7901, AGS, MKN-45, HGC-27 etc.) up-regulated Expression levels of lncRNA CCAT2 in gastric cancer tissues were significantly higher than those in adjacent non-tumor tissues. By statistical analyses, high lncRNA CCAT2 expression was observed to be closely correlated with higher incidence of lymph node metastasis and distance metastasis. Moreover, patients with high lncRNA CCAT2 expression had shorter overall survival and progression-free survival compared with the low lncRNA CCAT2 group. 25755774 2015 Long non-coding RNA CCAT2 is up-regulated in gastric cancer and associated with poor prognosis. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colorectal cancer C19.9 NA qPCR, RIP etc. CRC tissues, cell lines (COLO320DM, HCT116, RKO, HEK293 etc.) up-regulated Here, we report that CCAT2, a novel long noncoding RNA transcript (lncRNA) encompassing the rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tumor growth, metastasis, and chromosomal instability. Our results support a new mechanism of MYC and WNT regulation by the novel lncRNA CCAT2 in colorectal cancer pathogenesis, and provide an alternative explanation on the SNP-conferred cancer risk. 23796952 2013 CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 osteosarcoma NA M9180/3 qPCR, Western blot etc. osteosarcoma tissues, cell line (SAOS-2, MG63, U2-OS and Nhost) up-regulated We demonstrated that lncRNA CCAT2 expression was significantly upregulated in OS tissues compared to adjacent normal bone tissues. Higher lncRNA CCAT2 expression positively associated with larger tumor size, advanced tumor stage and poor overall survival (OS) rate of patients. In vitro, knockdown of lncRNA CCAT2 suppressed cell proliferation and colony formation ability. In contrast, overexpression of lncRNA CCAT2 showed promoting cell proliferation effects in OS. Also, we found that knockdown of lncRNA CCAT2 inhibited GSK3B/B-catenin signaling by reducing p-GSK3B and B-catenin expression, but increasing GSK3B expression. 29863240 2018 LncRNA CCAT2 enhances cell proliferation via GSK3β/β-catenin signaling pathway in human osteosarcoma. CCAT4 NA NA NA NA NA colorectal cancer C19.9 NA microarray, qPCR, Luciferase reporter assay etc. CRC tissues, cell lines (HCT116, RKO, HT29, SW620 etc.) up-regulated Of the seletced lncRNAs, four lncRNAs named CCAT3, CCAT4, CCAT5, and CCAT6 (also named MYCLo-2) are upregulated in CRC cell lines, and two lncRNAs named CCAT7 and CCAT8 are downregulated in CRC cell lines. MYC-regulated lncRNAs, named MYCLos. The MYC-regulated MYCLos may function in cell proliferation and cell cycle by regulating MYC target genes such as CDKN1A (p21) and CDKN2B (p15), suggesting new regulatory mechanisms of MYC-repressed target genes through lncRNAs. 25663692 2015 Role of MYC-regulated long noncoding RNAs in cell cycle regulation and tumorigenesis. CCAT6 NA NA NA NA NA colorectal cancer C19.9 NA microarray, qPCR, Luciferase reporter assay etc. CRC tissues, cell lines (HCT116, RKO, HT29, SW620 etc.) up-regulated Of the seletced lncRNAs, four lncRNAs named CCAT3, CCAT4, CCAT5, and CCAT6 (also named MYCLo-2) are upregulated in CRC cell lines, and two lncRNAs named CCAT7 and CCAT8 are downregulated in CRC cell lines. MYC-regulated lncRNAs, named MYCLos. The MYC-regulated MYCLos may function in cell proliferation and cell cycle by regulating MYC target genes such as CDKN1A (p21) and CDKN2B (p15), suggesting new regulatory mechanisms of MYC-repressed target genes through lncRNAs. 25663692 2015 Role of MYC-regulated long noncoding RNAs in cell cycle regulation and tumorigenesis. CCAT7 DLGAP4-AS1, CCAT7 101926987 ENSG00000232907 NR_109939 GRCh38_20:36507702-36573391 colorectal cancer C19.9 NA microarray, qPCR, Luciferase reporter assay etc. CRC tissues, cell lines (HCT116, RKO, HT29, SW620 etc.) down-regulated Of the seletced lncRNAs, four lncRNAs named CCAT3, CCAT4, CCAT5, and CCAT6 (also named MYCLo-2) are upregulated in CRC cell lines, and two lncRNAs named CCAT7 and CCAT8 are downregulated in CRC cell lines. MYC-regulated lncRNAs, named MYCLos. The MYC-regulated MYCLos may function in cell proliferation and cell cycle by regulating MYC target genes such as CDKN1A (p21) and CDKN2B (p15), suggesting new regulatory mechanisms of MYC-repressed target genes through lncRNAs. 25663692 2015 Role of MYC-regulated long noncoding RNAs in cell cycle regulation and tumorigenesis. CCAT8 NA NA NA NA NA colorectal cancer C19.9 NA microarray, qPCR, Luciferase reporter assay etc. CRC tissues, cell lines (HCT116, RKO, HT29, SW620 etc.) down-regulated Of the seletced lncRNAs, four lncRNAs named CCAT3, CCAT4, CCAT5, and CCAT6 (also named MYCLo-2) are upregulated in CRC cell lines, and two lncRNAs named CCAT7 and CCAT8 are downregulated in CRC cell lines. MYC-regulated lncRNAs, named MYCLos. The MYC-regulated MYCLos may function in cell proliferation and cell cycle by regulating MYC target genes such as CDKN1A (p21) and CDKN2B (p15), suggesting new regulatory mechanisms of MYC-repressed target genes through lncRNAs. 25663692 2015 Role of MYC-regulated long noncoding RNAs in cell cycle regulation and tumorigenesis. CCDC26 CCDC26, RAM 137196 ENSG00000229140 NR_130917 GRCh38_8:128634199-129683679 acute myeloid leukemia NA M9861/3 microarray, qPCR, Western blot etc. cell lines (HL-60, K562 etc.) up-regulated We found that CCDC26 transcripts were abundant in the nuclear fraction of K562 human myeloid leukemia cells. We suggest that CCDC26 controls growth of myeloid leukemia cells through regulation of KIT expression.A KIT inhibitor might be an effective treatment against the forms of AML in which CCDC26 is altered. 25928165 2015 Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression. CCDC26 CCDC26, RAM 137196 ENSG00000229140 NR_130917 GRCh38_8:128634199-129683679 pancreatic cancer C25 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. pancreatic cancer tissues, cell lines (AsPC-1, PANC-1, SW1990, BxPC-3, MIAPaca-2 and CFPAC-1) up-regulated We found that the CCDC26 expression was significantly higher in PC tissues than in normal tissues. CCDC26 levels were correlated with tumor size, tumor number, and reduced overall survival (OS). Knockdown of CCDC26 expression by small interfering RNA significantly promoted growth arrest and apoptosis. 27470572 2016 Long noncoding RNA CCDC26 as a potential predictor biomarker contributes to tumorigenesis in pancreatic cancer. CCHE1 CCEPR, CCHE1, lncRNA-CCHE1 105682749 NA NR_131782 NA cervical cancer C53 NA qPCR etc. cervical cancer tissues up-regulated Our results showed that higher CCHE1 expression was found in cervical cancer tissues compared with the match normal cervical tissues. Then, we found that high levels of CCHE1 expression correlated with FIGO stage, tumor size, lymph node metastasis and HPV. 28239824 2017 Long non-coding RNA CCHE1 overexpression predicts a poor prognosis for cervical cancer. CCHE1 CCEPR, CCHE1, lncRNA-CCHE1 105682749 NA NR_131782 NA hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Flow cytometry assay, MTT assay etc. HCC tissues, cell lines (MHCC97H, Huh-7, Hep3B, HepG2 and HCCLM3) up-regulated The level of CCHE1 expressed in all five HCC cell lines was significantly higher than the normal hepatocyte L02 cells. The higher expression of CCHE1 was significantly correlated with tumor number, tumor size and TNM stage. Multivariate analyses revealed that CCHE1 expression served as an independent predictor for overall survival. Moreover, the effect of CCHE1 on proliferation was evaluated by MTT assays, and cell apoptosis was detected by flow-cytometric analysis. Further experiments demonstrated that CCHE1 knockdown significantly promoted growth arrest and cell apoptosis. Importantly, we further confirmed that ERK/MAPK pathway was found to be inactivated in the HCC cells after CCHE1 knockdown. 27427851 2016 Long noncoding RNA CCHE1 indicates a poor prognosis of hepatocellular carcinoma and promotes carcinogenesis via activation of the ERK/MAPK pathway. CCHE1 CCEPR, CCHE1, lncRNA-CCHE1 105682749 NA NR_131782 NA cervical cancer C53 NA qPCR, RNAi, Western blot, RNA pull-down assay etc. cervical cancer tissues, cell lines (HeLa, SiHa) up-regulated In this study, we found that cervical carcinoma high-expressed lncRNA 1 (lncRNA-CCHE1) was significantly upregulated in cervical cancer tissues. The higher expression of CCHE1 was significantly correlated with large tumor size, advanced Federation of Gynecology and Obstetrics stage, uterine corpus invasion, and poor survival. CCHE1 plays a pivotal role in cervical cancer cell proliferation via increasing PCNA expression and serves as a potential prognostic biomarker and therapeutic target in human cervical cancer. 25921283 2015 Long noncoding RNA CCHE1 promotes cervical cancer cell proliferation via upregulating PCNA. CCND2-AS1 NA 103752584 ENSG00000255920 NR_125790 GRCh38_12:4248765-4276184 glioma NA M9380/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. glioma tissues, cell lines (U87, U251, HA) up-regulated We found that lncRNA CCND2-AS2 is significantly up regulated in malignant glioma tissues and cell lines. Both loss- and gain-functions assays show that CCND2-AS1 promotes glioma cells proliferation and growth. In addition, we also revealed that highly expressed CCND2-AS1 could enhance Wnt/B-catenin signaling in glioma. 27923660 2017 Highly expressed lncRNA CCND2-AS1 promotes glioma cell proliferation through Wnt/B-catenin signaling. CEBPA-AS1 NA NA ENSG00000267296 NA GRCh38_19:33302857-33305054 oral squamous cell carcinoma C06.9 M8070/3 Microarray, qPCR, Western blot,in vitro knockdown etc. cell lines (Tca8113,Cal27), OSCC tissues up-regulated CEBPA-AS1 localized in the cytoplasm and the peri-nuclear cellular compartment functioning as a potential oncogene up-regulated in OSCC was correlated with poor differentiation, lymph node metastasis and high clinical stage, which made it considered to be a prognostic biomarker. Silence of CEBPA-AS1 inhibited OSCC cells proliferation and induced cells apoptosis, migration and invasion by targeting CEBPA and via a novel pathway CEBPA/Bcl2. 29281558 2017 Long non-coding RNA CEBPA-AS1 correlates with poor prognosis and promotes tumorigenesis via CEBPA/Bcl2 in oral squamous cell carcinoma. CHIAP2 CHIAP2 NA ENSG00000203878 NA GRCh38_1:111280059-111286116 lung adenocarcinoma C34 M8140/3 RNA-seq, qPCR etc. LUAD tissues down-regulated The results showed that CHIAP2, LINC00472, LINC00961 and MGC27382 were downregulated in LUAD tumor tissues when compared with adjacent non-tumor lung tissues, while AFAP1-AS1, CHIAP2 and FER1L4 were upregulated in LUAD tumor tissues. 27826625 2016 Integrated analysis of long non-coding RNA-associated ceRNA network reveals potential lncRNA biomarkers in human lung adenocarcinoma. CHIAP2 CHIAP2 NA ENSG00000203878 NA GRCh38_1:111280059-111286116 lung adenocarcinoma C34 M8140/3 RNA-seq, qPCR etc. LUAD tissues up-regulated The results showed that CHIAP2, LINC00472, LINC00961 and MGC27382 were downregulated in LUAD tumor tissues when compared with adjacent non-tumor lung tissues, while AFAP1-AS1, CHIAP2 and FER1L4 were upregulated in LUAD tumor tissues. 27826625 2016 Integrated analysis of long non-coding RNA-associated ceRNA network reveals potential lncRNA biomarkers in human lung adenocarcinoma. cox-2 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. cell line (Hepal-6, HepG2), liver tissue down-regulated The lncRNA cox-2 siRNA reduces the ability of M1 macrophages to inhibit HCC cell proliferation, invasion, migration, EMT, angiogenesis and facilitate apoptosis while strengthening the ability of M2 macrophages to promote proliferation HCC cell growth and inhibit apoptosis. These findings indicate that lncRNA cox-2 inhibits HCC immune evasion and tumor growth by inhibiting the polarization of M2 macrophages 29131381 2017 Long non-coding RNA cox-2 prevents immune evasion and metastasis of hepatocellular carcinoma by altering M1/M2 macrophage polarization. CPS1-IT1 CPS1-IT1, CPS1-IT, CPS1IT, CPS1IT1, PRO0132 29034 ENSG00000280837 NR_002763 GRCh38_2:210617571-210619876 ovarian cancer C56.9 NA qPCR, Western blot, Luciferase report assay etc. EOC tissues, cell lines (A2780, CAOV-3, ES-2, HOSE) down-regulated CPS1-IT1 was significantly downregulated in EOC cell lines and tissue samples.EOC patients in the low tissue CPS1-IT1 expression group had significantly shorter 5-year overall survival time than those in the high tissue CPS1-IT1 expression group.Survival analysis wasper formed using the Kaplan-Meier method and Cox’s proportional hazards model. 28770969 2017 Long non-coding RNA CPS1-IT1 is a positive prognostic factor and inhibits epithelial ovarian cancer tumorigenesis. CPS1-IT1 CPS1-IT1, CPS1-IT, CPS1IT, CPS1IT1, PRO0132 29034 ENSG00000280837 NR_002763 GRCh38_2:210617571-210619876 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RNAi, Western blot, RNA pull-down assay, Cell proliferation assay etc. HCC tissues, cell lines (J7, HepG2, and SK-Hep1) down-regulated Expression of CPS1-IT1 was significantly decreased in 73% of HCC tissues, and patients with low CPS1-IT1 expression had poor survival outcomes. Furthermore, in vitro functional assays indicated that CPS1-IT1 significantly reduced cell proliferation, migration and invasion capacities through reduced Hsp90 binding to and activation of HIF-1a, thereby suppressing the epithelial-mesenchymal transition (EMT). 27248828 2016 Long noncoding RNA CPS1-IT1 suppresses the metastasis of hepatocellular carcinoma by regulating HIF-1a activity and inhibiting epithelial-mesenchymal transition. CPS1-IT1 CPS1-IT1, CPS1-IT, CPS1IT, CPS1IT1, PRO0132 29034 ENSG00000280837 NR_002763 GRCh38_2:210617571-210619876 intrahepatic cholangiocarcinoma C22 M8160/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. ICC tissues, cell lines (L-02, Huh-7, Bel-7402) up-regulated Carbamoyl-phosphate synthase 1 (CPS1) and its lncRNA CPS1 intronic transcript 1 (CPS1-IT1) were observed to be upregulated in ICC. CPS1 and CPS1-IT1 were co-upregulated in ICC tissues compared with non-cancerous tissues. Knockdown of CPS1 andor CPS1-IT1 reduced the proliferation and increased the apoptosis of ICC-9810 cells. Additionally, clinical analysis indicated that CPS1 and CPS1-IT1 were associated with poor liver function and reduced survival rates when the relative expression values were greater than 4 in cancer tissues. 26499888 2015 Co-expression of the carbamoyl-phosphate synthase 1 gene and its long non-coding RNA correlates with poor prognosis of patients with intrahepatic cholangiocarcinoma. CPS1-IT1 CPS1-IT1, CPS1-IT, CPS1IT, CPS1IT1, PRO0132 29034 ENSG00000280837 NR_002763 GRCh38_2:210617571-210619876 colorectal cancer C19.9 NA qPCR, Western blot colorectal cancer tissues, cell lines (LoVo, SW620, SW480, LS174T, HCT116 and HT29) down-regulated Expression of CPS1-IT1 was significantly decreased in CRC tissues and cell lines, and patients with low CPS1-IT1 expression had poor survival outcomes. 29145177 2017 LncRna CPS1-IT1 Suppresses Cell Proliferation, Invasion and Metastasis in Colorectal Cancer CPSF6 Cleavage and Polyadenylation Factor-6 NA ENSG00000111605 NA GRCh38_12:69239537-69274358 breast cancer C50 NA qPCR, Western blot etc. BC tissues, cell lines (MDA-MB-231, MDA-MB-453, SKBR3 and BT474) up-regulated Aggressive breast cancer cells require CPSF6 for viability and tumorigenesis. CPSF6 and paraspeckles core proteins are associated with poor outcome in breast cancer. Prolactin hormone reprograms cells to suppress CPSF6 interaction with paraspeckles and ADAR1, A-I RNA editing machinery. CPSF6 and all core paraspeckles proteins to be overexpressed in human breast cancer cases and their expression to correlate with poor patient outcomes. the important role and contribution of CPFS6 to survival and tumor formation of aggressive breast cancer cells. 28673861 2017 CPSF6 is a Clinically Relevant Breast Cancer Vulnerability Target: Role of CPSF6 in Breast Cancer. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 intrahepatic cholangiocarcinoma C22 M8160/3 qPCR, Western blot, in vitro knockdown etc. IHCC tissues, IHCC cell lines (HuCCT1, RBE, HCCC9810 and HUH28) up-regulated CRNDE ectopic expression in HCCC9810 cells promoted proliferation. Moreover, the migration and invasion of HuCCT1 cells were greatly repressed with CRNDE deficiency following Transwell and Matrigel assays. Accordingly, the motility of HCCC9810 cells was notably accelerated with CRNDE overexpression. Mechanistically, CRNDE was revealed to facilitate the epithelial-mesenchymal transition (EMT) of IHCC cells. CRNDE could promote the clinical progression and metastasis of IHCC by facilitating EMT. CRNDE may be a novel prognostic marker and therapeutic target in IHCC.High CRNDE expression was identified as an independent risk factor of IHCC poor OS and PFS. 29556285 2018 Overexpression of long non-coding RNA CRNDE facilitates epithelial-mesenchymal transition and correlates with poor prognosis in intrahepatic cholangiocarcinoma. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 ovarian cancer C56.9 NA microarray, qPCR etc. ovarian cancer tissues up-regulated We have shown that the elevated level of CRNDE transcripts significantly increases the risk of death and recurrence in ovarian cancer patients. Elevated levels of two different CRNDE transcripts were a negative prognostic factor; they increased the risk of death and recurrence in the group of patients treated with TP, but not PC (DNA-damaging agents only). 26556866 2015 The putative oncogene, CRNDE, is a negative prognostic factor in ovarian cancer patients. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 pancreatic cancer C25 NA qPCR, Luciferase reporter assay, Western blot pancreatic tumour tissues, cell lines (SW1990, PANC-1, CAPAN-1, JF305 and BxPC-3, HPDE6-C7, HEK293T) up-regulated Upregulation of the expression of CRNDE was found in pancreatic cancer tissues as well as cell lines, in comparison with the adjacent non-tumour tissues and human pancreatic duct epithelial cells.High expression of CRNDE was correlated with poor clinicpathological characteristics and shorter overall survival.We identified miR-384 as a direct target for CRNDE. Moreover, the CRNDE knockdown considerably inhibited pancreatic cancer cell proliferation, migration and invasion not only in vitro but also in vivo. In addition, CRNDE positively regulated IRS1 expression through sponging miR-384. 28940804 2017 Long non-coding RNA CRNDE sponges miR-384 to promote proliferation and metastasis of pancreatic cancer cells through upregulating IRS1. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 multiple myeloma C42.1 M9732/3 qPCR, RNAi, Luciferase reporter assay, Cell proliferation assay etc. MM tissues, cell lines (MM1.S, NCIH929, U266, RPMI8226) up-regulated CRNDE expression level, in MM sample and cell lines, is higher than control. Knockdown of CRNDE significantly inhibits the proliferative vitality of MM cells and induces cell cycle arrest in G0/G1 phase and apoptosis-promoting. Subsequently, miR-451 inhibitor rescues the tumorigenesis inhibition induced by CRNDE knockdown. 28276319 2017 Long Non-coding RNA CRNDE Promotes Multiple Myeloma Cell Growth By Suppressing MiR-451. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 breast cancer C50 NA qPCR breast cancer tissues, cell lines (MCF-7, MDA-MB-231, MDA-MB-468 and BT-549) up-regulated CRNDE expression is remarkably up-regulated in BC tissue specimens and cell lines in comparison to corresponding normal tissues and normal human breast epithelial cells. Up-regulated CRNDE expression was greatly associated with larger tumor size, advanced TNM stage and unfavorable prognosis of BC patients. We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of B-catenin, c-myc and cyclinD1. 28469804 2017 Long noncoding RNA CRNDE activates Wnt/B-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 acute myeloid leukemia NA M9861/3 qPCR bone marrow tissues, acute myeloid leukemia cell line (U937) up-regulated The expression of lncRNA-CRNDE in patients with AML and U937 cells was significantly higher than that in non-malignant hematological controls. Results of clinical data showed that the expression of lncRNA-CRNDE was associated with the classification and total survival of myeloid leukemia in clinical patients. After transfection of siRNA-CRNDE, the proliferation and cloning ability of U937 cells decreased, while the apoptosis increased (p < 0.01) and cells were arrested in G0-G1 phase.the expression of lncRNA-CRNDE might play an essential role in promoting the proliferation of U937 cells. 29461608 2018 High expression of lnc-CRNDE presents as a biomarker for acute myeloid leukemia and promotes the malignant progression in acute myeloid leukemia cell line U937. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC cancer tissues, cell lines (A549, PC-9 and SK-MES-1) up-regulated The expression of CRNDE was significantly up-regulated in NSCLC patients and cells. In addition, both loss and gain function assays revealed that CRNDE promoted NSCLC cell proliferation and growth both in vitro and in vivo. Moreover, CRNDE regulated the cell cycle transition from G0/G1 stage to S stage and modulated the expression of CDK4, CDK6 and CCNE1. CRNDE activated PI3K/AKT signaling in NSCLC cell lines. CRNDE was highly expressed in NSCLC malignant tissues and the heightened CRNDE strongly promoted NSCLC cell proliferation and growth through activating PI3K/AKT signaling; our results shed a light on utilizing CRNDE as a potential novel therapeutic target for the treatment of NSCLC. 28477368 2017 Highly expressed long non-coding RNA CRNDE promotes cell proliferation through PI3K/AKT signalling in non-small cell lung carcinoma. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 gallbladder cancer C23.9 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. GBC tissues, cell lines (GBC-SD and NOZ, HEK293T) up-regulated Results showed c-IAP1 and CRNDE had a higher expression level in GBC tissue; and DMBT1 had a lower expression in GBC tissue. DMBT1 and CRNDE had a negatively correlation and CRNDE and c-IAP1 had a positive correlation in GBC tissues. Which confirmed the results we done above. These results illustrated CRNDE may act as scaffold of DMBT1 and c-IAP1 to influence the migration and invasion of GBC cancer cells. 27637083 2016 Long non-coding RNA CRNDE promotes gallbladder carcinoma carcinogenesis and as a scaffold of DMBT1 and C-IAP1 complexes to activating PI3K-AKT pathway. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR, Cell proliferation assay etc. PDAC tissues, cell lines (AsPC-1, BxPC-3, Capan-2, CFPAC-1, HPAC, MIA PaCa-2, PANC-1 and SW1990) up-regulated The qRT-PCR results showed that CRNDE, NR_036488, ENSG00000244649, AFAP1-AS and UCA1 expression was significantly increased and ENSG00000218510 expression was remarkably decreased in PDAC tissues compared with paired normal pancreatic tissues. Consistent with the findings in PDAC tissues, CRNDE, NR_036488, ENSG00000244649, AFAP1-AS1 and UCA1 expression was dramatically enhanced and ENSG00000218510 reduced in all or most of 8 PDAC cell lines in relative to the nonmalignant HPDE6-C7 cells or hTERT-HPNE cells at the RNA level. 27628540 2016 Analysis of long non-coding RNA expression profiles in pancreatic ductal adenocarcinoma. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (U87, U251 etc.) up-regulated Herein, the function and potential molecular mechanisms of CRNDE and miR-384 were illustrated in glioma cells. CRNDE overexpression facilitated cell proliferation, migration, and invasion, while inhibited glioma cells apoptosis. Quantitative real-time polymerase chain reaction (PCR) demonstrated that miR-384 was downregulated in human glioma tissues and glioma cell lines. Moreover, restoration of miR-384 exerted tumor-suppressive functions. In addition, the expression of miR-384 was negatively correlated with CRNDE expression. A binding region between CRNDE and miR-384 was confirmed using luciferase assays. Moreover, CRNDE promoted cell malignant behavior by decreasing miR-384 expression. At the molecular level, treatment by CRNDE knockdown or miR-384 overexpression resulted in a decrease of piwi-like RNA-mediated gene silencing 4 (PIWIL4) protein. Besides, PIWIL4 was identified as a target of miR-384 and plays an oncogenic role in glioma. Similarly, downstream proteins of PIWIL4 such as STAT3, cyclin D1, VEGFA, SLUG, MMP-9, caspase 3, Bcl-2, and bcl-xL were modulated when treated with miR-384 and PIWIL4. Remarkably, CRNDE knockdown combined with miR-384 overexpression led to tumor regression in vivo. 27049681 2016 CRNDE Promotes Malignant Progression of Glioma by Attenuating miR-384/PIWIL4/STAT3 Axis CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 colorectal cancer C19.9 NA qPCR, microarray, RIP, Western blotting etc. cell lines (DLD1, HCT116, SW480, SW620, LoVo, LS174t, HT29) up-regulated CRNDE is upregulated in CRC tissues and cell lines. High CRNDE expression is associated with poor prognosis in CRC patients. CRNDE upregulates the expression of Ras/MAPK signaling genes. 28594403 2017 Long noncoding RNA CRNDE stabilized by hnRNPUL2 accelerates cell proliferation and migration in colorectal carcinoma via activating Ras/MAPK signaling pathways CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 glioma NA M9380/3 qPCR etc. glioma tissues up-regulated Compared with nonneoplastic brain tissues, the expression level of CRNDE was significantly increased in glioma tissues. CRNDE upregulation was correlated with larger tumor size, higher WHO grade, and recurrence. 27775801 2016 Expression of long non-coding RNA CRNDE in glioma and its correlation with tumor progression and patient survival. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 glioma NA M9380/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell proliferation assay etc. glioma tissues, cell lines (U87, U251, HEK 293T) up-regulated CRNDE overexpression facilitated cell proliferation, migration, and invasion, while inhibited glioma cells apoptosis. Moreover, CRNDE promoted cell malignant behavior by decreasing miR-384 expression. Knockdown of CRNDE combined with overexpression of miR-384 restrained tumor growth and exhibit high survival in nude mice. 27058823 2016 CRNDE Promotes Malignant Progression of Glioma by Attenuating miR-384/PIWIL4/STAT3 Axis. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 glioma NA M9380/3 qPCR, Western blot, in vitro knockdown glioma tissues, cell lines (D54) up-regulated We confirm that CRNDE acts as an oncogene that is highly up-regulated in glioma, and high CRNDE expression correlates with poor prognosis in glioma patients. 28493025 2017 CRNDE Expression Positively Correlates with EGFR Activation and Modulates Glioma Cell Growth CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay etc. hepatocellular carcinoma tissues, cell line(QSG-7701) up-regulated CRNDE is more commonly up-regulated in HCC malignant tissues and associated with poor clinical outcomes. Furthermore, both loss- and gain-functions assays revealed that CRNDE promotes HCC cell proliferation and growth in vitro and in vivo. In addition, we found that CRNDE regulates PI3K/Akt/GSK3B-Wnt/B-catenin axis to exert its oncogenic role in HCC cell proliferation and growth. The full length T1 and another variant T3, especially T1, were significantly elevated in HCC malignant tissues as compared with variant T2 and T4. 29864897 2018 Long non-coding RNA CRNDE promotes heptaocellular carcinoma cell proliferation by regulating PI3K/Akt /β-catenin signaling. CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated In CRC, upregulation of lncRNA CRNDE-h was significantly correlated with large tumor size, positive regional lymph node metastasis, and distant metastasis.Patients with CRC with high lncRNA CRNDE-h expression level had poorer overall survival than those with low lncRNA CRNDE-h expression.Further, multivariable Cox regression analysis suggested that increased expression of lncRNA CRNDE-h was an independent prognostic indicator for CRC.Furthermore, lncRNA CRNDE-h expression was positively correlated with IRX5 mRNA in CRC tissues. 27042112 2016 Increased expression of the long noncoding RNA CRNDE-h indicates a poor prognosis in colorectal cancer, and is positively correlated with IRX5 mRNA expression CRYM-AS1 NCRNA00169 400508 ENSG00000189149 NR_026675 GRCh38_16:21300849-21339037 thyroid cancer C73.9 NA qPCR, Western blot, etc. cell lines (BHT101, BCPAP) down-regulated whereas thyroid cancer patients with higher PAX8-AS1 or lower CRYM-AS1 expression levels had shorter RFS time 29923329 2018 Identification of differential expressed lncRNAs in human thyroid cancer by a genome-wide analyses. CTBP1-AS CTBP1-AS, PCAT10 285463 ENSG00000280927 NR_104331 GRCh38_4:1210120-1218591 prostate cancer C61.9 NA qPCR, Western blot, Northern blot, RIP etc. prostate cancer tissues, cell lines (VCaP, LNCaP, DU145, RWPE etc.) up-regulated CTBP1-AS is predominantly localized in the nucleus and its expression is generally upregulated in prostate cancer. CTBP1-AS promotes both hormone-dependent and castration-resistant tumour growth. Mechanistically, CTBP1-AS directly represses CTBP1 expression by recruiting the RNA-binding transcriptional repressor PSF together with histone deacetylases. CTBP1-AS also exhibits global androgen-dependent functions by inhibiting tumour-suppressor genes via the PSF-dependent mechanism thus promoting cell cycle progression. 23644382 2013 Androgen-responsive long noncoding RNA CTBP1-AS promotes prostate cancer. CTD-2574D22.4 NA NA NA NA GRCh38_16:29919634-29921905 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. hepatocellular carcinoma tissues, cell lines (MHCC97L, SMCC-7721, Huh-7, MHCC97H and LO4) up-regulated We totally identified a set of four lncRNAs(MIR100HG, SERHL, CTD-2574D22.4 and SNHG22) that were significantly correlated with patient's survival. We then measured the expression levels of these four lncRNAs using TCGA data, and found that it was significanct. 29684484 2018 Characterization of long non-coding RNAs to reveal potential prognostic biomarkers in hepatocellular carcinoma. DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 lung cancer C34 NA qPCR lung cancer tissues up-regulated DANCR upregulation was seen in lung cancer, particularly in high-grade lung cancer tissues and aggressive cancer cells. Ectopic DANCR expression induced lung cancer cell proliferation and colony formation, whereas DANCR silencing induced opposing effects. The miR-216a level in cancer cells was negatively correlated with DANCR expression. The DANCR knockdown reduced the growth of tumor xenografts in vivo. DANCR upregulation is a potential indicator of aggressive lung cancer. Silencing of DANCR has great potential as a potent therapeutic strategy in lung cancer.higher DANCR is linked to cases with lung cancer having higher clinical grade and poorer survival. 29651883 2018 LncRNA DANCR Promotes Lung Cancer by Sequestering miR-216a. DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 non small cell lung cancer C34 M8046/3 qPCR, Luciferase reporter assay, in vitro knockdown etc. cell lines (SPC-A, NCL-H1650, NCL-H1975, SK-MES-1, A549, NCL-H358 and NCI-H1299, 16HBE), NSCLC tissues up-regulated DANCR was markedly upregulated in NSCLC tumor tissues and cell lines compared with related normal controls.The ectopic expression of DANCR significantly increased the proliferation, migration and invasion of SPC-A1 and NCL-H1299 cells. Furthermore, we investigated whether DANCR regulates NSCLC tumor formation in vivo. Subsequently, we concluded that DANCR promotes NSCLC cell proliferation, migration and invasion by regulating the tumor suppressor miR-758-3p.the DANCR/miR-758-3p axis could be a potential target in the treatment of NSCLC. 29635134 2018 The long non-coding RNA-DANCR exerts oncogenic functions in non-small cell lung cancer via miR-758-3p. DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 retinoblastoma C69.2 M9510/3 qPCR, Western blot etc. retinoblastoma tissues, cell lines (Weri-Rb1, Y79, SO-RB50, HXO-RB44, ARPE-19 and hTERT-RPE1) up-regulated DANCR was up-regulated in RB tissue and cell lines.Moreover, the ectopic overexpression of DANCR indicated poor overall survivals and disease free survival (DFS) for RB patients.In vitro and in vivo experiments, DANCR knockdown suppress the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) correlated protein (N-cadherin, Vimentin) of RB cells. Bioinformatics analysis predicted that miR-34c and miR-613 targeted with 3'-UTR of DANCR, besides, miR-34c and miR-613 also targeted with 3'-UTR of MMP-9, which was validated by luciferase reporter assay. Functional experiments demonstrated that miR-34c and miR-613 could reverse the oncogenic function of DANCR in RB tumorigenesis. In conclusion, our results reveal that DANCR function as competing endogenous RNA (ceRNA) for miR-34c and miR-613 to modulate progression and metastasis in RB oncogenesis via targeting MMP-9, presenting the in-depth regulation of DANCR in RB and providing a novel insight for ceRNA mechanism for RB. 29744877 2018 Long noncoding RNA DANCR aggravates retinoblastoma through miR-34c and miR-613 by targeting MMP-9. DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 glioblastoma NA M9440/3 qPCR, Western blot etc. glioblastoma tissue, cell lines (U87, U251, SGC7901 and BGC823) up-regulated High expression of DANCR might be a poor prognostic factor in glioma patients. Results of loss-of function assay suggested that downregulated DANCR could inhibited glioma cell proliferation and migration. Additionally, western blot assay was conducted in glioma cells to demonstrate that the protein levels of the Wnt/B-catenin pathway related proteins was negatively modulated by si-DANCR. Finally, and the increased proliferation and migration of glioma cells were observed after the Wnt/B-catenin signals were activated. However, this tendency was reduced by si-DANCR. 29602127 2018 Overexpression of lncRNA DANCR positively affects progression of glioma via activating Wnt/B-catenin signaling. DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 triple negative breast cancer C50 NA qPCR, Western blot,RNAi, etc. breast cancer cell lines (MCF-7, T47D, MDA-MB-468, MDA-MB-231), TNBC tissues up-regulated In the present study, our results showed that DANCR expression was increased in TNBC tissues compared with the adjacent normal tissues using quantitative real-time PCR (qRT-PCR) in 63TNBC specimens. The correlation between lncRNA DANCR expression and the overall survival of TNBC patients. Kaplan-Meier analysis of overall survival was analyzed according to lncRNA DANCR expression levels. 28760736 2017 Targeting long non-coding RNA DANCR inhibits triple negative breast cancer progression. DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Our results showed that lncRNA DANCR expression was increased in CRC tissues compared with that in adjacent normal tissues. In addition, tumors with high lncRNA DANCR expression was correlated with TNM stage, histologic grade, and lymph node metastasis. Kaplan-Meier analysis showed that patients with high lncRNA DANCR expression had a shorter overall survival (OS) and disease-free survival (DFS) compared with the low lncRNA DANCR expression group. Moreover, in a multivariate Cox model, our results showed that lncRNA DANCR expression was an independent poor prognostic factor for both OS and DFS in CRC. 26617879 2015 Over-expression of lncRNA DANCR is associated with advanced tumor progression and poor prognosis in patients with colorectal cancer DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC cell lines up-regulated We found that lncRNA-DANCR is over-expressed in stem-like HCC cells and this can serve as a prognostic biomarker for HCC patients. Experiments showed that DANCR markedly increased stemness features of HCC cells to promote tumorigenesis and intra-/extra-hepatic tumor colonization.Our studies reveal a significance and mechanism of DANCR action in increasing stemness features and offer a potential prognostic marker and a therapeutic target for HCC. 25964079 2015 Long noncoding RNA DANCR increases stemness features of hepatocellular carcinoma via de-repression of CTNNB1. DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 osteosarcoma NA M9180/3 qPCR, Western blot etc. osteosarcoma tissue, cell lines (MG-63, U2OS, MNNG/HOS, 143B and hFOB) down-regulated an elevated DNACR was found in osteosarcoma tissue specimens and in osteosarcoma cell lines, and the elevated DNACR was closely correlated with poor prognosis in clinical patients. Functional experiments illustrated that a depression of DANCR suppressed ROCK1-mediated proliferation and metastasis in osteosarcoma cells. The results of western blot assays and qRT-PCR assays revealed that DANCR regulated ROCK1 via crosstalk with miR-335-5p and miR-1972. Further cellular behavioral experiments demonstrated that DNACR promoted ROCK1-meidated proliferation and metastasis through decoying both miR-335-5p and miR-1972. Finally, the outcomes of in vivo animal models showed that DANCR promoted tumor growth and lung metastasis of osteosarcoma. LncRNA DANCR work as an oncogene and promoted ROCK1-mediated proliferation and metastasis through acting as a competing endogenous RNA (ceRNA) in osteosarcoma. 29753317 2018 Long noncoding RNA DANCR, working as a competitive endogenous RNA, promotes ROCK1-mediated proliferation and metastasis via decoying of miR-335-5p and miR-1972 in osteosarcoma. DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay etc. tumor soft tissues, cell lines (MG63, U2OS, SaOS2, HOS, 143B) up-regulated Mechanistically, DANCR promoted osteosarcoma progression by mediating cancer stem cells (CSC) features. Moreover, pull-down assays and luciferase reporter assays indicated that DANCR upregulated expression of the receptor tyrosine kinase AXL by competitively binding to miR-33a-5p. Furthermore, DANCR enhanced the expression of proteins downstream of the AXL-Akt pathway. DANCR was consistently significantly increased in osteosarcoma tissues, and its expression was positively correlated with tumor size and metastasis as an independent poor prognostic factor. Furthermore, both in patient tumors and xenograft tumors, DANCR expression was positively related to AXL and negatively related to miR-33a-5p. Taken together, our results suggest that DANCR is a crucial upregulator of osteosarcoma and an independent predictor of prognosis. DANCR increases CSC function by upregulating AXL via competitively binding to miR-33a-5p, and this function is sequentially performed through the PI3K-Akt signaling pathway 28642170 2017 lncRNA DANCR promotes tumor progression and cancer stemness features in osteosarcoma by upregulating AXL via miR-33a-5p Q2 inhibition DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 gastric cancer C16 NA qPCR etc. gastric cancer tissues, cell lines (SGC7901, MGC803, and MKN-45) up-regulated Interestingly, DANCR was significantly upregulated in the GC tissues of the 118-patient cohort (Figure 1(a)). Kaplan–Meier analysis was used to evaluate the effects of DANCR expression and clinicopathological features on OS. 28618943 2017 Long non-coding RNA DANCR, a prognostic indicator, promotes cell growth and tumorigenicity in gastric cancer DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay, etc. glioma tissues, cell lines (U87, U251, LN229, T98G, HEB) up-regulated knockdown of DANCR increased the expression of miR-33a-5p, reduced EMT and increased apoptosis. 29940760 2018 Long non-coding RNA DANCR facilitates glioma malignancy by sponging miR-33a-5p. DBH-AS1 DBH-AS1, NCRNA00118 138948 ENSG00000225756 NR_002783 GRCh38_9:133654586-133657313 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot etc. HCC tissues, cell lines (HepG2, SMMC-7721, Hep3B, MHCC97H, SK-Hep1) up-regulated The levels of DBH-AS1 were positively correlated with hepatitis B surface antigen (HBsAg) and tumor size in HCC tissues. Overexpression of DBH-AS1 induced cell cycle progression by accelerating G1/S and G2/M transition concomitantly with upregulation of CDK6, CCND1, CCNE1 and downregulation of p16, p21 and p27. We also provide evidence that DBH-AS1 could be significantly induced by HBx protein and markedly down-regulated by p53. Thus, we concluded that DBH-AS1 can be induced by HBx and inactivated by p53, and consequently promote cell proliferation and cell survival through activation of MAPK signaling in HCC. 26393879 2015 HBx-related long non-coding RNA DBH-AS1 promotes cell proliferation and survival by activating MAPK signaling in hepatocellular carcinoma. DGCR5 DGCR5, LINC00037, NCRNA00037 26220 ENSG00000237517 NR_002733 GRCh38_22:18970514-18994628 lung cancer C34 NA qPCR, Western blot, Luciferase report assay etc. LC tissues, cell ines (BEAS-2B, H520, H157, SKMES1, H460, A549, H1299, HEK293T) down-regulated DGCR5 was downregulated and miR-1180 was upregulated in the sera and tissues of LC patients and was correlated with poor prognosis. a negative correlation between the expression of DGCR5 and miR-1180 in LC tissues and sera. DGCR5 negatively regulated miR-1180 expression. DGCR5 suppressed the proliferation, migration and invasion of LC cells by targeting miR-1180.Recently, a novel lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) was found to be downregulated in hepatocellular carcinoma (HCC), and low expression of DGCR5 was closely associated with poor five-year survival rate. 28744397 2017 Long non-coding RNA DGCR5 is involved in the regulation of proliferation, migration and invasion of lung cancer by targeting miR-1180. DGCR5 DGCR5, LINC00037, NCRNA00037 26220 ENSG00000237517 NR_002733 GRCh38_22:18970514-18994628 lung cancer C34 NA qPCR, western blot etc. lung cancer tissues, cell line A549 up-regulated Upregulation of DiGeorge syndrome critical region gene 5 (DGCR5) predicts better lung squamous cell carcinoma prognosis; therefore, we explore the role of DGCR5 in lung cancer in our present study. DGCR5 decreased the protein level of TUSC3 by miR-873-5p which was demonstrated by Western blot and immunofluorescence. 29790668 2018 The effects of aberrant expression of LncRNA DGCR5/miR‐873‐5p/TUSC3 in lung cancer cell progression DGCR9 NA 25787 ENSG00000273032 NR_024159 GRCh38_22:19017834-19020248 gastric cancer C16 NA qPCR etc. gastric cancer tissues, cell lines (GES-1, AGS, MGC803, HGC27, and SGC7901) up-regulated DGCR9 was shown to have increased expression in gastric cancer tissues and in gastric cancer cell lines. Further, DGCR9 was found to be associated with clinicopathological characteristics of patients with gastric cancer. In particular, DGCR9 was positively associated with lymph node invasion and tumor-node-metastasis (TNM) stage in gastric cancer patients. By in vitro functional analysis, knockdown of DGCR9 in gastric cancer cells suppressed cellular proliferation, migration, and glucose uptake. In contrast, overexpression of DGCR9 increased each of these cancer cell characteristics. 29719408 2018 Role of DiGeorge syndrome critical region gene 9, a long noncoding RNA, in gastric cancer. DKFZP434K028 DKFZP434K028 NA NA NA GRCh38_11:61754029-61757664 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues, cell lines (HCG-27, SGC-7901) down-regulated Linc00261, DKFZP434K028 and RPL34-AS1 had lower expression levels in gastric cancer tissues than the normal counterparts. In gastric cell lines, the three lncRNAs were also down-regulated compared with the respective normal gastric epithelial cell line GES-1. Moreover, the low expression levels of DKFZP434K028 and RPL34-AS1 positively correlated with the larger tumor size. 26237576 2015 Long non-coding RNA Linc00152 is involved in cell cycle arrest, apoptosis, epithelial to mesenchymal transition, cell migration and invasion in gastric cancer. DLEU2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 10301 ENSG00000176124 NR_002605 GRCh38_13:50082171-50723236 chronic lymphocytic leukemia NA M9823/3 microarray, qPCR, RNAi, ChIP, Luciferase reporter assay etc. blood up-regulated In contrast, the lncRNA genes DLEU1 and variant DLEU2/Alt1 that display DNA-hypomethylation at their 5' ends are significantly upregulated in CLL cells. We found a significant inverse correlation of gene expression of the lncRNA genes DLEU1 and the DLEU2 variant Alt1 with DNA-methylation levels in regions D6 and E6 that are localized at their transcriptional start sites. 23593011 2013 Epigenetic upregulation of lncRNAs at 13q14.3 in leukemia is linked to the In Cis downregulation of a gene cluster that targets NF-kB. DLEU2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 8847 ENSG00000231607 NR_002612 GRCh38_13:49982552-50125720 laryngeal cancer C32 NA qPCR, Luciferase reporter assay, in vitro knockdown etc. cell lines (TU212,A549), laryngeal cancer tissues down-regulated LncRNA Dleu2 and miR-16-1 levels were significantly declined in the laryngeal carcinoma tissue compared to para-carcinoma tissue.LncRNA Dleu2 and miR-16-1 up-regulation significantly reduced cell proliferation,migration,and invasion compared to the control group.Ago-miR16-1 transfection significantly enhanced the luciferase activity of wild-type Dleu2 compared to control group,suggesting their interaction with each other. LncRNA Dleu2 influences the proliferation, migration, and invasion of laryngeal cancer cells through miR-16-1. Therefore, lncRNA Dleu2 and miR-16-1 may serve as potential biomarkers and targets for laryngeal cancer diagnosis and treatment. 29687850 2018 Long non-coding RNA Dleu2 affects proliferation, migration and invasion ability of laryngeal carcinoma cells through triggering miR-16-1 pathway. DLEU2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 8847 ENSG00000231607 NR_002612 GRCh38_13:49982552-50125720 chronic lymphocytic leukemia NA M9823/3 qPCR, Northern blot etc. cell lines (I83E95) down-regulated Here, we demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression. 20060366 2010 The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia. DLEU7-AS1 NA NA ENSG00000237152 NA NA colorectal cancer C19.9 NA qPCR, Western blot colorectal cancer tissues, cell lines (HCT-8, HT-29, HCT-116 and SW-620) up-regulated The expression of DLEU7-AS1 is significantly increased in CRC, which is markedly associated with CRC staging, lymph node metastasis, distant metastasis and poor prognosis. DLEU7-AS1 may promote the proliferation, invasion and migration capacities of CRC through regulating the Wnt/B-catenin pathway.DLEU7-AS1 Expression was Correlated with Clinical Staging, Lymph Node Metastasis, Distant Metastasis and Overall Survival of CRC Patients 29364477 2018 Long non-coding RNA DLEU7-AS1 promotes the occurrence and development of colorectal cancer via Wnt/B-catenin pathway. DLX6-AS1 DLX6-AS1, DLX6-AS, DLX6AS, Evf-2, NCRNA00212 285987 ENSG00000231764 NR_015448 GRCh38_7:96955141-97014065 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay, Western blot hepatocellular carcinoma tissues, cell lines (MHCC97L, HCCLM3, HepG2, Hep3B, Huh7, LO2) up-regulated DLX6-AS1 expression level was up-regulated in 60 cases of HCC tissue samples compared with adjacent normal tissue.the aberrant overexpression of DLX6-AS1 indicated the poor prognosis of HCC patients. DLX6-AS1 knockdown inhibited the proliferation, migration and invasion of HCC cells in vitro, and decreased the tumor growth in vivo.miR-203a potentially targeted DLX6-AS1 3'-UTR, suggesting the interaction between miR-203a and DLX6-AS1. Furthermore, miR-203a also targeted MMP-2 mRNA 3'-UTR. 29145165 2017 Long non-coding RNA DLX6-AS1 aggravates hepatocellular carcinoma carcinogenesis by modulating miR-203a/MMP-2 pathway. DMTF1v4 NA NA NA NA NA colon cancer C18 NA qPCR, Western blot, etc. colon cancer tissues, cell line (HT-29) up-regulated lncRNA DMTF1v4 promotes colon cancer cell proliferation and migration, and inhibits apoptosis by downregulating the expression of p-ERK, p-JNK, and p-p38, thus affecting the progression of colon cancer. Compared with the control group, the cell survival rate in the DMTF1v4-siRNA group was significantly decreased. 29949153 2018 Study on the function and mechanism of long non-coding RNA DMTF1v4 in the occurrence of colon cancer. DPP10-AS1 DPP10-AS1, BC032913 389023 ENSG00000235026 NR_036580 GRCh38_2:115130935-115161343 colorectal cancer C19.9 NA Microarray, qPCR, Western blot, Luciferase reporter assay Human colorectal cancer cell lines (HCT116 , DLD-1) up-regulated Our findings indicate that the novel lncRNA BC032913 could serve as a novel prognostic marker and effective therapeutic target for CRC. A total of 115 CRC patients were included in the survival analysis, which was conducted using the Kaplan-Meier method. A log-rank test was employed to compare differences between survival curves. Although TIMP3 plays a significant role in cancers, limited data are available regarding the mechanism of TIMP3 dysregulation. It has been documented that aberrant methylation of TIMP-3 occurs in primary cancers of the colon, lung, breast, kidney, and brain. 28918047 2017 Long Noncoding RNA BC032913 as a Novel Therapeutic Target for Colorectal Cancer that Suppresses Metastasis by Upregulating TIMP3 DQ192290 KCNE2, ATFB4, LQT5, LQT6, MIRP1 NA NA NA GRCh38_21:34364024-34364151 gastric cancer C16 NA microarray, qPCR, RNAi etc. gastric cancer tissues down-regulated LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC. 25765901 2015 Reciprocal repression between TUSC7 and miR-23b in gastric cancer. DQ786243 NA NA NA NA NA gastric cancer C16 NA qPCR etc. GC tissues up-regulated High DQ786243 expression was closely associated with invasion depth, TNM stage and lymphatic metastasis. Moreover, Kaplan-Meier analysis showed that patients with DQ786243 high expression tumors had worse OSand PFS compared to patients with DQ786243 low expression tumors. DQ786243 was a significant and independent prognostic predictor for both OS and PFSof GC patients. 29762832 2018 LncRNA DQ786243 expression as a biomarker for assessing prognosis in patients with gastric cancer DQ786243 NA NA NA NA NA colorectal cancer C19.9 NA qPCR, RNAi, Western blot etc. tumour tissues, cell lines (SW620, HCT116, HT29 etc.) up-regulated The effects of LncRNA DQ786243 were assessed by silencing the LncRNA in vitro and in vivo Results showed that the expression level LncRNA DQ786243 was significantly higher in CRC tissues and cell lines. We also found LncRNA DQ786243 knockdown by RNA interference with siRNA significantly arrested the cell cycle in the G2/M-phase, promoted apoptosis and weaken the abilities of cell proliferation and invasion in vitro Further investigation into the mechanisms responsible for the growth inhibitory effects by DQ786243 silencing revealed that its knockdown resulted in the induction of cell cycle arrest and apoptosis through certain cell cycle-related and apoptosis-related proteins. Finally, xenograft experiments confirmed that the growth of xenograft tumours formed by CRC cells was suppressed after silencing LncRNA DQ786243 expression 26934980 2016 LncRNA DQ786243 contributes to proliferation and metastasis of colorectal cancer both in vitro and in vivo DRAIC DRAIC 145837 ENSG00000245750 NR_026979 GRCh38_15:69463026-69843120 prostate cancer C61.9 NA qPCR, Western blot etc. cell lines (VCap, PC3M-luc, LNCaP etc.) down-regulated This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAIC and PCAT29, that are prognostic for a wide variety of cancer types.This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAICand PCAT29, that are prognostic for a wide variety of cancer types. 25700553 2015 The lncRNA DRAIC/PCAT29 locus constitutes a tumor suppressive nexus. DREH NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HBV-associated HCC tissues, cell lines (HepG2, HepG2.2.15, Hep3B, Huh-7 and SMMC-7721) down-regulated DREH was frequently downregulated in hepatitis B virus (HBV) associated HCC tissues in comparison with adjacent non-cancerous hepatic tissues, and was inversely correlated with HBx mRNA expression in HBV associated HCC. the levels of DREH were inversely correlated with hepatitis B surface antigen and tumor size in HCC tissues. The forced expression of HBx in liver cell lines resulted in a significant decrease in the expression of DREH.This decrement was significantly correlated with poor survival in HCC patients. 28789433 2017 Downregulated long non-coding RNA DREH promotes cell proliferation in hepatitis B virus-associated hepatocellular carcinoma. DUXAP10 PCAN-3 NA NA NA GRCh38_14:19294785-19337674 ovarian cancer C56.9 NA qPCR cell lines (IOSE386,HEY, HO8910 and A2780) up-regulated DUXAP10 was significantly overexpressed in ovarian cancer tissues,and its expression was positively correlated with tumor size and FIGO stage in clinical patients. DUXAP10 played a role in promoting the proliferation of ovarian cancer cells and was expected to be a predictor and a potential therapeutic target of ovarian cancer. The overall survival rate of DUXAP10 overexpressing ovarian cancer patients was significantly lower than that of DUXAP10 low expression group. 29424918 2018 Highly expressed long non-coding RNA DUXAP10 promotes proliferation of ovarian cancer. DUXAP10 PCAN-3 NA NA NA GRCh38_14:19294785-19337674 colorectal cancer C19.9 NA qPCR etc. CRC tissues, cell lines (DLD-1, HCT116, SW480 and SW620) up-regulated Pseudogene derived lncRNAs are crucial regulators of cancer development and progression. DUXAP10,a pseudogene derived long non-coding RNA(lncRNA), is overexpression in colorectal cancer (CRC). DUXAP10 was up-regulated in CRC tissues which was positively correlated with advanced pathological stages, larger tumor sizes and lymph node metastasis. Additionally, knockdown of DUXAP10 inhibited cell proliferation, induced cell apoptosis and increase the number of G0/G1 cells significantly in the HCT116 and SW480 cell lines. Moreover, DUXAP10 silencing inhibited tumor growth in vivo. Further mechanism study showed that, by binding to histone demethylase lysine-specific demethylase 1 (LSD1), DUXAP10 promote CRC cell growth and reduced cell apoptosis through silencing the expression of p21 and phosphatase and tensin homolog (PTEN) tumor suppressor. Our findings suggested that the pseudogene-derived from lncRNA DUXAP10 promotes the biological progression of CRC and is likely to be a potential therapeutic target for CRC intervention. 28779166 2017 The pseudogene derived from long non-coding RNA DUXAP10 promotes colorectal cancer cell growth through epigenetically silencing of p21 and PTEN. DUXAP10 PCAN-3 NA NA NA GRCh38_14:19294785-19337674 pancreatic cancer C25 NA qPCR, in vitro knockdown etc. cell lines (AsPC-1, BxPC-3, and PANC-1), PC tissue up-regulated DUXAP10 was overexpressed in PC tissues compared with normal tissues. DUXAP10 expression was significantly higher in patients with an advanced TNM stage and positive lymph node metastasis. Bioinformatic analysis showed that cell cycle progression was increased in patients with high DUXAP10 expression. In vitro and in vivo assays of DUXAP10 alterations revealed a complex integrated phenotype affecting cell growth, apoptosis, migration, and invasion. Mechanistic studies revealed that DUXAP10 has a crucial role in G2/M arrest. We further showed that DUXAP10 regulated PC cell proliferation through interact with RNA-binding protein EZH2 and LSD1. Overall, our findings indicates that DUXAP10 is an oncogenic lncRNA that promotes PC proliferation and metastasis. 29286182 2017 Knockdown of pseudogene derived from lncRNA DUXAP10 inhibits cell proliferation, migration, invasion, and promotes apoptosis in pancreatic cancer. DUXAP10 PCAN-3 NA NA NA GRCh38_14:19294785-19337674 non small cell lung cancer C34 M8046/3 qPCR, RNAi, RIP, western blot non small cell lung cancer tissues, cell lines (A549, H1975, SPC-A1, PC-9, H1299, H226) up-regulated Firstly, we found that DUXAP10 was significantly up-regulated in 93 human NSCLC tissues and cell lines, and increased DUXAP10 was associated with patients poorer prognosis and short survival time. 28029651 2017 The pseudogene DUXAP10 promotes an aggressive phenotype through binding with LSD1 and repressing LATS2 and RRAD in non small cell lung cancer DUXAP10 PCAN-3 NA NA NA GRCh38_14:19294785-19337674 breast cancer C50 NA qPCR, RNAi etc. breast cancer tissues, cell line (MCF-7) up-regulated The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines. 27322459 2016 Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis. DUXAP8 NA NA ENSG00000206195 NA GRCh38_22:15784959-15829984 renal cell carcinoma C64.9 NA Microarray, qPCR,RNAi etc. renal cell carcinoma tissues up-regulated knockdown of DUXAP8 could impair RCC cells invasive ability in vitro. lots of lncRNAs expression levels are significantly associated RCC patients overall survival time, such as PVT1 and DUXAP8 . 29152119 2017 A genome-wide comprehensively analyses of long noncoding RNA profiling and metastasis associated lncRNAs in renal cell carcinoma. DUXAP8 NA NA ENSG00000206195 NA GRCh38_22:15784959-15829984 non small cell lung cancer C34 M8046/3 qPCR, RNAi, western blot non small cell lung cancer tissues, cell lines (PC9, SPC-A1, NCI-H1975, H1299, and A549) up-regulated We identified a transcribed pseudogene named DUXAP8 that is upregulated in tumor tissues. Patients with higher DUXAP8 expression exhibited shorter survival, suggesting DUXAP8 as a new candidate prognostic marker for NSCLC patients. Knockdown of DUXAP8 impairs cell growth, migration, and invasion, and induces apoptosis both in vitro and in vivo. 28131418 2017 The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB DUXAP8 NA NA ENSG00000206195 NA GRCh38_22:15784959-15829984 gastric cancer C16 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. primary GC tissues, cell lines (SGC7901, BGC823, GSE-1) up-regulated DUXAP8 was remarkably upregulated in GC. Additionally, a higher level of DUXAP8 expression in GC was significantly associated with greater tumor size, advanced clinical stage, and lymphatic metastasis. Patients with a higher level of DUXAP8 expression had a relatively poor prognosis. Further experiments revealed that knockdown of DUXAP8 significantly inhibited cell proliferation and migration, as documented in the SGC7901 and BGC823 cell lines. Furthermore, RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that DUXAP8 could epigenetically suppress the expression of PLEKHO1 by binding to EZH2 and SUZ12 (two key components of PRC2), thus promoting GC development. 27507049 2016 The pseudogene derived long noncoding RNA DUXAP8 promotes gastric cancer cell proliferation and migration via epigenetically silencing PLEKHO1 expression. DUXAP8 NA NA ENSG00000206195 NA GRCh38_22:15784959-15829984 gastric cancer C16 NA qPCR, Western blot, RIP etc. gastric cancer tissues, cell lines (SGC7901, BGC823) up-regulated Taken together, our findings suggest that the pseudogene-derived lncRNA DUXAP8 promotes the progression of GC and is a potential therapeutic target for GC intervention. Patients with a higher level of DUXAP8 expression had a relatively poor prognosis. 28881724 2016 The pseudogene derived long noncoding RNA DUXAP8 promotes gastric cancer cell proliferation and migration via epigenetically silencing PLEKHO1 expression DUXAP8 NA NA ENSG00000206195 NA GRCh38_22:15784959-15829984 esophageal cancer C15 NA qPCR, western blot esophageal cancer tissue, cell lines (TE-1, ESCCA109, ESCCA9706 and KYSE520) up-regulated DUXAP8 expression was significantly correlated with tumor stage, lymph node metastasis and poor prognosis of ESCC patients. DUXAP8 may promote the occurrence of ESCC via Wnt/B-catenin pathway. 29771416 2018 Long non-coding RNA DUXAP8 regulates proliferation and invasion of esophageal squamous cell cancer DUXAP8 NA NA ENSG00000206195 NA GRCh38_22:15784959-15829984 bladder cancer C67 NA qPCR, Western blot, etc. bladder cancer tissues, cell lines (SV-HUC-1, T24, RT4, J82) up-regulated it was in a positive correlation with the TNM stage and tumor size, but negatively correlated with the total survival time. promote the progression of bladder cancer through inhibiting PTEN. 29917188 2018 Mechanism of lncRNA DUXAP8 in promoting proliferation of bladder cancer cells by regulating PTEN. ecCEBPA NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. cell lines (Hl-60 and theU939) down-regulated Our outcomes revealed that SAM particularly when given at the starting phase downregulates ecCEBPA and UCA1 gene transcripts and ameliorate histopathological alterations in DEN-initiated HCC. Interestingly, SAM attenuates DEN-induced upregulation of PI3K/Akt protein expression. However, SAM upregulates the antioxidant enzymes mRNA transcripts and effectively diminishing DNA oxidation. The results of a DNA fragmentation assay further support the capacity of SAM to ameliorate DEN-induced hepatic malignancy. These results revealed the role of ecCEBPA and UCA1 in HCC and suggest that these lncRNAs may be helpful as prognostic and analytical biomarkers of HCC. 29748795 2018 Role of lncRNAs as prognostic markers of hepatic cancer and potential therapeutic targeting by S-adenosylmethionine via inhibiting PI3K/Akt signaling pathways. ecCEBPA NA NA NA NA NA gastric cancer C16 NA qPCR etc. cell lines (HEK-293, HUVECs, SKBR3, A542, MCF7, NT2) up-regulated Our results showed ecCEBPA and UCA1 over-expression in GC tissues. Furthermore, lncRNAs associations with clinicopathological features were demonstrated both in the current and TCGA cohort. Kaplan-Meier analysis indicated that patients with higher UCA1 expression had a worse overall survival in the case of pancreatic and lung adenocarcinomas but not other solid cancer types including GC. These data demonstrate UCA1 and ecCEBPA involvement in GC and suggest that these lncRNAs might be useful as diagnostic/ prognostic biomarkers in cancer. 29147491 2017 Augmented expression levels of lncRNAs ecCEBPA and UCA1 in gastric cancer tissues and their clinical significance EFNA3 EFNA3, EFL2, EPLG3, Ehk1-L, LERK3 1944 ENSG00000143590 NA GRCh38_1:155078872-155087538 breast cancer C50 NA qPCR, RIP etc. breast cancer tissues up-regulated We demonstrate that sustained expression of both Ephrin-A3 and novel EFNA3 lncRNAs increased the metastatic potential of human breast cancer cells, possibly by increasing the ability of tumor cells to extravasate from the blood vessels into surrounding tissue. In agreement, we found a strong correlation between high EFNA3 expression and shorter metastasis-free survival in breast cancer patients. hypoxia could contribute to metastatic spread of breast cancer via HIF-mediated induction ofEFNA3lncRNAs and subsequent Ephrin-A3 protein accumulation. 25023702 2014 EFNA3 long noncoding RNAs induced by hypoxia promote metastatic dissemination. EGFLAM-AS1 EGFLAM-AS1 100874117 ENSG00000249491 NA GRCh38_5:38425036-38427376 gastric cancer C16 NA qPCR, RNAi, Western blot etc. gastric cancer tissues, cell lines (SGC-7901, AGS, BGC-823, HG-27, GES-1) down-regulated Significantly reduced expression of lncRNA-LOWEG was found in gastric cancer tissues and cell lines (SGC-7901, AGS, BGC-823 and HG-27) compared with patient-matched nontumorous adjacent tissues or the normal gastric cell line GES-1. Lastly, western blot and real-time PCR analysis suggested that lncRNA-LOWEG is positively correlated with the expression of leukemia inhibitory factor receptor (LIFR) gene at the translational level. 26537802 2015 A novel long noncoding RNA-LOWEG is low expressed in gastric cancer and acts as a tumor suppressor by inhibiting cell invasion. EGFR-AS1 NA 100507500 ENSG00000224057 NR_047551 GRCh38_7:55179750-55188934 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RNAi, Western blot, Flow cytometry assay etc. HCC tissues, cell lines (SMMC-7721, LM-9, Huh-7, HepG2) up-regulated It was verified that EGFR and EGFR-AS1 were relatively upregulated in HCC tissue, and they were significantly related to some clinical characteristics and patient prognosis. Furthermore, EGFR-AS1 was determined to promote HCC development by improving the ability of invasion and proliferation of HCC cells in vitro, and it was also found to affect the cell cycle. Our study identified that EGFR-AS1 may promote HCC genesis and development. EGFR-AS1 may act as a prognostic factor in HCC. 26271667 2015 The long noncoding RNA, EGFR-AS1, a target of GHR, increases the expression of EGFR in hepatocellular carcinoma. EGOT EGOT, EGO, NCRNA00190 100126791 ENSG00000235947 NR_004428 GRCh38_3:4749192-4751590 breast cancer C50 NA qPCR etc. breast cancer tissues down-regulated EGOT expression was lower in breast cancer compared with the adjacent noncancerous tissues, and low levels of EGOT expression were significantly correlated with larger tumor size, more lymph node metastasis, and higher Ki-67 expression. Moreover, patients with low levels of EGOT expression showed significantly worse prognosis for overall survival. Multivariate analysis suggested that low levels of EGOT were a poor independent prognostic predictor for breast cancer patients 26159853 2015 Downregulation of the long noncoding RNA EGOT correlates with malignant status and poor prognosis in breast cancer EGOT EGOT, EGO, NCRNA00190 100126791 ENSG00000235947 NR_004428 GRCh38_3:4749192-4751590 gastric cancer C16 NA qPCR, Western blot gastric cancer tissues, cell lines (MGC80-3,AGS, NCI-N87, MKN-45 and SGC-7901, GES-1) up-regulated The expression of EGOT was observably elevated in GC. Upregulation of EGOT was related with lymphatic metastasis and TNM stage. knockdown of EGOT by siRNA could significantly inhibit GC cell proliferation and arrest cycle progression in G1 phase. Moreover, EGOT mediated cyclin D1 expression in GC cells which was regulated by Hedgehog pathway. loss of EGOT downregulated Hedgehog signaling pathway in GC cells. EGOT functions as an oncogene in GC, and may be useful as a conceivable diagnostic and prognostic biomarker for GC tumorigenesis.low levels of EGOT expression had signally longer overall survival (OS) time than that in high-EGOT group. 29209988 2017 LncRNA EGOT Promotes Tumorigenesis Via Hedgehog Pathway in Gastric Cancer. EGOT EGOT, EGO, NCRNA00190 100126791 ENSG00000235947 NR_004428 GRCh38_3:4749192-4751590 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) down-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. EINCR1 NA NA NA NA NA lung adenocarcinoma C34 M8140/3 qPCR etc. cell lines (MCF10A, A549, MCF7, MDA-MD-231 and HEK293T) up-regulated EINCR1 is specifically expressed in normal human heart tissues and is up-regulated in cancer. in several cancers EINCR1 shows elevated expression levels which correlate with poor survival in lung adenocarcinoma patients. In the context of lung adenocarcinomas, EINCR1 expression is anti-correlated with the expression of several protein coding EGF-regulated genes. A potential functional connection is demonstrated as EINCR1 overexpression is shown to reduce the expression of EGF-regulated protein coding genes including FOS and FOSB. 28732076 2017 EINCR1 is an EGF inducible lincRNA overexpressed in lung adenocarcinomas. ENSG00000177133 LINC00982, FLJ42875, RP1-163G9.1 440556 ENSG00000177133 NR_015440 GRCh38_1:3059615-3068437 clear cell renal cell carcinoma C64.9 M8005/0 microarray, qPCR etc. ccRCC tissues down-regulated To validate the microarray data, we examined the expression of these three lncRNAs in 71 ccRCC and adjacent normal renal tissue samples. Decreased expression of three lncRNAs (ENSG00000177133, TCL6, and ENSG00000244020) was observed in ccRCC compared to adjacent normal tissue. 27494890 2016 Decreased TCL6 expression is associated with poor prognosis in patients with clear cell renal cell carcinoma. ENSG00000177133 LINC00982, FLJ42875, RP1-163G9.1 440556 ENSG00000177133 NR_015440 GRCh38_1:3059615-3068437 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. gastric cancer tissues, cell lines (SGC7901, BGC823, MGC803, AGS, MKN45) down-regulated In this study, we identified a novel lncRNA LINC00982, whose expression was downregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. Furthermore, knockdown of LINC00982 expression by small interfering RNA (siRNA) could promote cell proliferation and cell cycle progression, while ectopic expression of LINC00982 inhibited cell proliferation and rendered cell cycle arrest in GC cells partly via regulating P15 and P16 protein expressions. 26334618 2015 Upregulated expression of long non-coding RNA LINC00982 regulates cell proliferation and its clinical relevance in patients with gastric cancer. ENSG00000244020 MT1HL1, MT1P2 NA ENSG00000244020 NA GRCh38_1:237004103-237004418 clear cell renal cell carcinoma C64.9 M8005/0 microarray, qPCR etc. ccRCC tissues down-regulated To validate the microarray data, we examined the expression of these three lncRNAs in 71 ccRCC and adjacent normal renal tissue samples. Decreased expression of three lncRNAs (ENSG00000177133, TCL6, and ENSG00000244020) was observed in ccRCC compared to adjacent normal tissue. 27494890 2016 Decreased TCL6 expression is associated with poor prognosis in patients with clear cell renal cell carcinoma. ENSG00000244649 LINC02086 105371809 ENSG00000244649 XR_001752925 GRCh38_17:48646923-48707346 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR, Cell proliferation assay etc. PDAC tissues, cell lines (AsPC-1, BxPC-3, Capan-2, CFPAC-1, HPAC, MIA PaCa-2, PANC-1 and SW1990) up-regulated The qRT-PCR results showed that CRNDE, NR_036488, ENSG00000244649, AFAP1-AS and UCA1 expression was significantly increased and ENSG00000218510 expression was remarkably decreased in PDAC tissues compared with paired normal pancreatic tissues. Consistent with the findings in PDAC tissues, CRNDE, NR_036488, ENSG00000244649, AFAP1-AS1 and UCA1 expression was dramatically enhanced and ENSG00000218510 reduced in all or most of 8 PDAC cell lines in relative to the nonmalignant HPDE6-C7 cells or hTERT-HPNE cells at the RNA level. 27628540 2016 Analysis of long non-coding RNA expression profiles in pancreatic ductal adenocarcinoma. ENSG00000261684 RP11-265N6.1 NA ENSG00000261684 NA GRCh38_15:42531867-42532840 glioblastoma NA M9440/3 microarray, qPCR etc. glioblastoma tissues up-regulated Our real-time RT-PCR confirmed aberrant expression patterns of all the lncRNA and genes that were observed inthe microarray data, suggesting that these lncRNAs and genes were dysregulated in GBM patient samples and that they might have important roles in GBM pathology. 27784795 2016 The Potential Roles of Long Noncoding RNAs (lncRNA) in Glioblastoma Development. ENST00000421965 AC006159.4 NA NA NA GRCh38_7:116563594-116571234 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. ENST00000426615 HAGLROS 102800310 ENSG00000226363 NR_110457 GRCh38_2:176177717-176179008 gastric cancer C16 NA RNA-seq, Microarray, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP GC tissues, gastric cancer cell lines (SGC-7901, BGC-823, HGC-27, MGC-803 and AGS) up-regulated HAGLROS,whose expression was significantly increased and correlated with outcomes of GC patients Exogenous down-regulation of HAGLROS expression significantly suppressed the cell proliferation,invasion and migration.HAGLROS was a direct target of transcriptional factor STAT3.Moreover,HAGLROS knockdown decreased mTOR expression and increased autophagy-related genes ATG9A and ATG9B expression.Further,HAGLROS regulated mTOR signals in two manners.HAGLROS competitively sponged miR-100-5p to increase mTOR expression by antagonizing miR-100-5p-mediated mTOR mRNA inhibition. 29329543 2018 STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy. ENST00000435885 NA NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. OSCC tissues differential expression we identified a three-lncRNA signature (including the lncRNAs ENST00000435885.1, XLOC_013014 and ENST00000547963.1) which classified the patients into two groups with significantly different overall survival . The signature was applied to the test group and independent cohort and showed similar prognostic values in both. 24522499 2014 LncRNA profile study reveals a three-lncRNA signature associated with the survival of patients with oesophageal squamous cell carcinoma. ENST00000438550 RPS24P1, RPS24P NA ENSG00000236477 NA GRCh38_Y:12244,52-12245457 nasopharyngeal cancer C11 NA microarray, qPCR etc. NPC tissues up-regulated All four lncRNAs (LOC84740, ENST00000498296, AL359062, and ENST00000438550) were differentially expressed in the metastatic and primary NPC tumors based on microarray analysis, which was validated via QPCR using the same tissues. The validation results of the four lncRNAs indicated that the microarray data strongly correlated with the QPCR results. These lncRNAs displayed higher expression levels in NPC primary tumors with progression than in those without progression. 26448942 2015 Long Noncoding RNA Expression Signatures of Metastatic Nasopharyngeal Carcinoma and Their Prognostic Value. ENST00000439577 RP1-20B21.4 NA NA NA GRCh38_1:17406760-17407382 non small cell lung cancer C34 M8046/3 microarray, qPCR, Western blot, Luciferase reporter assay etc. NSCLC tissues, cell lines (A549, H1299, H1975 and PC9) up-regulated Two of the lncRNAs, LOC146880 and ENST00000439577, were positively correlated with expression of two cancer-related genes, KPNA2 and RCC2, respectively. High expression of LOC146880 and ENST00000439577 were also associated with poor survival. Analysis of lncRNA expression in relation to DNA methylation showed that LOC146880 expression was down-regulated by DNA methylation in its promoter. Lowering the expression of LOC146880 or ENST00000439577 in tumor cells could inhibit cell proliferation, invasion and migration. 27849024 2016 Analysis of Microarray Data on Gene Expression and Methylation to Identify Long Non-coding RNAs in Non-small Cell Lung Cancer. ENST00000457457 AC016735.1 NA ENSG00000224739 NA GRCh38_2:43001355-43006060 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow up-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. ENST00000457799 FCRL3, CD307c, FCRH3, IFGP3, IRTA3, SPAP2 115352 ENSG00000160856 NA GRCh38_1:157674321-157700857 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow down-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. ENST00000464359 LINC00635 151658 ENSG00000241469 NR_015414 GRCh38_3:107840228-107882000 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. hepatocellular carcinoma tissues up-regulated The results showed that the levels of ENSG00000258332.1 and LINC00635 in the HCC group were significantly higher than those in the other groups (all P < 0.05). A high ENSG00000258332.1 level in HCC was associated with portal vein tumor emboli, lymph node metastasis, TNM stage, and overall survival (OS; all P < 0.05), and a high LINC00635 level was related to lymph node metastasis, TNM stage, and OS (all P < 0.05). ENSG00000258332.1 discriminated HCC from CHB, gaining an area under the ROC curve (AUC) of 0.719 (cutoff value of 1.345); LINC00635 gained an AUC of 0.750 (cutoff value of 1.690). The results suggested that the combination of serum exosomal ENSG00000258332.1, LINC00635, and AFP may be a valuable assay in diagnosis and prognosis of HCC. 29650788 2018 Serum Exosomal Long Noncoding RNAs ENSG00000258332.1 and LINC00635 for the Diagnosis and Prognosis of Hepatocellular Carcinoma. ENST00000480669 RP11-641D5.2, LOC105374205 NA NA NA GRCh38_3:169447867-169477052 esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues down-regulated Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. ENST00000480739 RPL13AP23, RPL13A_10_1240 NA ENSG00000242990 NA GRCh38_12:57674665-57675250 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, Western blot, Luciferase reporter assay, ELISA etc. PDAC tissues down-regulated We determined that the ENST00000480739 expression level was remarkably decreased in tumorous tissues compared with their corresponding non-tumorous tissues. The expression of ENST00000480739 was negatively associated with tumour node metastasis stage and lymph node metastasis. Overexpression of ENST00000480739 significantly increased both mRNA and protein levels of OS-9, and the luciferase assays confirmed that ENST00000480739 positively regulates OS-9 by activating the transcription level of the OS-9 promoter. We further found that ENST00000480739 may target hypoxia-inducible factor-1a (HIF-1a) expression by upregulating OS-9. 25314054 2014 A novel long non-coding RNA ENST00000480739 suppresses tumour cell invasion by regulating OS-9 and HIF-1a in pancreatic ductal adenocarcinoma. ENST00000498296 RPLP0P11, RPLP0_4_1600 NA ENSG00000239780 NA GRCh38_18:50457887-50458795 nasopharyngeal cancer C11 NA microarray, qPCR etc. NPC tissues up-regulated All four lncRNAs (LOC84740, ENST00000498296, AL359062, and ENST00000438550) were differentially expressed in the metastatic and primary NPC tumors based on microarray analysis, which was validated via QPCR using the same tissues. The validation results of the four lncRNAs indicated that the microarray data strongly correlated with the QPCR results. These lncRNAs displayed higher expression levels in NPC primary tumors with progression than in those without progression. 26448942 2015 Long Noncoding RNA Expression Signatures of Metastatic Nasopharyngeal Carcinoma and Their Prognostic Value. ENST00000507950 LINC02121 NA ENSG00000250529 NA GRCh38_5:5069192-5078311 renal cell carcinoma C64.9 NA microarray, qPCR etc. RCC tissues down-regulated From five paired samples we identified hundreds of significantly differentiated lncRNAs. Specifically, the most upregulated lncRNAs were: uc001vjj.1, ENST00000414223, BC047917, uc003erl.1, and uc009wkz.1, of which uc001vjj.1 was the highest. The most highly downregulated were: ENST00000507950, uc001aka.2, NR_026860, NR_024256, and BC070168, of which ENST00000507950 showed the largest downregulation. 24905231 2014 Expression pattern of long non-coding RNAs in renal cell carcinoma revealed by microarray. ENST00000509150 ATP2C1, ATP2C1A, BCPM, HHD, PMR1, SPCA1, hSPCA1 27032 ENSG00000017260 NA GRCh38_3:130850595-131016712 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow up-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. ENST00000539535 NA NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues up-regulated Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. ENST00000547963 LINC01234, LCAL84, onco-lncRNA-32 100506465 ENSG00000249550 NR_110026 GRCh38_12:113744577-113773683 esophageal squamous cell cancer NA NA microarray, qPCR etc. OSCC tissues differential expression we identified a three-lncRNA signature (including the lncRNAs ENST00000435885.1, XLOC_013014 and ENST00000547963.1) which classified the patients into two groups with significantly different overall survival . The signature was applied to the test group and independent cohort and showed similar prognostic values in both. 24522499 2014 LncRNA profile study reveals a three-lncRNA signature associated with the survival of patients with oesophageal squamous cell carcinoma. ENST00000547963 LINC01234, LCAL84, onco-lncRNA-32 100506465 ENSG00000249550 NR_110026 GRCh38_12:113679459-113773683 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, RIP etc. gastric cancer tissues, cell lines (GES-1, BGC823, SGC7901, AGS, HGC27, MGC803) up-regulated LINC01234 expression was significantly upregulated in gastric cancer tissues and was associated with larger tumor size, advanced TNM stage,lymph node metastasis,and shorter survival time.Furthermore,knockdown of LINC01234-induced apoptosis and growth arrest in vitro and inhibited tumorigenesis in mouse xenografts.Mechanistic investigations indicated that LINC01234 functioned as a ceRNA for miR-204-5p,thereby leading to the derepression of its endogenous target core-binding factor B (CBFB). LINC01234 is significantly overexpressed in gastric cancer, and LINC01234-miR-204-5p-CBFB axis plays a critical role in gastric cancer tumorigenesis. 29386218 2018 Long Noncoding RNA LINC01234 Functions as a Competing Endogenous RNA to Regulate CBFB Expression by Sponging miR-204-5p in Gastric Cancer. EPB41L4A-AS2 NA NA ENSG00000278921 NA GRCh38_5:112419583-112420978 head and neck squamous cell carcinoma C76.0 M8070/3 RNA-seq, Microarray, qPCR,Western blot NPC cell line (CNE1) down-regulated The relationship of EPB41L4A-AS2 with the clinicopathological features and prognosis of HNSCC patients was evaluated.EPB41L4A-AS2 may be involved in processes associated with the tumor-associated signaling pathway, especially the TGF-B signaling pathway. Low EPB41L4A-AS2 expression was determined,and overexpression of this gene inhibited cell migration and invasion in the EMT model. Moreover, EPB41L4A-AS2 suppressed TGFBR1 expression.A major mechanism of lncRNAs in regulating gene expression involves the interaction with Polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 lysine 27 (H3K27me3) to repress the transcription of specific genes. Considering that the promoter region of TGFBR1 is rich in methylation, we hypothesized that EPB41L4A-AS2 plays a role in inducing the methylation of the TGFBR1 promoter. Competing endogenous RNA (ceRNA) is currently under intense study as a novel mechanism for lncRNA functions, which indicates that RNA transcripts communicate with one another by miRNA response elements. 29490660 2018 Identification and validation a TGF-B-associated long non-coding RNA of head and neck squamous cell carcinoma by bioinformatics method. EPB41L4A-AS2 NA NA ENSG00000278921 NA GRCh38_5:112419583-112420978 breast cancer C50 NA qPCR, Flow cytometry assay etc. cell lines (MDA-MB-231, A549 and 786-O) down-regulated we investigated the expression of EPB41L4A-AS2 in breast cancer tissues and evaluated its relationship with the clinicopathological features and prognosis of patients with breast cancer. This entailed conducting a meta-analysis and prognosis validation study using two cohorts from the Gene Expression Omnibus (GEO). In addition, we assessed EPB41L4A-AS2 expression and its relationship with the clinicopathological features of renal and lung cancers using the Cancer Genome Atlas cohort and a GEO dataset. We also clarified the role of EPB41L4A-AS2 expression in mediating cancer cell proliferation in breast, renal, and lung cancer cell lines transfected with an EPB41L4A-AS2 expression vector. We found that high EPB41L4A-AS2 expression is associated with favorable disease outcomes. Gene ontology enrichment analysis revealed that EPB41L4A-AS2 may be involved in processes associated with tumor biology. Finally, overexpression of EPB41L4A-AS2 inhibited tumor cell proliferation in breast, renal, and lung cancer cell lines 26980733 2016 The long non-coding RNA EPB41L4A-AS2 inhibits tumor proliferation and is associated with favorable prognoses in breast cancer and other solid tumors EPEL NA NA NA NR_027107 GRCh38_4:182138658-182144515 lung cancer C34 NA RNA-seq, Microarray,RIP, qPCR cell lines (A549,NCI-H1299) up-regulated EPEL,known as LOC90768 and MGC45800, was associated with the relapse and survival of lung cancer patients and promoted lung cancer cell proliferation through the activation of E2F target genes. EPEL knockdown specifically down-regulated the expression of cell cyclerelated E2F target genes, including Cyclin B1 (CCNB1), in lung cancer cells but not that of apoptosis- or metabolism-related E2F target genes. EPEL interacted with E2F1 and regulated the expression of the E2F target genes by changing the binding efficiency of E2F1 to the E2F target promoters. Moreover, the expression levels of EPEL and CCNB1 both alone and in combination were robust prognostic markers for lung cancer. 29448242 2018 The LncRNA EPEL Promotes Lung Cancer Cell Proliferation Through E2F Target Activation EPIC1 NA NA NA NA NA breast cancer C50 NA qPCR, Western blot, in vitro knockdown, RIP etc. cell lines (MCF10A,BT-20,BT-474,HCC1937,Hs578T,MDA-MB-231,MDA-MB-361,MDA-MB-468,MCF-7,T-47D,ZR-75-1,A2780,A2780cis,IGR-OV-1NIH:OVCAR-3,OVCAR-4,OVCAR-8,SK-OV-3), breast cancer tissues up-regulated Overexpression of EPIC1 is associated with poor prognosis in luminal B breast cancer patients and enhances tumor growth in vitro and in vivo. Mechanistically, EPIC1 promotes cell-cycle progression by interacting with MYC through EPIC1's 129-283 nt region. EPIC1 knockdown reduces the occupancy of MYC to its target genes (e.g., CDKN1A, CCNA2, CDC20, and CDC45). MYC depletion abolishes EPIC1's regulation of MYC target and luminal breast cancer tumorigenesis in vitro and in vivo. 29622465 2018 lncRNA Epigenetic Landscape Analysis Identifies EPIC1 as an Oncogenic lncRNA that Interacts with MYC and Promotes Cell-Cycle Progression in Cancer. ESRPS-AS 1810019D21Rik NA NA NA NA breast cancer C50 NA qPCR, RNA-seq, western blot etc. cell lines (M28N2, M27H4, M6, M6C) up-regulated ESRPs were shown previously to have a dual role in carcinogenesis. Both gain and loss have been associated with poor prognosis in human cancers, but the mechanisms regulating expression are not known. Indepth analyses indicate that coordinate overexpression of Esrp2 and Esrp2-as inversely correlates with DNA methylation. Using the Kaplan–Meier plotter survival analysis tool,we could confirm that high ESRP2 mRNA levels reduce the fraction of relapse-free survival, overall survival, and distant metastasis-free survival of breast cancer cases analyzed together or when cases were subdivided into breast cancer subtypes. 28759043 2017 Genome-wide screen for differentially methylated long noncoding RNAs identifies Esrp2 and lncRNA Esrp2-as regulated by enhancer DNA methylation with prognostic relevance for human breast cancer EWSAT1 EWSAT1, LINC00277, NCRNA00277, TMEM84 283673 ENSG00000212766 NR_026949 GRCh38_15:69072926-69095820 nasopharyngeal cancer C11 NA qPCR, Cell transfection, Western blot, Luciferase reporter assay, RNA pull-down assay etc. NPC tissues, cell lines (SUNE-1, CNE-1, HNE-1, CNE-2, C666-1 and HONE-1) up-regulated Herein, we identified that EWSAT1 was up-regulated in NPC tissues and cell lines, and higher expression of EWSAT1 resulted in a markedly poorer survival time. EWSAT1 over-expression facilitated, while EWSAT1 silencing impaired cell growth in NPC. In addition, mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive 'sponge' of miR-326/330-5p clusters. 27816050 2016 Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p. EWSAT1 EWSAT1, LINC00277, NCRNA00277, TMEM84 283673 ENSG00000212766 NR_026949 GRCh38_15:69072926-69095820 osteosarcoma NA M9180/3 qPCR osteosarcoma tissues up-regulated EWSAT1 levels were significantly higher in osteosarcoma tissues compared with matched non-cancerous tissues. The level of EWSAT1 expression was significantly associated with clinical stage and distant metastasis.high EWSAT1 expression level was associated with poorer OS and DFS. EWSAT1 expression was an independent prognostic factor for both OS and DFS in osteosarcoma patients 29243774 2017 Clinical significance of long non-coding RNA EWSAT1 as a novel prognostic biomarker in osteosarcoma. EWSAT1 EWSAT1, LINC00277, NCRNA00277, TMEM84 283673 ENSG00000212766 NR_026949 GRCh38_15:69072926-69095820 osteosarcoma NA M9180/3 qPCR, RNAi, RIP, Luciferase reporter assay etc. cell lines (HOS, MG63 and HOS) up-regulated EWSAT1 enhanced OS cell proliferation, migration, and invasion. Further mechanistic studies found that EWSAT1 positively regulated lncRNA MEG3 expression in the transcriptional level. Finally, we observed that EWSAT1 facilitates OS cell growth and metastasis through regulation of MEG3 27860482 2016 Long Noncoding RNA EWSAT1 Promotes Osteosarcoma Cell Growth and Metastasis Through Suppression of MEG3 Expression. F11-AS1 F11-AS1 285441 ENSG00000251165 NR_033901 GRCh38_4:186286094-186500997 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. cell lines (SW1990, BxPC etc.) down-regulated We selected two upregulated lncRNAs (LINC00152 and CASC9) that were reported to be upregulated in other cancers, and two mostly downregulated lncRNAs (LINC00226 and F11-AS1) for further validation in PDAC cell lines and the normal cell line HPDE. F11-AS1 was only downregulated in 6 cell lines compared with HPDE cells. 28220683 2017 Analysis of distinct long noncoding RNA transcriptional fingerprints in pancreatic ductal adenocarcinoma. FABP5P3 NA 220832 ENSG00000241735 NA GRCh38_7:152436895-152443187 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay, in vitro knockdown etc. cell line (LO2, Hep3B, HepG2, Huh7), HCC tissues up-regulated FABP5P3 that was up-regulated in HCC tissues.Patients with higher FABP5P3 expression displayed poorer survival rate.FABP5P3 depletion in HCC cell lines and sample cells remarkably inhibited the abilities of proliferation, migration and invasion. FABP5P3 bond to miR-589-5p which served as a tumor suppressor. MiR-589-5p targeted directly the mRNA of ZMYND19 whose function has not been defined in HCC.FABP5P3 promoted HCC development and progression by sponging miR-589-5p and up-regulating ZMYND19 expression.FABP5P3/miR-589-5p/ZMYND19 axis regulates cell proliferation and migration in HCC,which may serve as a new target for HCC treatment. 29522715 2018 LncRNA FABP5P3/miR-589-5p/ZMYND19 axis contributes to hepatocellular carcinoma cell proliferation, migration and invasion. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 acute lymphoblastic leukemia NA M9835/3 qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p21 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 breast cancer C50 NA qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p22 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 chronic myelogenous leukemia NA M9875/3 qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p23 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 colon cancer C18 NA qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p24 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 glioblastoma NA M9440/3 qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p25 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 large cell immunoblastic lymphoma NA M9714/3 qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p26 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 melanoma NA M8720/3 qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p27 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 myeloma C42.1 M9732/3 qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p28 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 prostate cancer C61.9 NA qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p32 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 renal cancer C64.9 NA qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p33 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 non small cell lung cancer C34 M8046/3 qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p29 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 ovarian cancer C56.9 NA qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p30 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 ovarian cancer C56.9 NA qPCR, RNA pull-down assay etc. cell lines (BT20, HCC1428, HCC202, MCF7, MALME-3M etc.) up-regulated We identified an oncogene, FAL1, we measured the copy number of FAL1 in 99 cancer cell lines using qPCR and observed FAL1 copy-number gain in 46% of the cell lines. We then extracted the FAL1 RNA expression data from the aforementioned custom RNA array containing 40 cancer cell lines and found a significant and positive correlation between the genomic copy-number and RNA expression of FAL1. FAL1 associates with the epigenetic repressor BMI1 and regulates its stability in order to modulate the transcription of a number of genes including CDKN1A. The oncogenic activity of FAL1 is partially attributable to its repression of p21. FAL1-specific siRNAs significantly inhibit tumor growth in vivo. 25203321 2014 A functional genomic approach identifies FAL1 as an oncogenic long noncoding RNA that associates with BMI1 and represses p31 expression in cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 osteosarcoma NA M8260/3 qRT-PCR, Western blot analysis Human osteosarcoma cell lines (U2OS, HOS, SAOS‐2, 143B, and SW1353 cells from female patients and MG‐63 cells from a male patient) and human osteoblast cell lines (hFOB1.19 and NHOst), The osteosarcoma specimens and matched nontumor tissues, osteosarcoma blood samples up-regulated FAL1 expression was significantly upregulated in human osteosarcoma tissues and cell lines compared with their normal controls. FAL1 expression level was positively correlated with the distance metastasis (P?=?.008) and tumor stage ( P?=?.013).our study showed that lncRNA FAL1 exhibits an important pro-oncogenic effect on osteosarcoma progression by targeting EMT, which may serve as a potential therapeutic target for osteosarcoma. 29987852 2018 LncRNA FAL1 is a negative prognostic biomarker and exhibits pro-oncogenic function in osteosarcoma. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 melanoma NA M8720/3 qPCR, Western blot, RIP melanoma tissues, cell lines (HEMn, M21, B16, MEL-RM) up-regulated FALEC was more highly expressed in melanoma tissues and cell lines than in non-neoplastic nevi tissues and normal cell lines.silenced FALEC suppressed the proliferation of melanoma cells, resulted in cell cycle arrest, and induced apoptosis.FALEC boosted melanoma progression via epigenetically repressing p21 through recruiting EZH2 to the promoter of p21.FALEC acted as an oncogene in melanoma and had the potential to be a prognostic biomarker and therapeutic target for melanoma. 29196104 2017 Up-regulation of long noncoding RNA FALEC predicts poor prognosis and promotes melanoma cell proliferation through epigenetically silencing p21. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN50), gastric adenocarcinomas tissues down-regulated Downregulation of LINCROR, POU3F3, HOTAIR, FALEC, NBAT1, and ZEB2-AS1 lncRNAs in TCGA gastric tumor datasets 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 100874054 ENSG00000228126 NR_051960 GRCh38_1:150515757-150518032 prostate cancer C61.9 NA qPCR, Western blot, Luciferase reporter assay etc. prostate cancer tissues, cell lines (WPMY-1, PC-3, DU145, 22RV-1 and LNCaP) up-regulated In a total of 85 patients, FALEC expression was significantly increased in clinical PCa tissues compared to adjacent normal tissues, and can be considered as an independent prognostic factor in patients with PCa. Downregulation of FALEC could inhibit cell proliferation, migration and invasion in vitro. In vivo tumorigenesis study and orthotopic bioluminescence image also support the evidence that FALEC may promote the progression of prostate cancer. We also find FALEC is a potential hypoxia induced lncRNA and can be induced by the hypoxia master regulator HIF-1a. A dramatically shorter BCR time of patients with high levelofFALECwereobservedwhencomparedwiththosewithlowlevel ofFALEC( P = 0.033). 28585762 2018 Upregulation of the long non-coding RNA FALEC promotes proliferation and migration of prostate cancer cell lines and predicts prognosis of PCa patients. FAM212B-AS1 FAM212B-AS1 100506343 ENSG00000227811 NA GRCh38_1:111739841-111747798 endometrial cancer NA M8380/3 microarray, qPCR etc. endometrial carcinoma tissues down-regulated Real-time PCR verified that 6 of the 7 lncRNAs are dramatically downregulated in EC, which is consistent with the microarray data. 27748922 2016 Distinct expression profile of lncRNA in endometrial carcinoma. FAM215A FAM215A, APR-2, C17orf88, LINC00530 23591 ENSG00000267496 NR_026770 GRCh38_17:43917194-43917985 epithelial ovarian cancer C56.9 NA qPCR etc. primary EOC tissues differential expression We observed high expression of ASAP1-IT1, FAM215A and LINC00472 more frequently in low grade tumors and early stage disease compared to high grade tumors and late stage disease, respectively. 27667152 2016 Long non-coding RNAs, ASAP1-IT1, FAM215A, and LINC00472, in epithelial ovarian cancer. FAM83H-AS1 FAM83H-AS1, onco-lncRNA-3 100128338 NA NR_033849 NA pancreatic ductal adenocarcinoma C25.3 M8500/3 RNA-seq, qrT-PCR, Western blot cell lines (PANC-1 PANC1, BxPC3, MiaPaCa2 and Aspc1) up-regulated We identified lncRNAs in genomic regions with SCNA and single nucleotide polymorphisms associated with lifetime risk of PDA and associated with clinical outcome using genomic and clinical data in PDA. Systems biology and experimental functional analysis of two epithelial lncRNAs (LINC00673 and FAM83H-AS1) suggest they regulate the transcriptional profile of pancreatic tumour samples and PDA cell lines.We also detected lncRNAs located in proximity to GATA6 and FOXA2, both important transcription factors involved in pancreas development. PDA is characterised by high penetrance mutations in four genes (KRAS, TP53, CDKN2A and SMAD4). We performed a similar analysis and identified five candidate lncRNAs within loci that harboured somatic SNP variants associated with increased risk of PDA 29440233 2018 Comprehensive characterisation of compartment-specific long non-coding RNAs associated with pancreatic ductal adenocarcinoma. FAM83H-AS1 FAM83H-AS1, onco-lncRNA-3 100128338 NA NR_033849 NA lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay, Cell migration and invasion assay etc. LAD tissues, cell lines (HCC4006, H1975, H358, H44, H1650 etc.) up-regulated FAM83H-AS1 was found to be overexpressed in tumors relative to normal lung and significantly associated with worse patient survival in LUAD. Cell proliferation, migration and invasion were decreased after FAM83H-AS1 knockdown using siRNAs in lung cancer cells. Flow cytometry analysis indicated the cell cycle was arrested at the G2 phase after FAM83H-AS1 knockdown. Mechanistically, we found that MET/EGFR signaling was regulated by FAM83H-AS1. 28198463 2017 Overexpression of FAM83H-AS1 indicates poor patient survival and knockdown impairs cell proliferation and invasion via MET/EGFR signaling in lung cancer. FAM83H-AS1 FAM83H-AS1, onco-lncRNA-3 100128338 NA NR_033849 NA colorectal cancer C19.9 NA RT-qPCR, Western blot, in vitro knockdown CRC tissues paired adjacent tissues, colonic cancer cell lines (SW480, LoVo, HCT116, HT29) up-regulated The levels of FAM83H-AS1, Notch1 and Hes1 were significantly increased in CRC samples and cell lines. Cell proliferation was markedly inhibited when FAM83H-AS1 was knocked down and this effect mediated by FAM83H-AS1 could be reversed by Notch1 regulators. Thus, downregulated FAM83H-AS1 exhibited an anti-proliferative role in CRC by repressing the Notch signaling pathway. 29434883 2017 lncRNA FAM83H-AS1 is associated with the prognosis of colorectal carcinoma and promotes cell proliferation by targeting the Notch signaling pathway. FAM83H-AS1 FAM83H-AS1, onco-lncRNA-3 100128338 NA NR_033849 NA colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues, cell lines (HCT116, SW480, HT29 and SW620) up-regulated Notably, the overexpression of FAM83H-AS1 and VPS9D1-AS1 indicated shorter OS time than lower expression. The overexpression of FAM83H-AS1 and VPS9D1-AS1 was validated in cancerous tissues. Thus, FAM83H-AS1 and VPS9D1-AS1 may potentially enhance carcinogenesis or may be developed as prognostic biomarkers for CRC. 27895773 2016 Dysregulation of long non-coding RNA profiles in human colorectal cancer and its association with overall survival. FAM83H-AS1 FAM83H-AS1, onco-lncRNA-3 100128338 NA NR_033849 NA glioma NA M9380/3 qPCR, RIP, Western blot etc. glioma tissues, cell line (U87 and U251) up-regulated FAM83H-AS1 was upregulated in glioma tissues and cell lines and high level of FAM83H-AS1 was associated with poor prognosis of glioma. Loss-of-function assays demonstrated that silenced FAM83H-AS1 obviously suppressed cell proliferation via regulating the cell-cycle distribution and cell apoptosis rate, and mechanistic experiments revealed that FAM83H-AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A, thereby influencing the cell cycle and proliferation. Moreover, the the Kaplan–Meier method (log-rank test) was used to analyze the correlation between FAM83HAS1 expression and overall survival of all patients and we found that high level of FAM83H‐AS1 was associated with poor prognosis ( p < 0.001, log-rank test). 29870057 2018 Long noncoding RNA FAM83H-AS1 exerts an oncogenic role in glioma through epigenetically silencing CDKN1A (p21). FAS-AS1 FAS-AS1, FAS-AS, FASAS, SAF 100302740 NA NR_028371 NA B-cell lymphoma NA M9591/3 qPCR, RIP, ChIP, ELISA etc. blood, cell lines (B-lymphocytes, Granta-519) down-regulated We found that the alternative splicing of Fas in lymphomas is tightly regulated by a long-noncoding RNA corresponding to an antisense transcript of Fas (FAS-AS1). Levels of FAS-AS1 correlate inversely with production of sFas, and FAS-AS1 binding to the RBM5 inhibits RBM5-mediated exon 6 skipping. EZH2, often mutated or overexpressed in lymphomas, hyper-methylates the FAS-AS1 promoter and represses the FAS-AS1 expression. EZH2-mediated repression of FAS-AS1 promoter can be released by DZNeP (3-Deazaneplanocin A) or overcome by ectopic expression of FAS-AS1, both of which increase levels of FAS-AS1 and correspondingly decrease expression of sFas. 24811343 2014 FAS-antisense 1 lncRNA and production of soluble versus membrane Fas in B-cell lymphoma. FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 400550 ENSG00000268388 NR_033925 GRCh38_16:86474529-86509099 neuroendocrine prostate cancer NA NA RNA-seq, Microarray, qPCR etc. neuroendocrine prostate cancer tissues down-regulated Top candidate lncRNAs FENDRR, H19, LINC00514, LINC00617, and SSTR5-AS1 identified in this study are implicated in the development of NEPC. 29757368 2018 The long noncoding RNA landscape of neuroendocrine prostate cancer and its clinical implications. FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 400550 ENSG00000268388 NR_033925 GRCh38_16:86474529-86509099 lung adenocarcinoma C34 M8140/3 qPCR etc. NSCLC tissues down-regulated 4 lncRNAs were also selected and validated by qRT-PCR in 20 pairs of lung cancer tissues and adjacent tissues. Expression patterns of all 4 lncRNAs were consistent with our analysis results, showing the analysis results were solid. 26918601 2016 Comprehensive analysis of lncRNA expression profiles and identification of functional lncRNAs in lung adenocarcinoma. FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 400550 ENSG00000268388 NR_033925 GRCh38_16:86474529-86509099 prostate cancer C61.9 NA qPCR, Luciferase reporter assay, in vitro knockdown cell lines (RWPE-1, P69 ,VCaP, LNCaP, 22Rv1, PC3, DU145), PCa tissues down-regulated FENDRR acts as a molecular sponge for miR-18a-5p. Upregulation of FENDRR inhibited cell proliferation, increased apoptosis and decreased invasion and migration ability,which was inhibited by miR-18a-5p mimic. Knockdown of FENDRR resulted in a significant increase of PCa cell proliferation and decrease of apoptosis and this effect was inhibited miR-18a-5p inhibitor.FENDRR and RUNX1 contain potential target sites for miR-18a-5p. miR-18a-5p mimic inhibited RUNX1 expression and luciferase activity.FENDRR could increase RUNX1 expression,which was inhibited by miR-18a-5p.The effect of FENDRR on cell proliferation, apoptosis and invasion and migration ability was suppressed by silence of RUNX1. 29465000 2018 Long non-coding RNA FENDRR reduces prostate cancer malignancy by competitively binding miR-18a-5p with RUNX1. FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 400550 ENSG00000268388 NR_033925 GRCh38_16:86474529-86509099 breast cancer C50 NA qPCR, in vitro knockdown etc. cell lines (MCF-7, BT-474, SK-BR-3, HCC1937, MDA-MB-231), breast cancer tissues down-regulated FENDRR inhibits breast cancer cell proliferation and migration and promotes cell apoptosis, while FENDRR knockdown promotes breast cancer cell proliferation and migration and suppresses cell apoptosis. FENDRR overexpression could inhibit tumor growth in a xenograft model. FENDRR inhibits breast cancer cell proliferation, promotes cell apoptosis, and is associated with good prognosis in breast cancer. 29559798 2018 Long non-coding RNA FENDRR inhibits cell proliferation and is associated with good prognosis in breast cancer. FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 400550 ENSG00000268388 NR_033925 GRCh38_16:86474529-86509099 gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissues, cell lines (MGC803, BGC823, MKN28, MKN45, SGC7901) down-regulated FENDRR was downregulated in gastric cancer cell lines and cancerous tissues, as compared with normal gastric epithelial cells and adjacent noncancerous tissue samples. Low FENDRR expression was correlated with deeper tumor invasion, higher tumor stage, and lymphatic metastasis. Histone deacetylation was involved in the downregulation of FENDRR in gastric cancer cells. FENDER overexpression suppressed invasion and migration by gastric cancer cells in vitro, by downregulating FN1 and MMP2/MMP9 expression. 25167886 2014 Decreased expression of the long non-coding RNA FENDRR is associated with poor prognosis in gastric cancer and FENDRR regulates gastric cancer cell metastasis by affecting fibronectin1 expression. FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 400550 ENSG00000268388 NR_033925 GRCh38_16:86474529-86509099 osteosarcoma NA M9180/4 qPCR, RIP, ChIP, Western blot etc. osteosarcoma tissues, cell line (hFOB1.19, HOS, Saos2, MG63, and U2OS) up-regulated We confirmed that FOXP4-AS1 was overexpressed in OS tissues than that of paracancerous tissues. The disease-free survival and overall survival of OS patients were not correlated with age, gender and tumor location, but remarkably correlated with FOXP4-AS1 expression, tumor size and lung metastasis. For in vitro experiments, MG63?cells expressed a higher expression of FOXP4-AS1, whereas U2OS cells expressed a lower expression, which were selected for the following studies. Overexpressed FOXP4-AS1 led to enhanced proliferation, migration and invasion, shortened G0/G1 phase, as well as inhibited cell cycle. Knockdown of FOXP4-AS1 in MG63?cells obtained the opposite results. Furthermore, RIP assay indicated that FOXP4-AS1 could inhibit LATS1 expression by binding to LSD1 and EZH2, so as to participate in OS development. In conclusion, these results revealed that FOXP4-AS1 is overexpressed in OS, and is the independent risk factor in OS prognosis. Upregulated FOXP4-AS1 promotes the proliferation, migration and cell cycle, but inhibits apoptosis of OS cells. Furthermore, FOXP4-AS1 participates in the development and progression of OS by downregulating LATS1 via binding to LSD1 and EZH2. 29859193 2018 FOXP4-AS1 participates in the development and progression of osteosarcoma by downregulating LATS1 via binding to LSD1 and EZH2. FER1L4 FER1L4, C20orf124 NA ENSG00000088340 NA GRCh38_20:35558737-35607562 osteosarcoma NA M9180/3 qPCR etc. osteosarcoma tissues down-regulated LncRNA FER1L4 expression was decreased in osteosarcoma samples. LncRNA FER1L4 was not related to the gender and age of patients, but was significantly associated with disease stage, metastasis, and tumor differentiation.Low-expression of lncRNA FER1L4 might be a prognostic marker in osteosarcoma. 29762833 2018 Low-expression of lncRNA FER1L4 might be a prognostic marker in osteosarcoma. FER1L4 FER1L4, C20orf124 NA ENSG00000088340 NA GRCh38_20:35558737-35607562 lung adenocarcinoma C34 M8140/3 RNA-seq, qPCR etc. LUAD tissues up-regulated The results showed that CHIAP2, LINC00472, LINC00961 and MGC27382 were downregulated in LUAD tumor tissues when compared with adjacent non-tumor lung tissues, while AFAP1-AS1, CHIAP2 and FER1L4 were upregulated in LUAD tumor tissues. 27826625 2016 Integrated analysis of long non-coding RNA-associated ceRNA network reveals potential lncRNA biomarkers in human lung adenocarcinoma. FER1L4 FER1L4, C20orf124 NA ENSG00000088340 NA GRCh38_20:35558737-35607562 glioblastoma NA M9440/3 qPCR etc. glioma tissues, cell lines (U373-MG, U251, LN-18, U87-MG and SHG-44) down-regulated FER1L4 was downregulated in 91.80% of gastric cancer tissues studied.low expression of FER1L4 was associated with tumor size, histological staging, tumor infiltration depth, lymph node metastasis, distant metastasis, tumor-node-metastasis staging, angioneurotic infiltration and serum CA72-4 antigen levels.Patients that receive surgical treatment for this disease typically have a poor prognosis, particularly those with glioblastoma multiforme (GBM), for which the average survival time is <2 years.etal bovine serum (FBS), 0.25% trypsin and Dulbecco's modified Eagle's medium (DMEM) were purchased from Invitrogen. 28789454 2017 Long non-coding RNA Fer-1-like family member 4 is overexpressed in human glioblastoma and regulates the tumorigenicity of glioma cells. FER1L4 FER1L4, C20orf124 NA ENSG00000088340 NA GRCh38_20:35558737-35607562 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated FER1L4 expression levels in gastric cancer tissues are significantly decreased. The low FER1L4 level were associated with tumor size, histologic grade, general classification, depth of invasion, lymphatic metastasis , distant metastasis, TNM stage, vessel or nerve invasion.FER1L4 might play a crucial role in human gastric cancer and may be a new potential biomarker for clinical prognosis evaluation. 24961353 2014 Clinical significance of the low expression of FER1L4 in gastric cancer patients. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 osteosarcoma NA M9180/3 RT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown OS cell lines (U2OS, SAOS2, SW1353, and MG63), fetal osteoblastic cell line hFOB up-regulated FEZF1-AS1 sponged miR-4443 to promote NUPR1 expression in U2OS and MG63 cells.Furthermore,knockdown of miR-4443 abrogated FEZF1-AS1 silence-induced inhibition of cell proliferation,migration and invasion in osteosarcoma.Finally,we found that restoration of NUPR1 rescued the proliferation,migration and invasion abilities of FEZF1-AS1-depleted U2OS and MG63 cells. In collection,FEZF1-AS1 could promote osteosarcoma progression by sponging miR-4443 to promote NUPR1 expression.The FEZF1-AS1/miR-4443/NUPR1 axis may act as a novel therapeutic strategy for osteosarcoma treatment. 29510778 2018 Long non-coding RNA FEZF1-AS1 promotes osteosarcoma progression by regulating miR-4443/NUPR1 axis. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 pancreatic ductal adenocarcinoma C25.3 M8500/3 Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP PDAC tissues, PC cell lines (PANC-1, Capan-2, MIAPaCa-2, SW1990, and BxPC-3) up-regulated A novel lncRNA FEZF1-AS1 and its sense-cognate gene ZNF312B were found to be highly expressed in human PDAC tissues and cell lines, which is associated with disease progression and predicts clinical outcome in PDAC patients.FEZF1-AS1 may act as an endogenous sponge by competing for miR-107, thereby modulating the derepression of ZNF312B. Downregulation of FEZF1-AS1 or ZNF312B significantly inhibited proliferation, colony formation, migration, and invasion of PDAC cells in vitro, whereas the miR-107 inhibitor abrogated the effect of dow-regulation of FEZF1-AS1 or ZNF312B in reducing oncogenic capacities of PDAC cells.In addition, FEZF1-AS1/miR-107/ZNF312B axis-induced promotion of PDAC cells proliferation appeared to be mediated by modulation of the apoptosis and the G1-S checkpoint. 29348628 2018 FEZF1-AS1/miR-107/ZNF312B axis facilitates progression and Warburg effect in pancreatic ductal adenocarcinoma. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 colorectal cancer C19.9 NA qPCR, RNAi, Flow cytometry assay, Cell proliferation assay etc. CRC tissues, cell lines (DLD-1, HT29, HCT116, SW480, SW620, Lovo) up-regulated Here, we discovered a novel lncRNA FEZF1-AS1 is markedly upregulated in human primary CRC and associated with CRC metastasis and poor prognosis. Moreover, the downregulation of FEZF1-AS1 expression significantly inhibited the CRC cells proliferation, migration and invasiveness, suppressed S-phase entry in vitro, and repressed tumor growth and metastasis in vivo. In contrast, overexpression of FEZF1-AS1 could promote the aggressive behaviors of CRC cells. 26848625 2016 Long non-coding RNA FEZF1-AS1 facilitates cell proliferation and migration in colorectal carcinoma. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 lung adenocarcinoma C34 M8140/3 qPCR, Western bolt, RIP, ChIP etc. LAD tissues, cell lines (SPCA-1, NCI-H1299, A549, NCI-H441, LTEP-a2) up-regulated FEZF1-AS1 was increased in lung adenocarcinoma tissues and cell lines and high level of FEZF1-AS1 was associated with poor prognosis of lung adenocarcinoma.Besides,we also uncovered that FEZF1-AS1 could suppress p57 expression through recruiting EZH2 and LSD1 to the promoter of p57, thus influenced the cell cycle and proliferation.we determined the expression level of FEZF1-AS1 in LAD cells and found that FEZF1-AS1 was mainly located in nucleus, indicating that FEZF1-AS1 regulated target gene probably at transcriptional level. 29262540 2017 LincRNA FEZF1-AS1 contributes to the proliferation of LAD cells by silencing p57 expression FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 gastric cancer C16 NA qPCR, Western blot, RNAi gastric cancer tissues, cell lines (MGC-803, MKN-49P, BGC-823, SGC-7901, AGS,NCI-N87,GES-1) up-regulated lncRNA FEZF1-AS1 was observably upregulated in human GC tissues and GC cell lines.high expression of lncRNA FEZF1-AS1 was significantly associated with later stage and higher grade. lncRNA FEZF1-AS1 may be an independent prognostic factor in GC.whenever the lncRNA FEZF1-AS1 was silenced, the proliferation of GC cells were significantly inhibited and the cell cycle was arrested at a G0/G1 stage in GC cells.downregulation of lncRNA FEZF1-AS1 could suppress the activation of the Wnt/B-catenin signaling pathway. 29239821 2017 Long noncoding RNA FEZF1-AS1 indicates a poor prognosis of gastric cancer and promotes tumorigenesis via activation of Wnt signaling pathway. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, ChIP, MTT assay etc. gastric cancer tissues, cell lines (MGC-803, SGC-7901, AGS) up-regulated FEZF1-AS1 was overexpressed in gastric cancer. Further experiments revealed that knockdown FEZF1-AS1 significantly inhibited gastric cancer cells proliferation by inducing G1 arrest and apoptosis, whereas endogenous expression FEZF1-AS1 promoted cell growth. Additionally, RIP assay and RNA-pulldown assay evidenced that FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1, the first discovered demethylase. 28209170 2017 LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation through LSD1-Mediated H3K4me2 demethylation. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, etc. The human HCC cells( HepG2, SK-hep1, Huh7, HCCLM3), normal liver cell line (LO2) up-regulated In conclusion, the present study for the first time demonstrated that FEZF1-AS1 serves as an oncogenic lncRNA in human HCC and implicated FEZF1-AS1 as a valuable therapeutic target for HCC treatment. Kaplan-Meier analysis of overall survival (OS) in 139 HCC patients based on FEZF1-AS1 expression. 29957463 2018 Long non-coding RNA FEZF1-AS1 promotes cell invasion and epithelial-mesenchymal transition through JAK2/STAT3 signaling pathway in human hepatocellular carcinoma. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 cervical cancer C53 NA qPCR cervical cancer tissues up-regulated High expressions of FEZF1-AS1 were significantly association with poorer histological grade (p = 0.004), positive distant metastasis (p = 0.002) and advanced FIGO stage (p = 0.001). patients with low FEZF1-AS1 expression lived shorter than those with high FEZF1-AS1 expression. 29917186 2018 Long non-coding RNA FEZF1-AS1 is up-regulated and associated with poor prognosis in patients with cervical cancer. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 colorectal cancer C19.9 NA qPCR, microarray, RNA-seq, Luciferase reporter assay, RIP, Western blot, etc. colorectal cancer tissues, cell lines (LoVo, Caco2, HT29, HCT8, HCT116, SW480) up-regulated Increased FEZF1-AS1 expression is associated with poor survival. Functional assays revealed that FEZF1-AS1 promotes CRC cell proliferation and metastasis. FEZF1-AS1 could bind and increase the stability of the pyruvate kinase 2 (PKM2) protein, resulting in increased cytoplasmic and nuclear PKM2 levels. 29914894 2018 LncRNA-FEZF1-AS1 promotes tumor proliferation and metastasis in colorectal cancer by regulating PKM2 signaling. FGF14-AS2 FGF14-AS2 283481 ENSG00000272143 NR_036487 GRCh38_13:102394630-102395703 breast cancer C50 NA qPCR, RIP etc. breast cancer tissues down-regulated In this study, we demonstrated that FGF14 antisense RNA 2 (FGF14-AS2), a novel long non-coding RNA, was significantly down-regulated in breast cancer tissue compared with adjacent normal tissue both in validated cohort and TCGA cohort. Reduced expression of FGF14-AS2 was correlated with larger tumor size, more lymph node metastasis and advanced clinical stage in both cohorts. 26820525 2016 A novel long non-coding RNA FGF14-AS2 is correlated with progression and prognosis in breast cancer. FGFR3-AS1 NA NA NA NA NA osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay etc. osteosarcoma tissues up-regulated The effects of FGFR3-AS1 on osteosarcoma cell proliferation and cell cycle were determined by Cell Counting Kit-8, Ethynyl deoxyuridine incorporation assay and flow cytometry. FGFR3-AS1 was upregulated in osteosarcoma. Increased FGFR3-AS1 expression correlates with large tumor size, advanced Enneking stage, metastasis and poor survival. Through antisense pairing with FGFR3 3'UTR, FGFR3-AS1 increases FGFR3 mRNA stability and upregulates FGFR3 expression. The expression of FGFR3-AS1 and FGFR3 is positively correlated in osteosarcoma tissues. Knockdown of FGFR3-AS1 inhibits the proliferation and cell cycle progression of osteosarcoma cells in vitro. Moreover, knockdown of FGFR3-AS1 inhibits xenograft tumor growth of osteosarcoma cells in vivo. 27022737 2016 Long noncoding RNA FGFR3-AS1 promotes osteosarcoma growth through regulating its natural antisense transcript FGFR3 FILNC1 NA 100132735 ENSG00000231426 NR_038399 GRCh38_6:139677639-139860476 renal tumor C64.9 NA qPCR, microarray, Western blot, Luciferase reporter assay etc. cell lines (HEK293T, RCC4, 786-O, 769P) down-regulated We show that FILNC1 deficiency leads to enhanced glucose uptake and lactate production through upregulation of c-Myc. Upon energy stress, FILNC1 interacts with AUF1, a c-Myc mRNAbinding protein, and sequesters AUF1 from binding c-Myc mRNA, leading to downregulation of c-Myc protein. FILNC1 is specifically expressed in kidney, and is downregulated in renal cell carcinoma; also, its low expression correlates with poor clinical outcomes in renal cell carcinoma. Together, our study not only identifies FILNC1 as a negative regulator of renal cancer with potential clinical value, but also reveals a regulatory mechanism by long non-coding RNAs to control energy metabolism and tumor development. 28978906 2017 Energy stress-induced lncRNA FILNC1 represses c-Myc-mediated energy metabolism and inhibits renal tumor development FLJ22447 LncRNA-CAF NA NA NA GRCh38_14:61570540-61654713 oral squamous cell carcinoma C06.9 M8070/3 RNA-seq, qPCR, RIP breast cancer tissues, cell lines (HSC-3) up-regulated lncRNA FLJ22447, which was remarkably up-regulated in CAFs, referred to LncRNA-CAF (Lnc-CAF) hereafter. Interleukin-33 (IL-33) was mainly located in the stroma and positively co-expressed with Lnc-CAF to elevate the expression of CAF markers (a-SMA, vimentin and N-cadherin) in fibroblasts. In a co-culture system, IL-33 knockdown impaired Lnc-CAF-mediated stromal fibroblast activation, leading to decreased proliferation of tumor cells. Mechanistically, Lnc-CAF up-regulated IL-33 levels and prevented p62-dependent autophagy-lysosome degradation of IL-33, which was independent of LncRNA-protein scaffold effects. Treatment with the autophagy inducer, rapamycin, impaired the proliferative effect of Lnc-CAF/IL-33 by promoting IL-33 degradation. In turn, tumor cells further increased Lnc-CAF levels in stromal fibroblasts via exosomal Lnc-CAF. 29346528 2018 A novel stromal lncRNA signature reprograms fibroblasts to promote the growth of oral squamous cell carcinoma via LncRNA-CAF/interleukin-33. FLVCR1-AS1 NA NA ENSG00000198468 NA GRCh38_1:212852108-212858088 hepatocellular carcinoma C22.0 M8170/3 qPCR, in vitro knockdown, Luciferase reporter assay etc. cell line (LO2, Hep3B, HepG2, Huh7, and PLC/PRF-5), HCC tissues up-regulated lncRNA FLVCR1-AS1 was extremely up-regulated in HCC tissues and cell lines. FLVCR1-AS1 expression level was positively correlated with tumor severity.FLVCR1-AS1 knockdown remarkably inhibited HCC cell proliferation,migration,and invasion in vitro and in vivo while induced cell apoptosis. In mechanism, FLVCR1-AS1 acted as a competitive endogenous RNAs to sponge miR-513c which targeted the mRNA of MET for degradation. By directly sponging miR-513c, FLVCR1-AS1 increased MET expression in HCC, and then promoted HCC progression. FLVCR1-AS1 played a positive role in HCC development and progression according to the study in its mechanism,function and clinical manifestation, so that it could be expected to become a new target in HCC prevention and treatment. 29574975 2018 LncRNA FLVCR1-AS1 acts as miR-513c sponge to modulate cancer cell proliferation, migration, and invasion in hepatocellular carcinoma. FOXC2-AS1 FOXC2-AS1, ODRUL 103752587 ENSG00000260944 NR_125795 GRCh38_16:86565145-86567761 breast cancer C50 NA qPCR, Western blot etc. cell line (MCF-10A, MDA-MB-468, MDA-MB-231, MDA-MB-436, MCF-7), BC tissue up-regulated Cyclin D1 Cyclin D2, and Cyclin D3 were all partly positively modulated by FOXC2-AS1 in BC. FOXC2-AS1 may serve as a promising prognostic biomarker and therapeutic target for BC patients. FOXC2-AS1 significantly suppressed the proliferation ability and flow cytometric analysis illustrated the influence of FOXC2-AS1 on cell cycle and apoptosis rate. 29562954 2018 Long non-coding RNA FOXC2-AS1 predicts poor survival in breast cancer patients and promotes cell proliferation FOXCUT FOXCUT, LINC01379, TCONS_00011636 101927703 ENSG00000280916 NR_125804 GRCh38_6:1605531-1606079 esophageal squamous cell cancer NA NA qPCR, RNAi etc. ESCC tissues, cell lines (KYSE30, KYSE70, KYSE140, KYSE150, KYSE180 etc.) up-regulated Notably elevated FOXCUT and FOXC1 expression levels were observed in cancerous tissues compared to adjacent noncancerous tissues, showing strong correlations with poor differentiation, advanced lymph node classification and metastasis. The expression of FOXCUT was positively correlated with expression of FOXC1 in ESCC specimens. And the expression of FOXC1 was also decreased as the FOXCUT expression was silenced by siRNA. Assays in vitro demonstrated that knockdown of either FOXCUT or FOXC1 remarkably inhibited cell proliferation, colony formation, migration, invasion in ESCC cells. 25031703 2014 A novel long non-coding RNA FOXCUT and mRNA FOXC1 pair promote progression and predict poor prognosis in esophageal squamous cell carcinoma. FOXD2-AS1 NA 84793 ENSG00000237424 NR_026878 GRCh38_1:47432133-47434641 nasopharyngeal cancer C11 NA qPCR, Western blot, in vitro knockdown etc. cell lines (SUNE-1, CNE-1, HNE-1, CNE-2, C666-1,HONE-1), NPC tissues up-regulated The aberrant overexpression of FOXD2-AS1 indicated the poor prognosis of NPC patients. Silence of FOXD2-AS1 was able to repress NPC cell growth in vitro while overexpression of FOXD2-AS1 inversed this process. 29248577 2017 Long non-coding RNA FOXD2-AS1 aggravates nasopharyngeal carcinoma carcinogenesis by modulating miR-363-5p/S100A1 pathway FOXD2-AS1 NA 84793 ENSG00000237424 NR_026878 GRCh38_1:47432133-47434641 esophageal squamous cell cancer NA NA qRT-PCR ESCC tissue, esophageal squamous cell carcinoma cell lines (KYSE510, KYSE520, KYSE150, KYSE30 and KYSE140) up-regulated FOXD2-AS1 expression was upregulated in ESCC tissue than that in adjacent non-tumor tissue samples (P< 0.001). Kaplan-Meier analysis showed that high FOXD2-AS1 expression was correlated with poor prognosis in ESCC patients. Patients with a high level of FOXD2-AS1 had a shorter OS and DFS than those with a low level of FOXD2-AS1 (P= 0.005 and 0.0001, respectively). On multivariate analysis, the hazard ratio of FOXD2-AS1 expression was 1.66 (95% CI = 1.04-2.64, P= 0.033) for OS and 2.68 (95% CI = 1.49-4.82, P= 0.001) for DFS. 29286915 2018 Upregulation of the long noncoding RNA FOXD2-AS1 predicts poor prognosis in esophageal squamous cell carcinoma. FOXD2-AS1 NA 84793 ENSG00000237424 NR_026878 GRCh38_1:47432133-47434641 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc. NSCLC tissues, cell lines (H1299, A549, H1650 and H2291) up-regulated We found that lncRNA FOXD2-AS1 is significantly up-regulated in NSCLC tissues. Loss- and gain-function assays revealed that FOXD2-AS1 promotes NSCLC cell growth and NSCLC tumor progression. Furthermore, we also revealed that FOXD2-AS1 modulates Wnt/B-catenin signaling in NSCLC cells. 28132805 2017 Highly expressed long non-coding RNA FOXD2-AS1 promotes non-small cell lung cancer progression via Wnt/B-catenin signaling. FOXD2-AS1 NA 84793 ENSG00000237424 NR_026878 GRCh38_1:47432133-47434641 colorectal cancer C19.9 NA qPCR, Western blot etc. CRC tissues, cell lines (RKO, HCT15, HCT28, HCT116, and SW480) up-regulated FOXD2- AS1 expression was significantly increased in CRC tissues as well as in CRC cell lines. down-regulation of FOXD2-AS1 suppressed cell, proliferation, invasion and migration in vitro. FOXD2-AS1 promoted the progression of CRC by regulating EMT and Notch signaling pathway. Thus, targeting FOXD2-AS1 may be an effective strategy for CRC treatment.Although recent advances have been made in diagnostic procedures and therapeutic strategies, the 5-year survival rate for metastatic CRC is only 10-15%3,4.Waltham,MA, USA) Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% fetal bovine serum (FBS), Sigma-Aldrich. 28925486 2017 Long non-coding RNA FOXD2-AS1 functions as a tumor promoter in colorectal cancer by regulating EMT and Notch signaling pathway. FOXD2-AS1 NA 84793 ENSG00000237424 NR_026878 GRCh38_1:47432133-47434641 bladder cancer C67 NA Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP bladder cancer tissues, bladder cancer cell lines (T24 and UM-UC-3) up-regulated FOXD2-AS1 promotes bladder cancer cell proliferation, migration, and invasion in vitro and in vivo. Microarray analysis demonstrated that FOXD2-AS1 negatively regulates the expression of Tribbles pseudokinase 3 (TRIB3), a negative regulator of Akt. Mechanistically, FOXD2-AS1 forms an RNA-DNA complex with the promoter of TRIB3, the transcriptional activity of which is subsequently repressed, and leads to the activation of Akt, which further increases the expression of E2F1, a vital transcription factor involved in the G/S transition. Interestingly, E2F1 could bind to the FOXD2-AS1 promoter region and subsequently enhance its transcriptional activity, indicating that FOXD2-AS1/Akt/E2F1 forms a feedback loop. 29445134 2018 Human NPC cell lines CNE2 and 5-8FThe long non-coding RNA FOXD2-AS1 promotes bladder cancer progression and recurrence through a positive feedback loop with Akt and E2F1. FOXD2-AS1 NA 84793 ENSG00000237424 NR_026878 GRCh38_1:47432133-47434641 gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissues, cell lines (BGC823, MGC803, AGS, SGC790, and MKN45) up-regulated A comprehensive analysis identified that FOXD2-AS1 enrichment was upregulated markedly in GC and positively correlated with a large tumor size, a later pathologic stage, and a poor prognosis. 29789713 2018 Upregulation of the long noncoding RNA FOXD2-AS1 promotes carcinogenesis by epigenetically silencing EphB3 through EZH2 and LSD1, and predicts poor prognosis in gastric cancer FOXD2-AS1 NA 84793 ENSG00000237424 NR_026878 GRCh38_1:47432133-47434641 thyroid cancer C73.9 NA qPCR, Western blot, etc. cell lines (BHT101, BCPAP) down-regulated thyroid cancer patients with higher RUNDC3A-AS1 or lower FOXD-AS1 expression levels had shorter OS time. 29923329 2018 Identification of differential expressed lncRNAs in human thyroid cancer by a genome-wide analyses. FOXD3-AS1 FOXD3-AS1, pasFOXD3 100996301 ENSG00000230798 NR_121634 GRCh38_1:63320884-63324441 neuroblastoma NA M9500/3 RNA-Seq, qPCR, Western blot, Luciferase reporter assay,in vitro knockdown, RIP etc. cell lines (NB-1643, SK-N-BE(2), NB-1691, IMR32,BE(2)-C, SK-N-AS, SH-SY5Y, SK-N-SH), NB tissue down-regulated FOXD3-AS1 is downregulated in NB tissues and cell lines, and ectopic expression of FOXD3-AS1 induces neuronal differentiation and decreases the aggressiveness of NB cells in vitro and in vivo.Mechanistically, as a nuclear lncRNA, FOXD3-AS1 interacts with poly(ADP-ribose) polymerase 1 (PARP1) to inhibit the poly(ADP-ribosyl)ation and activation of CCCTC-binding factor (CTCF), resulting in derepressed expression of downstream tumor-suppressive genes. FOXD3-AS1 harbors tumor-suppressive properties by inhibiting the oncogenic roles of PARP1 or CTCF and plays crucial roles in all-trans-retinoic-acid-mediated therapeutic effects on NB. 29398485 2018 Risk-Associated Long Noncoding RNA FOXD3-AS1 Inhibits Neuroblastoma Progression by Repressing PARP1-Mediated Activation of CTCF FOXD3-AS1 FOXD3-AS1, pasFOXD3 100996301 ENSG00000230798 NR_121634 GRCh38_1:63320884-63324441 glioma NA M9380/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. glioma tissues, cell lines (U87, A172 and U251) up-regulated FOXD3-AS1 was markedly up-regulated in high-grade glioma tissues (WHO grade III-IV) compared with that in low-grade glioma (WHO grade I-II) and normal brain tissues, and patients with low FOXD3-AS1 expression had grater survival probability. FOXD3-AS1 knockdown significantly inhibited cell proliferation, induced cell cycle S-phase arrest, and impaired cell migration and invasion in malignant glioma cells. As expected, we also found that the expression of FOXD3-AS1 was positively correlated with FOXD3 mRNA. Knockdown of FOXD3-AS1 reduced the protein level of FOXD3 in cultured U251 and A172 cell lines. 27829996 2016 Down-regulation of long non-coding RNA FOXD3 antisense RNA 1 (FOXD3-AS1) inhibits cell proliferation, migration, and invasion in malignant glioma cells. FRLnc1 NA NA NA NA NA gastric cancer C16 NA qPCR gastric cancer tissues up-regulated Increased FRLnc1 expression was associated with depth of tumor,differentiation degree,distant metastasis, TNM stage and lymph node metastasis.FRLnc1 expression was an independent prognostic marker for survival in patients with GC.overall patient survival for those with low FRLnc1 expression was significantly longer than those patients with high FRLnc1 expression. 29424899 2018 Clinical prognostic value of A FOXM1 related long non-coding RNA expression in gastric cancer. FTH1P3 FTH1P3, FTHL3, FTHL3P NA ENSG00000213453 NA GRCh38_2:27392784-27393367 oral squamous cell carcinoma C06.9 M8070/3 qPCR, Cell transfection, Western blot, Luciferase reporter assay, RNA pull-down assay etc. OSCC tissues, cell lines (SCC1, SCC25, TU183, HSU3, FADU, OEC-M1, SNU1041 etc.) up-regulated FTH1P3 was over-expressed in OSCC and decreased the survival rate of OSCC patients.Ectopic expression of FTH1P3 facilitates cell proliferation and colony formation in OSCC cells.Moreover, FTH1P3 acted as a ceRNA, effectively becoming sponge for miR-224-5p and thereby modulating the expression of fizzled 5. Importantly, expression analysis revealed that both FTH1P3 and fizzled 5 were up-regulated in OSCC cell lines and tissues, and over-expression of fizzled 5 also functioned as an oncogene in OSCC cells. 28093311 2017 Long non-coding RNA FTH1P3 facilitates oral squamous cell carcinoma progression by acting as a molecular sponge of miR-224-5p to modulate fizzled 5 expression. FTX FTX, LINC00182, MIR374AHG, NCRNA00182 100302692 ENSG00000230590 NR_028379 GRCh38_X:73946555-74293574 glioma NA M9380/3 qPCR, Cell transfection, Western blot, MTT assay etc. glioma tissues, cell lines (U87MG and LN18) up-regulated the expression of FTX and miR-342-3p was associated with progression of gliomas. FTX directly inhibited the expression of miR-342-3p, which subsequently regulates the expression of AEG-1. Collectively, FTX is critical for proliferation and invasion of glioma cells by regulating miR-342-3p and AEG-1. 28112756 2017 Long noncoding RNA FTX is upregulated in gliomas and promotes proliferation and invasion of glioma cells by negatively regulating miR-342-3p. FTX FTX, LINC00182, MIR374AHG, NCRNA00182 100302692 ENSG00000230590 NR_028379 GRCh38_X:73946555-74293574 hepatocellular carcinoma C22.0 M8170/3 RIP etc. Frozen HCC tumors, cell lines (SMMC-7721, HCCLM3, Hep3B, HepG2, Huh7, 97H and GSG7701) down-regulated lnc-FTX is expressed at higher levels in female livers than in male livers and is significantly downregulated in HCC tissues compared with normal liver tissues. Patients with higher lnc-FTX expression exhibited longer survival, suggesting that lnc-FTX is a useful prognostic factor for HCC patients. lnc-FTX inhibits HCC cell growth and metastasis both in vitro and in vivo. Mechanistically, lnc-FTX represses Wnt/B-catenin signaling activity by competitively sponging miR-374a and inhibits HCC cell epithelial-mesenchymal transition and invasion. In addition, lnc-FTX binds to the DNA replication licensing factor MCM2, thereby impeding DNA replication and inhibiting proliferation in HCC cells. 27065331 2016 Long noncoding RNA FTX inhibits hepatocellular carcinoma proliferation and metastasis by binding MCM2 and miR-374a FTX FTX, LINC00182, MIR374AHG, NCRNA00182 100302692 ENSG00000230590 NR_028379 GRCh38_X:73946555-74293574 colorectal cancer C19.9 NA qPCR, RNAi etc. CRC tissues, cell lines (HT-29, SW1116, SW480, COLO205) up-regulated Long non-coding RNA FTX was significantly upregulated in colorectal cancer tissues, and low long non-coding RNA FTX expression was significantly correlated with differentiation grade, lymph vascular invasion, and clinical stage. Patients with high long non-coding RNA FTX showed poorer overall survival than those with low long non-coding RNA FTX. Multivariate analyses indicated that status of long non-coding RNA FTX was an independent prognostic factor for patients. Functional analyses showed that upregulation of long non-coding RNA FTX significantly promoted growth, migration, invasion, and increased colony formation in colorectal cancer cells. 26629053 2015 Biological significance of long non-coding RNA FTX expression in human colorectal cancer FTX FTX, LINC00182, MIR374AHG, NCRNA00182 100302692 ENSG00000230590 NR_028379 GRCh38_X:73946555-74293574 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Cell proliferation assay, MTT assay etc. HCC tissues, cell lines (HepG2, Hep3B, Huh7, SMMC-7721 and Bel-7402) up-regulated The results showed that the expression of lncRNA Ftx and miR-545 in HCC tissues were significantly higher than that in the non-tumor tissues and correlated with each other. Further results confirmed that lncRNA Ftx and miR-545 were upregulated in a panel of HCC cell lines compared with that in non-transformed LO2 hepatic cell line. LncRNA Ftx and miR-545functions to enhance proliferation, tumorigenicity and cell cycle progression of HCC cells. 26992218 2016 Ftx non coding RNA-derived miR-545 promotes cell proliferation by targeting RIG-I in hepatocellular carcinoma. FTX FTX, LINC00182, MIR374AHG, NCRNA00182 100302692 ENSG00000230590 NR_028379 GRCh38_X:73946555-74293574 colorectal cancer C19.9 NA qPCR, RIP, etc. CRC tissues, cell lines (HT29, LS513, SW480, HCT8, HCT116, FHC) up-regulated Overexpression of lncRNA FTX was significantly associated with the bigger tumor diameter, the advanced TNM stage, the lymph node, and distant metastasis, and also predicted poor prognosis of patients with CRC. FTX directly interacted with miR-215 and suppressed miR-215 expression. The results showed that patients with higher FTX levels had shorter overall survival time than those with lower FTX levels. 29925853 2018 LncRNA FTX sponges miR-215 and inhibits phosphorylation of vimentin for promoting colorectal cancer progression. GACAT3 GACAT3, LINC01458, lncRNA-AC130711 104797537 ENSG00000236289 NR_126559 GRCh38_2:16050427-16085801 gastric cancer C16 NA qPCR, Luciferase reporter assay, Western blot cell lines (BGC-823,SGC-7901, MKN-45, AGS, 293T,GES-1) up-regulated GACAT3 showed a higher expression in GC tissues and cell lines. Increased GACAT3 level was significantly associated with a shorter overall survival of patients with GC.knockdown of GACAT3 significantly inhibited proliferation, colony formation, migration, and invasion of GC cells in vitro. Moreover, underexpression of GACAT3 decreased tumorigenesis in vivo.GACAT3 directly binds to microRNA-497 (miR-497), and GACAT3 expression was inversely correlated with miR-497 expression. 29091858 2017 LncRNA GACAT3 promotes gastric cancer progression by negatively regulating miR-497 expression. GAPLINC GAPLINC, LINC01540 100505592 ENSG00000266835 NR_110429 GRCh38_18:3466250-3478978 bladder cancer C67 NA qPCR, Western blot etc. bladder cancer tissues, cell lines (UM-UC-3, T24, J82, 5637, RT4 and SV-HUC-1) up-regulated We demonstrated that gastric adenocarcinoma associated, positive CD44 regulator, long intergenic noncoding RNA (GAPLINC) was significantly upregulated in bladder cancer tissues compared with normal tissues in The Cancer Genome Atlas (TCGA) cohort (P=0.039) and a validated cohort of 80 patients with bladder cancer (P=0.021). Statistical analysis revealed that GAPLINC expression level was associated with tumor stage in the validated cohort (P=0.017). Kaplan-Meier analysis demonstrated that patients in the high GAPLINC expression group had a worse overall survival (P=0.0386), indicating that GAPLINC may be a sensitive prognostic biomarker for patients with bladder cancer. Furthermore, knockdown of GAPLINC inhibited cell proliferation and colony formation, promoted cells cycle arrest at G1 phase and suppressed cells migration and invasion. The findings of the present study suggest that GAPLINC exhibits an oncogenic role in bladder cancer and may be a potential prognostic biomarker and therapeutic target. 29725414 2018 Upregulated GAPLINC predicts a poor prognosis in bladder cancer patients and promotes tumor proliferation and invasion. GAPLINC GAPLINC, LINC01540 100505592 ENSG00000266835 NR_110429 GRCh38_18:3466250-3478978 colorectal cancer C19.9 NA microarray, qPCR, Western blot, RNA pull-down assay etc. cell lines (HCT116, HT29, SW480, DLD-1, SW620) up-regulated The increased expression of GAPLINC was found to be positively correlated with larger tumor size, advanced tumor stage (T stage), advanced node stage (N stage), increased death, and shorter survival of patients with CRC by in situ hybridization analysis. Besides, the decreased expression of GAPLINC could significantly repress CRC cell invasion in vitro and also inhibit proliferation in vitro and in vivo. RNA pull-down with mass spectrum experiments revealed that PTB-associated splicing factor (PSF) and non-POU-domain-containing octamer-binding (NONO) protein bound to GAPLINC and reversed the effect of GAPLINC on cell invasion. 27259250 2016 Long noncoding RNA GAPLINC promotes invasion in colorectal cancer by targeting SNAI2 through binding with PSF and NONO. GAPLINC GAPLINC, LINC01540 100505592 ENSG00000266835 NR_110429 GRCh38_18:3466250-3478978 gastric cancer C16 NA microarray, ISH etc. gastric cancer tissues up-regulated GAPLINC is a 924-bp-long lncRNA that is highly expressed in gastric cancer tissues. GAPLINC suppression and with gene expression profiling in gastric cancer cells revealed alterations in cell migration pathways, with CD44 expression the most highly correlated. Manipulating GAPLINC expression altered CD44 mRNA abundance and the effetcs of GAPLINC on cell migration and proliferation were neutralized by suppressing CD44 expression. 25277524 2014 Long Noncoding RNA GAPLINC Regulates CD44-Dependent Cell Invasiveness and Associates with Poor Prognosis of Gastric Cancer. GAPLINC GAPLINC, LINC01540 100505592 ENSG00000266835 NR_110429 GRCh38_18:3466250-3478978 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, ChIP, Luciferase reporter assay etc. gastric cancer tissues, cell lines (GEF-1, HFE-145, MKN45, SGC7901, HEK-293T) up-regulated GAPLINC was overexpressed in GC tissues and promoted tumor migration and invasive behavior. GAPLINC overexpression was associated with poor prognosis in GC patients. Luciferase reporter assays and chromatin immunoprecipitation assays confirmed that HIF-1a binds to the promoter region of GAPLINC and activates its transcription. GAPLINC knockdown inhibited hypoxia-induced tumor proliferation in vivo. 27729869 2016 Hypoxia Promotes Gastric Cancer Malignancy Partly through the HIF-1a Dependent Transcriptional Activation of the Long Non-coding RNA GAPLINC. GAS5 GAS5, NCRNA00030, SNHG2 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 glioblastoma NA M9440/3 microarray, qPCR etc. glioblastoma tissues up-regulated Our real-time RT-PCR confirmed aberrant expression patterns of all the lncRNA and genes that were observed inthe microarray data, suggesting that these lncRNAs and genes were dysregulated in GBM patient samples and that they might have important roles in GBM pathology. 27784795 2016 The Potential Roles of Long Noncoding RNAs (lncRNA) in Glioblastoma Development. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 thyroid cancer C73.9 NA qPCR thyroid cancer tissues down-regulated There was a decrease in the lncRNA GAS5 expression in TC tissues in comparison to benign tumor tissues. Expression of lncRNA GAS5 showed significant association with tumor node metastasis (TNM) staging, lymph node metastasis and the multiple cancer foci of TC. The survival rate of TC patients with high lncRNA GAS5 expression was higher than that of TC patients with low lncRNA GAS5 expression during the DFS and OS periods. 28506768 2017 Low expression of long non-coding RNA GAS5 is associated with poor prognosis of patients with thyroid cancer GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 nasopharyngeal cancer C11 NA DNA Extraction and genotyping, SNPs selections etc. NPC tissues differential expression the potential role of lncRNA GAS5 polymorphisms rs2067079 and rs6790 as predictive biomarkers for chemoradiotherapy induced toxic reactions in NPC patients.This decrement was significantly correlated with poor survival in HCC patients. 28977945 2017 Genetic polymorphisms of long non-coding RNA GAS5 predict platinum-based concurrent chemoradiotherapy response in nasopharyngeal carcinoma patients. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 lymphoma NA M9590/3 RNAi etc. cell lines (Jeko-124 and Z-138) down-regulated Downregulation of GAS5 substantially reduced the effects of each rapalogue on cell viability, DNA synthesis, and colony-forming ability.Stimulation of expression of candidate tumor suppressor GAS5 is responsible for much of the cytotoxic and cytostatic effects of rapalogues in MCL, suggesting that improved targeting of this pathway may allow improvements in the therapy of this intractable lymphoma. 24703244 2014 Role of GAS5 noncoding RNA in mediating the effects of rapamycin and its analogues on mantle cell lymphoma cells GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 glioma NA M9380/3 qPCR, Lentiviral infection, Western blot, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc. cell lines (MCF-7, T47D, MDA-MB-231) down-regulated Here, Gas5 is found to be downregulated in glioma specimens and U87 and U251 glioma cell lines. We showed that the introduction of Gas5 by plasmid transfection increased the expression of tumor suppressor Bcl-2-modifying factor (bmf) and Plexin C1 via directly targeting and reducing the expression of miR-222. Downregulated expression of miR-222 inhibited U87 and U251 cell proliferation and promoted the apoptosis by upregulating bmf. 26370254 2015 Gas5 Exerts Tumor-suppressive Functions in Human Glioma Cells by Targeting miR-222. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 esophageal squamous cell cancer NA NA qPCR etc. cell lines (KYSE30, KYSE180 and HEK 293T) differential expression In this study, we found that GAS5 was over-expressed in ESCC tissue compared with that in normal esophageal tissue in a public database. Functional studies showed that GAS5 could inhibit ESCC cell proliferation, migration and invasion in vitro. Further analysis revealed that GAS5 was regulated by interferon (IFN) responses via the JAK-STAT pathway. Moreover, as an IFN-stimulated gene (ISG), GAS5 was a positive regulator of IFN responses. The feedback loop between GAS5 and the IFN signaling pathway plays an important antitumor role in ESCC, thus providing novel potential therapeutic targets. 29743093 2018 Long non-coding RNA GAS5 is induced by interferons and plays an antitumor role in esophageal squamous cell carcinoma. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay etc. glioblastoma tissues up-regulated The present study characterized the expression and function of long non-coding RNA growth arrest specific 5 (GAS5) in GSCs in order to elucidate the molecular mechanisms by which GAS5 contributes to glioma pathogenesis. We demonstrate that GAS5 suppresses GSC malignancy by binding to miR-196a-5p. miR-196a-5p, an onco-miRNA, stimulates GSC proliferation, migration, and invasion, in addition to reducing levels of apoptosis. miR-196a-5p specifically downregulates the expression of forkhead box protein O1 (FOXO1) by targeting its 3′ untranslated region (3′-UTR). FOXO1 upregulates expression of phosphotyrosine interaction domain containing 1 (PID1), thereby inhibiting GSC tumorigenicity and growth. FOXO1 also upregulates migration and invasion inhibitory protein(MIIP), resulting in attenuation of migration and invasion activities. Interestingly, we also show that FOXO1 promotes GAS5 transcription, thus forminga positive feedback loop. 28666797 2017 GAS5 suppresses malignancy of human glioma stem cells via a miR-196a-5p/FOXO1 feedback loop GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 pancreatic cancer C25 NA qPCR, Western blot, RIP cell lines (SW1990 and PATU8988, SW1990/GEM, PATU8988/5-FU, PANC-1) down-regulated GAS5 expression was significantly down-regulated, miR-181c-5p expression was significantly up-regulated in pancreatic cancer cells.Overexpresson of GAS5 obviously inhibited cell viability, while GAS5 knockdown showed the opposite outcome. GAS5 regualtes Hippo signaling pathway via miR-181c-5p to antagonize the development of multidrug resistance in pancreatic cancer cells.cells transfected si-GAS5 had a significantly higher survival rate than that in control group. 29112934 2017 Long non-coding RNA GAS5 antagonizes the chemoresistance of pancreatic cancer cells through down-regulation of miR-181c-5p. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 bladder cancer C67 NA Microarray, qPCR etc. bladder cancer tissues down-regulated In the training set, uc004cox.4 was up-regulated and GAS5 was down-regulated in BC patients. Moreover, the expression of urinary uc004cox.5 was an independent predictor for the recurrence of NMIBC patients. 29516641 2018 Cell-free lncRNA expression signatures in urine serve as novel non-invasive biomarkers for diagnosis and recurrence prediction of bladder cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 cervical cancer C53 NA qPCR, RNAi etc. cervical cancer tissues down-regulated We found that GAS5 expression was markedly downregulated in cervical cancer tissues than in corresponding adjacent normal tissues. Decreased GAS5 expression was significantly correlated with FIGO stage, vascular invasion and lymph node metastasis. Moreover, cervical cancer patients with GAS5 lower expression have shown significantly poorer overall survival than those with higher GAS5 expression. And GAS5 expression was an independent prognostic marker of overall survival in a multivariate analysis. 25400758 2014 Decreased expression of lncRNA GAS5 predicts a poor prognosis in cervical cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Flow cytometry assay, Cell proliferation assay, ISH etc. cell lines (Huh7, Hep3B, HepG2, QGY-7701, MHCC97L and HCCLM9he) down-regulated Low expression of GAS5 was significantly correlated with differentiation and portal vein tumor thrombosis. Further experiments demonstrated that overexpression of GAS5 significantly suppressed the proliferation and invasion of hepatoma cells in vitro. Overexpression of GAS5 significantly promoted the apoptosis of hepatoma cells. 26707238 2016 Decreased expression of long non-coding RNA GAS5 indicates a poor prognosis and promotes cell proliferation and invasion in hepatocellular carcinoma by regulating vimentin. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 ovarian cancer C56.9 NA qPCR, Cell transfection, Western blot, Cell proliferation assay etc. ovarian cancer tissues, cell lines (IOSE25, A2780, OVCAR3, SKOV3 and 3AO) down-regulated GAS5 was markedly decreased in tumor tissues and a lower expression of GAS5 was detected in tumors with larger size, deeper invasive depth and higher tumor stage. Patients with low GAS5 expression level had poorer disease-free and overall survival than those with high GAS5 expression. Moreover, overexpression of GAS5 was demonstrated to suppress ovarian cancer cell proliferation in vitro and in vivo. Finally, we found that GAS5 influenced ovarian cancer cell proliferation, partly via regulating cyclin D1, p21 and apoptosis protease activating factor 1 (APAF1) expression. 27779700 2016 Decreased expression of long non-coding RNA GAS5 promotes cell proliferation, migration and invasion, and indicates a poor prognosis in ovarian cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues down-regulated The expression level of GAS5 was reduced in HCC in comparison to normal matched tissues. It is also proved that GAS5 expression was to be associated with HCC tumor size, lymphnode metastasis and clinical stage. In addition, the Kaplan-Meier survival curves revealed that low GAS5 expression was associated with poor prognosis in HCC patients. GAS5 expression was an independent prognostic marker of overall HCC patient survival in a multivariate analysis. 25120813 2014 Down-regulation of long non-coding RNA GAS5 is associated with the prognosis of hepatocellular carcinoma. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 cervical cancer C53 NA qPCR, RNAi cervical cancer tissues, Cervical cancer cell line (HeLa) down-regulated GAS5 expression in cervical cancer tissues was significantly inhibited compared to that in adjacent tissues (p<0.05). GAS5 expression was correlated with FIGO stage and metastatic tumor parameters of cervical cancer patients (p<0.01). RNA interference data showed that the down-regulation of GAS5 significantly enhanced cell proliferation and invasion potency (p<0.05). 29509242 2018 Correlation between long strand non-coding RNA GASS expression and prognosis of cervical cancer patients. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 prostate cancer C61.9 NA qPCR, Western blot etc. cell lines (PC3, DU145, PNT2C2) down-regulated GAS5 expression is significantly decreased in prostate cancer cells compared with prostate epithelial cells. GAS5 interacted with E2F1 and enhanced the binding of E2F1 to the P27Kip1 promoter. GAS5 functions as a tumor suppressor in prostate cancer development and progression via targeting P27Kip1. 28396462 2017 LncRNA GAS5 Inhibits Cellular Proliferation by Targeting P27Kip1. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues down-regulated The expression of all 18 candidate lncRNAs was evaluated by RT-qPCR, using 80 pairs of CRC and control tissue samples. Among these, eight lncRNAs (MALAT-1, NR_029373, NR_046321, NR_034119, GAS5, BANCR, NR_026817 and PCAT-1) were found significantly dysregulated in CRC tumor tissues compared with controls. 27591862 2016 Identification of long noncoding RNAs as potential novel diagnosis and prognosis biomarkers in colorectal cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA qPCR, RNAi etc. cell lines (MCF-7, T-47D) down-regulated In this preclinical study, the consequences of decreased GAS5 expression for breast cancer cell survival following treatment with chemotherapeutic agents are addressed. GAS5 lncRNA promoted the apoptosis of triple-negative and oestrogen receptor-positive cells but only dual PI3K/mTOR inhibition was able to enhance GAS5 levels in all cell types. Reduced GAS5 expression attenuates apoptosis induction by classical chemotherapeutic agents in breast cancer cells, providing an explanation for the relationship between GAS5 expression and breast cancer patient prognosis. 24789445 2014 Regulation of apoptosis by long non-coding RNA GAS5 in breast cancer cells: implications for chemotherapy. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 colorectal cancer C19.9 NA qPCR, Flow cytometry assay etc. CRC tissues down-regulated The lower expression of GAS5 was significantly correlated with large tumor size, low histological grade and advanced TNM stage. Multivariate analyses revealed that GAS5 expression served as an independent predictor for overall survival. Further experiments revealed that overexpressed GAS5 significantly repressed the proliferation both in vitro and in vivo. 25326054 2014 Long noncoding RNA GAS5 affects cell proliferation and predicts a poor prognosis in patients with colorectal cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA qPCR etc. cell lines (HEK 293T, LNCaP, W7.2c etc.) down-regulated We have found that, in some cell lines, GAS5 expression induces growth arrest and apoptosis independently of other stimuli. GAS5 transcript levels were significantly reduced in breast cancer samples relative to adjacent unaffected normal breast epithelial tissues. 18836484 2009 GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 prostate cancer C61.9 NA qPCR etc. cell lines (HEK 293T, LNCaP, W7.2c etc.) down-regulated Real-time RTPCR was therefore carried out and the level of GAS5 expression was quantified in these cell lines relative to 22Rv1. 22Rv1, P4E6 and PNT2C2 cell linesexpressed similar levels of GAS5, whereas LNCaP and PC3 expressed much lower levels of GAS5. 18836484 2009 GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Luciferase reporter assay, MTT assay etc. NSCLC tissues, cell lines (A549 and H1975) down-regulated GAS5 was down-regulated and miR-135b was up-regulated in NSCLC tissues and cells. The expressions of GAS5 and miR-135b changed inversely in response to irradiation. Gain of function experiments revealed that GAS5 overexpresion and miR-135b downregulation significantly suppressed tumorigenesis by repressing cell proliferation, invasion and enhanced radiosensitivity of NSCLC cells by reducing colony formation rates. Moreover, rescue experiments demonstrated that miR-135b upregulation markedly abolished GAS5 overexpression-induced tumorigenesis inhibition and radiosensitivity improvement. 28117028 2017 LncRNA GAS5 Inhibits Tumorigenesis and Enhances Radiosensitivity By Suppressing miR-135b Expression in Non-Small Cell Lung Cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. HCC tissues, cell lines (Bel-7402, SMMC-7721, HCCLM3 etc.) up-regulated The levels of GAS5 and miR-21 were correlated with the clinicopathological characteristics of HCC. HCC patients with higher levels of GAS5 or with the lower levels of miR-21 have longer survival times. There are lower levels of GAS5 and higher levels of miR-21 in HCC cell lines (Be7402, SMMC-7721, and HCCLM3) than in normal liver L-02 cells, and the levels correlate with the aggression of the HCC cell lines. Knockdown of GAS5 upregulates miR-21 levels in Bel-7402 cells (weakly aggressive). Moreover, GAS5 that upregulated or downregulated the expression of PDCD4 and PTEN was reversed by inhibiting or overexpressing miR-21 level in Bel-7402 and HCCLM3 cells. Then, overexpression of GAS5 suppresses the migration and invasion of HCC cells and high expression of miR-21 largely eliminates GAS5-mediated suppression of HCC cell migration and invasion. 26404135 2015 Long noncoding RNA GAS5 suppresses the migration and invasion of hepatocellular carcinoma cells via miR-21. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901 and MKN54), gastric adenocarcinomas tissues up-regulated Overexpression of tumor suppressor lncRNAs PTENP1-AS and GAS5 might,in turn,reduce the oncogenic role of miR-21.We observed upregulation of PTENP1-AS that could increase the EGFR and AGO4 expression in tumors and also noticed that GAS5 could compete with AGO4 and regulate the miR-21.Compared to PTENP1-AS,the GAS5 expression was predominantly upregulated in the gastric tumor samples and the expression level was comparatively higher than competing mRNA AGO4. Collectively,these observations suggest that overexpression of PTENP1-AS and GAS5 in gastric cancer could be abrogating oncogenic activity of miR-21 and confirms that lncRNAs could act as tumor suppressive ceRNAs. 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 prostate cancer C61.9 NA qPCR, RNA interference and transient transfection etc. prostate cancer tissues, cell lines (LNCaP, 22RV1, DU145, PC3, WPMY-1) up-regulated GAS5-007 was reduced by androgen treatment and inhibited by AR. Functional analysis of GAS5 showed it was related to regulating translational elongation, protein biosynthesis, and transcription. Moreover, we observed GAS5-007 knockdown inhibited the proliferation, cell cycle and promoted cell apoptosis of PCa. We also constructed a GAS5-miRNA network to explain the different roles of different GAS5 transcripts in PCa. This study provides novel insights to identify potential diagnostic biomarker and therapy target for prostate cancer in clinical treatment. 28771526 2017 An androgen reduced transcript of LncRNA GAS5 promoted prostate cancer proliferation. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 colorectal cancer C19.9 NA qRT-PCR, Western blot CRC and normal tissues, CRC cell lines (HCT-8, HT-29, HCT-116, SW-480) down-regulated Gas5 expression was lower in CRC tissues compared to the adjacent normal tissues, and is also lower in CRC cell lines than FHC cell line.Meanwhile, elevated Gas5 expression inhibited mRNA expression of Akt and Erk and protein expression of p-Akt and p-Erk, which promoted Casp9 mRNA and pho-Casp9 protein expression but inhibited Casp3 mRNA and pho-Casp3 protein expression. 29308053 2018 Effect of long non-coding RNA Gas5 on proliferation, migration, invasion and apoptosis of colorectal cancer HT-29 cell line. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. breast cancer tissues, cell lines (MDA-MB-453, MDA-MB-231, MCF-7 and T47D) down-regulated Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly. High level of Notch-1 provided a poor prognosis in breast cancer. Interference of Notch-1 significantly suppressed proliferation of T47D cell, and significantly increased the level of GAS5. 26550436 2015 Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 gastric cancer C16 NA qPCR, RNAi, Western blot etc. gastric cancer tissues, cell lines (SGC7901, BGC823, MGC803, MKN45, MKN28) down-regulated GAS5 expression was markedly downregulated in gastric cancer tissues. Moreover, ectopic expression of GAS5 was demonstrated to decrease gastric cancer cell proliferation and induce apoptosis, while downregulation of endogenous GAS5 could promote cell proliferation. GAS5 could influence gastric cancer cells proliferation, partly via regulating E2F1 and P21 expression. 24884417 2014 Decreased expression of long noncoding RNA GAS5 indicates a poor prognosis and promotes cell proliferation in gastric cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA qPCR, Western blot breast cancer tissues, cell lines (MDA-MB-231 and MDA-MB-468) down-regulated Here, we show that levels of the lncRNA, growth arrest-specific transcript 5 (GAS5), are decreased in TNBC tissues, and this down-regulation of GAS5 is associated with an aggressive tumor phenotype in patients, affecting clinical stage, lymph node metastasis and overall survival. These data suggest that GAS5 can suppress TNBC progression by competitively binding miR-196a5p, therefore GAS5 may be a prognostic biomarker of TNBC. 29793177 2018 Long noncoding RNA GAS5 suppresses triple negative breast cancer progression through inhibition of proliferation and invasion by competitively binding miR-196a-5p GAS6-AS1 NA 650669 ENSG00000233695 NR_044995 GRCh38_13:113815630-113845744 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues down-regulated In this study, we reported a new lncRNA GAS6-AS1, whose expression was downregulated in tumor tissues in 50 patients with NSCLC compared with those in the adjacent normal tissues. Furthermore, decreased GAS6-AS1 expression was negatively correlated with lymph node metastasis and advanced tumor node metastasis stage. Univariate and multivariate analyses showed that GAS6-AS1 expression served as an independent predictor for overall survival. Altered lncRNA GAS6-AS1 expression might be involved in the development and progression of NSCLC by influencing its host gene and promised to be a potential diagnostic target in patients with NSCLC. 23979857 2013 Low expression of long noncoding RNA GAS6-AS1 predicts a poor prognosis in patients with NSCLC. GAS8-AS1 NA 750 ENSG00000221819 NR_122031 GRCh38_16:90028908-90029901 papillary thyroid cancer NA M8260/3 qPCR, Western blot,in vitro knockdown etc. cell line (BCPAP, Nthy-ori-3-1, K1), PTC tissues down-regulated Overexpression of GAS8-AS1 inhibited proliferation, significantly increased the ratio of LC3-II/LC3-I, and reduced p62 expression, whereas GAS8-AS1 knockdown demonstrated opposite effects.silencing of ATG5 attenuated autophagy activation and rescued the inhibition of cell proliferation caused by GAS8-AS1. 29327301 2017 LncRNA GAS8-AS1 inhibits cell proliferation through ATG5-mediated autophagy in papillary thyroid cancer. GCASPC lnc-SOD2-1, RP1-56L9.7-001, TCONS_00011605 112441427 ENSG00000224073 NA NA gallbladder cancer C23.9 NA qPCR, RIP, RNA pull-down assay, Mass Spetcrometry etc. GBC tissues, cell lines (GBC-SD, SGC-996, NOZ and OCUG-1) down-regulated GCASPC levels were significantly lower in gallbladder cancer than adjacent nontumor tissues and were associated with tumor size, American Joint Committee on Cancer tumor stage, and patient outcomes. GCASPC overexpression suppressed cell proliferation in vitro and in vivo, whereas GCASPC silencing had opposite effects. By RNA pull-down and mass spectrometry, we identified pyruvate carboxylase as an RNA-binding protein that associated with GCASPC. 27450454 2016 Long Noncoding RNA GCASPC, a Target of miR-17-3p, Negatively Regulates Pyruvate Carboxylase-Dependent Cell Proliferation in Gallbladder Cancer. GHET1 GHET1, lncRNA-GHET1 102723099 ENSG00000281189 NR_130107 GRCh38_7:148987527-148989432 gastric cancer C16 NA qPCR, Western blot etc. cell lines (SGC-7901, AGS and BGC-823) up-regulated We found an lncRNA, AK123072, which was up-regulated by hypoxia. AK123072 was frequently up-regulated in GC samples and promoted GC migration and invasion in vivo and in vitro. Furthermore, AK123072 could mediate the metastasis of hypoxia-induced GC cells. Next, we identified EGFR, which was a metastasis-related gene regulated by AK123072. In addition, we found that the expression of EGFR was positively correlated with that of AK123072 in the clinical GC samples used in our study. Furthermore, we found that the EGFR gene CpG island methylation was significantly increased in GC cells depleted of AK123072. Intriguingly, EGFR expression was also increased by hypoxia, and EGFR up-regulation by AK123072 mediated hypoxia-induced GC cell metastasis 26884908 2015 Hypoxia/lncRNA-AK123072/EGFR pathway induced metastasis and invasion in gastric cancer GHET1 GHET1, lncRNA-GHET1 102723099 ENSG00000281189 NR_130107 GRCh38_7:148987527-148989432 bladder cancer C67 NA qPCR, RNAi, Western blot, in vitro knockdown etc. bladder cancer tissues up-regulated In this study, we demonstrated that GHET1 was upregulated in bladder cancer tissues compared to adjacent normal tissues and its over-expression correlates with tumor size, advanced tumor and lymph node status, and poor survival. GHET1 knockdown suppressed the proliferation and invasion of bladder cancer cells in vitro. In the meantime, inhibition of GHET1 reversed the epithelial-mesenchymal-transition in bladder cancer cell line. 25400817 2014 Long noncoding RNA GHET1 promotes the development of bladder cancer. GHET1 GHET1, lncRNA-GHET1 102723099 ENSG00000281189 NR_130107 GRCh38_7:148987527-148989432 head and neck cancer C76.0 NA qPCR etc. head and neck cancer tissues, cell lines (HOK, FaDu, OECM1, SCC25, SAS and Cal-27) up-regulated The expression level of GHET1 was significantly increased in HNC tissues, compared with paired adjacent normal tissues. High GHET1 expression was significantly associated with advanced Tumor-Node-Metastasis stages and poor prognosis. Furthermore, inhibition of GHET1 suppressed cell proliferation, induced cell apoptosis and caused cell cycle arrest in vitro. In addition, GHET1 silencing inhibited cell migration and invasion. Taken together, the results of the present study indicated that GHET1 acts as an oncogene in HNC and may represent a novel therapeutic target. 29725422 2018 Long non-coding RNA gastric carcinoma highly expressed transcript 1 promotes cell proliferation and invasion in human head and neck cancer. GHET1 GHET1, lncRNA-GHET1 102723099 ENSG00000281189 NR_130107 GRCh38_7:148987527-148989432 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RIP etc. hepatocellular carcinoma tissues, cell lines (HepG2, Hep3B, Bel-7402, SMMC-7721 and L02) up-regulated GHET1 expression was significantly up-regulated in HCC tissues and the higher level of GHET1 was related to vascular invasion, cirrhosis, tumor size, edmindson grade, and poor prognosis. Moreover, knockdown of GHET1 inhibited cell proliferation of HCC, and also caused cell cycle arrest and induced apoptosis in HCC cell lines. We also found that GHET1 could epigenetically repress transcription of Kruppel-like factor 2 (KLF2) in HCC cells by recruiting PRC2 into KLF2 promoter region. Our results indicated that lncRNA GHET1, as a growth regulator, might serve as a novel prognostic biomarker and therapy target for HCC. patients with high expression level of GHET1 had a significantly shorter overall survival than those with low expression level of GHET1. 29139562 2018 LncRNA GHET1 predicts poor prognosis in hepatocellular carcinoma and promotes cell proliferation by silencing KLF2. GHET1 GHET1, lncRNA-GHET1 102723099 ENSG00000281189 NR_130107 GRCh38_7:148987527-148989432 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. gastric cancer tissues, cell lines (MKN45, AGS etc.) up-regulated In this study, we found that lncRNA gastric carcinoma high expressed transcript 1 (lncRNA-GHET1) was up-regulated in gastric carcinoma. The over-expression of this lncRNA correlates with tumor size, tumor invasion and poor survival. Gain-of-function and loss-of-function analyses demonstrated that GHET1 over-expression promotes the proliferation of gastric carcinoma cells in vitro and in vivo. Knockdown of GHET1 inhibits the proliferation of gastric carcinoma cells. 24397586 2014 Long non-coding RNA GHET1 promotes gastric carcinoma cell proliferation by increasing c-Myc mRNA stability. GHET1 GHET1, lncRNA-GHET1 102723099 ENSG00000281189 NR_130107 GRCh38_7:148987527-148989432 breast cancer C50 NA qPCR, western blot etc. breast cancer tissues, cell lines (SKBR3, ZR-75- 681, BT-20 and MCF-7) up-regulated Our results demonstrated that GHET1 was up-regulated in breast cancer tissues and cell lines, and promoted breast cancer cell proliferation, invasion and migration by affecting EMT. 29843220 2018 up-regulated GHRLOS NA 100126793 ENSG00000240288 NR_004431 GRCh38_3:10285754-10293449 colorectal cancer C19.9 NA qPCR etc. colorectal tissues down-regulated GHRLOS is downregulated at a high frequency in human CRC tissues. To the best of our knowledge, for the first time, we revealed that GHRLOS may have clinical potential not only as a prospective biomarker for metastatic phenotype of CRC but also as a promising prognostic predictor in CRC. Our findings encourage further functional studies, which will explore its potential as a therapeutic target that may be used for the control of CRC metastasis and progression. 29187879 2017 Aberrant Expression of the Long Non-coding RNA GHRLOS and Its Prognostic Significance in Patients with Colorectal Cancer GIHCG NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Northern blot, RIP, ChIP, RNA pull-down assay, Cell proliferation assay etc. HCC tissues, cell lines (L02, QSG7701, SMMC7721, Hep3B, Huh7, and HCCLM3) up-regulated Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression. 27380494 2016 Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. GIHCG NA NA NA NA NA tongue squamous cell carcinoma C02 M8070/3 qPCR TSCC tissues, cell lines (SCC4, SCC1, UM1, Cal27, NHOK) up-regulated we indicated that high GIHCG expression was positively associated with poor overall survival. Elevated expression of GIHCG inhibited the miR-429 expression in TSCC cells. 29953645 2018 Long noncoding RNA GIHCG enhanced tongue squamous cell carcinoma progression through regulating miR-429. GPC3-AS1 NA 110806308 NA NR_148713 NA hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. HCC tissues, cell lines (QSG-7701, SMMC-7721, Huh7, and HepG2) up-regulated We observed a significant upregulation of GPC3-AS1 in HCC. GPC3-AS1 expression was strongly correlated with GPC3 in HCC tissues. Gain-of-function and loss-of-function analyses showed that GPC3-AS1 overexpression enhanced HCC cell proliferation and migration in vitro and xenograft tumor growth in vivo. GPC3-AS1 knockdown inhibited HCC cell proliferation and migration. Moreover, the effects of GPC3-AS1 on HCC cell proliferation and migration were dependent on the upregulation of GPC3. 27573079 2016 Long noncoding RNA glypican 3 (GPC3) antisense transcript 1 promotes hepatocellular carcinoma progression via epigenetically activating GPC3. GS1-5L10.1 GS1-5L10.1 NA NA NA GRCh38_8:91975908-91977418 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. GUARDIN NA NA NA NA NA colon cancer C18 NA Microarray, Luciferase reporter assay, in vitro knockdown, RNAi etc. cell line (HCT116, U2OS, A549, H1299, 293T and HAFF), colon cancer tissues up-regulated GUARDIN is necessary for preventing chromosome end-to-end fusion through maintaining the expression of telomeric repeat-binding factor 2 (TRF2) by sequestering microRNA-23a.Moreover, GUARDIN also sustains breast cancer 1 (BRCA1) stability by acting as an RNA scaffold to facilitate the heterodimerization of BRCA1 and BRCA1-associated RING domain protein 1 (BARD1).As such, GUARDIN silencing triggered apoptosis and senescence,enhanced cytotoxicity of additional genotoxic stress and inhibited cancer xenograft growth. Thus, GUARDIN may constitute a target for cancer treatment. GUARDIN functions to regulate TRF2 and IRF1 through sequestering miR-23a. 29593331 2018 GUARDIN is a p53-responsive long non-coding RNA that is essential for genomic stability. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric adenocarcinoma C16 M8140/3 other gastric adenocarcinoma tissues up-regulated The rs2839698 SNP of H19 may have potential as a novel prognostic factor for survival in T3 gastric adenocarcinoma after surgery alone; these finding have special relevance to patients who are not suitable for postoperative chemotherapy. 29479897 2018 The rs2839698 Single Nucleotide Polymorphism of lncRNA H19 is Associated with Post-Operative Prognosis in T3 Gastric Adenocarcinoma. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 neuroendocrine prostate cancer NA NA RNA-seq, Microarray, qPCR etc. neuroendocrine prostate cancer tissues up-regulated Top candidate lncRNAs FENDRR, H19, LINC00514, LINC00617, and SSTR5-AS2 identified in this study are implicated in the development of NEPC. 29757368 2018 The long noncoding RNA landscape of neuroendocrine prostate cancer and its clinical implications. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 embryonal carcinoma NA M9070/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. cell lines (NCCIT, NT2 and HES-1) up-regulated H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. SCID-Beige mice transplanted with H19 down-regulated hEC cells exhibited slower kinetics of tumor formation, resulting in an increased animal survival. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. 26415227 2015 The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 chronic myeloid leukemia NA M9863/3 qPCR, Western blot etc. cell line (K562) up-regulated We observed that H19 was highly expressed in Bcr-Abl-expressing primary CML cells derived from 4 patients, and imatinib treatment greatly decreased the expression of H19 in these cells but not in normal control cells. Loss of either Bcr-Abl expression or Abl kinase activity caused decrease of c-Myc levels with simultaneously reduced levels of H19. Furthermore, we demonstrated that depletion of c-Myc alone in K562 cells significantly decreased the level of H19, suggesting that H19 is expressed in a c-Myc dependent manner in K562 leukemic cells. 24685695 2014 High expression of long non-coding RNA H19 is required for efficient tumorigenesis induced by Bcr-Abl oncogene. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 retinoblastoma C69.2 M9510/3 Western blot, qPCR, in vitro knockdown RIP etc. cell lines (WERI-Rb-1, SO-RB50, and Y7, ARPE-19), retinoblastoma tissues down-regulated H19 is downregulated in retinoblastoma tissues and cell lines. Mechanistically, we identified seven miR-17-92 cluster binding sites on H19, and found that H19 directly bound to miR-17-92 cluster via these seven binding sites. Through binding to miR-17-92 cluster, H19 relieves the suppressing roles of miR-17-92 cluster on p21. Furthermore, H19 represses STAT3 activation induced by miR-17-92 cluster. Hence, our results revealed that H19 upregulates p21 expression,inhibits STAT3 phosphorylation, and downregulates the expression of STAT3 target genes BCL2, BCL2L1, and BIRC5. In conclusion, our data suggested that H19 inhibits retinoblastoma progression via counteracting the roles of miR-17-92 cluster, and implied that enhancing the action of H19 may be a promising therapeutic strategy for retinoblastoma. 29143996 2017 Long non-coding RNA H19 suppresses retinoblastoma progression via counteracting miR-17-92 cluster. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 malignant melanoma NA M8720/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell line (A375, SK-MEL-1, SK-MEL-5), melanoma tissues up-regulated LncRNA H19 was increased in melanoma tissue,and lncRNA H19 was correlated with poor prognosis of melanoma patients.miR-106a-5p acts as a tumour suppressor in melanoma by targeting E2F3.E2F3 affects the melanoma cell glucose metabolism and growth.lncRNA H19 may function as the sponge of miR-106a-5p to up-regulate E2F3 expression,and consequently promote the glucose metabolism and growth of melanoma. 29350287 2018 Long non-coding RNA H19 promotes glucose metabolism and cell growth in malignant melanoma via miR-106a-5p/E2F3 axis. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 oral squamous cell carcinoma C06.9 M8070/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (SCC-4, SCC-15 , CAL-27, HSC-3,HSC-2), OSCC tissues up-regulated The correlation between H19 and microRNA miR-138 was detected.H19 was found to be upregulated in OSCC tissues and its high expression level was associated with the TNM stage and nodal invasion,and also correlated with a shorter overall survival of patients with OSCC.The knockdown of H19 significantly inhibited OSCC cell proliferation,migration,invasion and epithelial-mesenchymal transition (EMT),and induced apoptosis in vitro.it also suppressed subcutaneous tumor growth in vivo.H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR-138,the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells. 29344674 2018 Long non-coding RNA H1 promotes cell proliferation and invasion by acting as a ceRNA of miR-138 and releasing EZH2 in oral squamous cell carcinoma. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 thyroid cancer C73.9 NA qPCR etc. TC tissues up-regulated TC patients with a lower 5-year survival rate showed upregulated levels of lncRNA H19 expression and,downregulated levels of miRNA let7a expression.This study aims to explore the effects of long non-coding RNA H19 (lncRNA H19) and microRNA let7a (miRNA let7a) expression on the prognosis of thyroid cancer.TC patients with a lower 5-year survival rate showed upregulated levels of lncRNA H19 expression and, downregulated levels of miRNA let7a expression.LncRNA H19 and miRNA let7a expression, tumor diameter, TNM stage and lymph node metastasis were independent prognostic factors of TC. increased lncRNA H19 and decreased miRNA let7a expression levels are associated with poor prognosis in TC patients. 28655518 2017 Effects of long non-coding RNA H19 and microRNA let7a expression on thyroid cancer prognosis. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 laryngeal squamous cell cancer C32.3 NA qPCR, Western blot, Luciferase reporter assay etc. LSCC tissues, cell line (Hep-2) up-regulated We identified microRNA miR-148a-3p as an inhibitory target for H19. Overexpression of miR-148a-3p reduced LSCC migration, invasion and proliferation cell, while inhibition of miR-148a-3p did the opposite. The inhibition of LSCC progression induced by H19 knockdown required the activity of miR-148a-3p. We also identified DNA methyltransferase enzyme DNMT1 as a target of miR-148a-3p. Cellular DNA methylation levels were inhibited by both miR-148a-3p overexpression and H19 knockdown 26872375 2016 Regulation of laryngeal squamous cell cancer progression by the lncRNA H19/miR-148a-3p/DNMT1 axis H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 cervical cancer C53 NA qPCR, Luciferase Reporter Assay, Western Blot. cervical cancer tissues down-regulated Function assays showed that overexpression of miR-138-5p reduced cervical cancer cell proliferation, arrested cells in the G0 /G1 phase, and induced cell apoptosis in vitro. Remarkably, SIRT1 was confirmed as a direct target of miR-138-5p in cervical cancer, and miR-138-5p exerted the reduced tumor functions by suppressing SIRT1 expression. Moreover, we further identified that lncRNA H19 could act as a molecular sponge of miR-138-5p in cervical cancer progression. Taken together, these results suggested that miR-138-5p could suppress cervical cancer cell progression by targeting SIRT1.This decreased expression of miR-138-5p correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, poor differentiation, lymph nodes metastasis, and poor overall survival of cervical cancer patients. 28797320 2017 Decreased Expression of MiR-138-5p by LncRNA H19 in Cervical Cancer Promotes Tumor Proliferation. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 cholangiocarcinoma NA M810/3 qPCR, Western blot etc. CCA tissue, cell lines (RBE, HCCC-9810, QBC939, Huh-28, HuCCT1, KMBC and CCLP-1) up-regulated expression levels of H19 were investigated in CCA tissues and cell lines and were correlated with clinicopathological features.H19 was upregulated in CCA tissue samples and cell lines, and this upregulation was associated with tumor size,TNM stage, postoperative recurrence and overall survival in 56 patients with CCA. knockdown of H19 followed by RNA silencing restrained cell proliferation and promoted apoptosis.In addition,H19 suppression impaired migration and invasion potential by reversing EMT. Overall, our findings may help to develop diagnostic biomarkers and therapeutics that target H19 for the treatment of CCA. H19 acts as a tumor-promoting role by regulating miR-675 in gastric cancer cells, indicating a correlation between H19 and miRNAs in cancer cells. 28528181 2017 Overexpression of long noncoding RNA H19 indicates a poor prognosis for cholangiocarcinoma and promotes cell migration and invasion by affecting epithelial-mesenchymal transition. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, RNAi, Cell proliferation assay etc. ccRCC tissues, cell lines (786-O, ACHN, and Caki-1) up-regulated The relative level of H19 was significantly higher in ccRCC compared to the adjacent normal renal tissues. And higher expression of H19 was found in renal cancer cells compared to the nonmalignant renal cells HK-2. Furthermore, The ccRCC patients with higher H19 expression had more advanced clinical stage and poorer prognosis than those with lower expression, Kaplan-Meier analysis revealed that patients with higher H19 expression had a poorer overall survival and H19 expression could be an independent prognostic marker for ccRCC patient. The results of in vitro assays indicated that knockdown of H19 reduced cell proliferation, invasion, and migration. 25866221 2015 Down-regulated long non-coding RNA H19 inhibits carcinogenesis of renal cell carcinoma. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 head and neck squamous cell carcinoma C76.0 M8070/3 qPCR, Cell transfection, Cell proliferation assay, Cell migration and invasion assay etc. acute lymphoblastic leukemia tissues up-regulated We observed that both H19 and miR-675 were significantly overexpressed in a cohort of 65 primary tumor samples and two HNSCC cell lines. Importantly, when paired with patient follow-up data, higher expression of either H19 or miR-675 was significantly correlated with higher risk of patient relapse, and associated with worse overall survival and poor disease-free survival. Knockdown miR-675 caused significant reduction of cell viability, migratory and invasive capabilities. 27994496 2016 Overexpression of lncRNA H19/miR-675 promotes tumorigenesis in head and neck squamous cell carcinoma. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 acute myeloid leukemia NA M9861/3 qPCR etc. acute myeloid leukemia tissues, cell lines (HL60 and K562) up-regulated H19 expression was significantly increased in AML patients but not associated with embedded miR-675 expression. Moreover, H19 overexpression was not dependent on the methylation pattern in H19 differentially methylated region/imprinting control region. Strong association was observed between H19 overexpression and patients' characteristics including sex, higher white blood cells, older age, and intermediate karyotype, FLT3-ITD, and DNMT3A mutations. In addition, H19 overexpression correlated with lower complete remission (CR) rate and shorter overall survival, and further confirmed by multivariate analyses. Importantly, the prognostic effect of H19 expression was validated by TCGA and GEO data. In the follow-up of patients, H19 expression in CR phase was lower than diagnosis time and returned at relapse time. 29643943 2018 H19 overexpression promotes leukemogenesis and predicts unfavorable prognosis in acute myeloid leukemia. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gallbladder cancer C23.9 NA qPCR, Western blot etc. GBC tissues cell lines (NOZ, GBC-SD, SGC-996, and EH-GB1) up-regulated In vitro, both TGF-B1 and IL-6 treatment induced upregulation of H19, downregulated the protein level of E-cadherin while increased Vimentin, indicating an epithelial-mesenchymal transition (EMT) phenotype in GBC. The overexpression of H19 in GBC cells enhanced tumor invasion and promoted EMT by upregulated transcription factor Twist1. On the contrary, Loss of function studies indicated that H19 interference in GBC suppressed tumor cell invasion and promoted mesenchymal-epithelial transition (MET) via suppressing Twist expression. In vivo, the volume of the tumors in H19-inteference group was significantly decreased compared to those in the control group of nude mice. 27073719 2015 Upregulation of H19 indicates a poor prognosis in gallbladder carcinoma and promotes epithelial-mesenchymal transition H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (A549, H1299 and BES-2B) up-regulated H19 was upregulated in A549 and H1299 cells compared to normal lung epithelial BEAS-2B cells. Meanwhile,miR-17 was downregulated in NSCLC cell lines. Overexpression of miR-17 was able to inhibit the progression of NSCLC cells while reversely miR-17 inhibitors reversed this process.In addition, signal transducers and activators of transcription (STAT3),as an mRNA target of miR-17,was presented in our research.Moreover, we discovered that H19 demonstrated its biological functions via regulating miR-17 and STAT3 in vitro.Silencing H19 greatly increased STAT3 expression by sponging miR-19 in vitro.It was hypothesized that H19 may serve as a competing endogenous RNA (ceRNA) to modulate STAT3 by attaching miR-17 in lung cancer. 29693721 2018 H19 promotes non-small-cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR-17. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 non small cell lung cancer C34 M8046/3 qPCR, RNAi, ChIP, Luciferase reporter assay etc. NSCLC cell lines (A549, SPCA1) up-regulated The higher expression of H19 was positively correlated with advanced tumor-node-metastasis (TNM) stage and tumor size. Multivariate analyses found that H19 expression could serve as an independent prognostic factor for overall survival of NSCLC. Moreover, chromatin immunoprecipitation (ChIP) assays revealed that H19 was a direct transcriptional target of c-Myc. And, knockdown of H19 significantly inhibited NSCLC cell proliferation both in vitro and in vivo. 26482621 2015 c-Myc-regulated long non-coding RNA H19 indicates a poor prognosis and affects cell proliferation in non-small-cell lung cancer H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colon cancer C18 NA qPCR, Western blot etc. colorectal cancer tissues, cell lines (HCT-116 and SW-481) up-regulated overexpression of H20 is associated with decreased recurrence-free survival and overall survival rates in patients with colorectal cancer, and increased viability and migration in colon cancer cells. H19 may function as a competing endogenous RNA for miR-138 and miR-200a, antagonizing their functions and thus leading to the derepression of their endogenous targets vimentin, zinc finger E-box-binding homeobox (ZEB) OL-9705-NPS 1 and ZEB2, all of which were associated with the EMT process. 28781681 2017 Overexpression of long non-coding RNA H20 is associated with unfavorable prognosis in patients with colorectal cancer and increased proliferation and migration in colon cancer cells. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 osteosarcoma NA M9180/3 qPCR, Western blot etc. steosarcoma tissues, cell lines(hFOB, MG-63, U2OS and SAOS-2) up-regulated Expression level of H19 was significantly elevated in tumor tissue compared with adjacent healthy tissue. Expression level of H19 was positively associated with distant metastasis of osteosarcoma (P<0.01), but not with gender and age. Overall survival of patients with osteosarcoma with high H19 level was significantly shorter compared with patients with low H19 expression (P<0.05). H19 knockdown significantly reduced migration and invasion ability of osteosarcoma cells. Significantly decreased levels of p-PI3K and p-AKT, and elevated level of IkBa were observed in H19 knockdown osteosarcoma cells compared with control osteosarcoma cells, while no significant differences in levels of PI3K and AKT were observed. 29568924 2018 Downregulation of lncRNA H19 inhibits migration and invasion of human osteosarcoma through the NF-kB pathway. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioblastoma NA M9440/3 qPCR, RNAi, Cell migration and invasion assay etc. glioblastoma tissues, cell lines (U87, U373) up-regulated H19 is significantly overexpressed in glioblastoma tissues. Overexpression of H19 promotes glioblastoma cell invasion and angiogenesis in vitro. Interestingly, H19 was also significantly overexpressed in CD133+ glioblastoma cells, and overexpression of H19 was associated with increased neurosphere formation of glioblastoma cells. Finally, stable overexpression of H19 was associated with increased tumor growth in the murine xenograft model. 28306408 2017 Increased level of H19 long noncoding RNA promotes invasion, angiogenesis, and stemness of glioblastoma cells. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioblastoma NA M9440/3 qPCR, Neurosphere Formation assay etc. glioblastoma tissues, cell lines (U87, U373) up-regulated H19 is significantly overexpressed in glioblastoma tissues, and the level of expression was associated with patient survival. In the subsequent investigations, the authors found that overexpression of H19 promotes glioblastoma cell invasion and angiogenesis in vitro. Interestingly, H19 was also significantly overexpressed in CD133+ glioblastoma cells, and overexpression of H19 was associated with increased neurosphere formation of glioblastoma cells. 26274999 2015 Increased level of H19 long noncoding RNA promotes invasion, angiogenesis, and stemness of glioblastoma cells. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 bladder cancer C67 NA ISH etc. bladder cancer tissues differential expression More than 5% of cells expressed H19 in 47 of the 56 (84%) biopsies. There was a decrease in the number of cells expressing H19 with increasing tumour grade (loss of differentiation). Disease free survival from the first biopsy to first recurrence was significantly shorter in patients with tumours having a larger fraction of H19 expressing cells, controlling for tumour grade. This was also supported by the selective analysis of tumour recurrence in patients with grade I tumours. 11193051 2000 The imprinted H19 gene is a marker of early recurrence in human bladder carcinoma. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA microarray, qPCR, RIP, ChIP etc. cell lines (DLD1, HCT116, HT29 and SW480) differential expression H19 silencing blocked G1-S transition, reduced cell proliferation, and inhibited cell migration. Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. We further demonstrated that reduced CDK8 expression underlies changes of B-catenin activity, and identified that H19 interacts with macroH2A, an essential regulator of CDK8 gene transcription. 27789274 2016 H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-B-Catenin Signaling in Colorectal Cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA qPCR, Western blot, RIP, Flow cytometry assay etc. cell lines (HCT116, HT29, Lovo, SW480, CCD-18Co) up-regulated We observed higher expression of H19 was significantly correlated with tumor differentiation and advanced TNM stage in a cohort of 83 CRC patients. Multivariate analyses revealed that expression of H19 served as an independent predictor for overall survival and disease-free survival. Further experiments revealed that overexpression of H19 promoted the proliferation of CRC cells, while depletion of H19 inhibited cell viability and induced growth arrest. 26989025 2016 Long noncoding RNA H19 indicates a poor prognosis of colorectal cancer and promotes tumor growth by recruiting and binding to eIF4A3 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Among them, AFAP1-AS1, BCAR4, H19, HOXA-AS2, MALAT1 and PVT1 were significantly up-regulated, and ADAMTS9-AS2 was significantly down-regulated in cancer tissue samples. 27596298 2016 Differentially expressed long non-coding RNAs and the prognostic potential in colorectal cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioma NA M9380/3 qPCR, RNAi, Cell proliferation assay etc. glioma tissues, cell lines (U251 and U87) up-regulated LncRNA H19 was overexpressed in glioma tissue and cell lines. In tissue, higher expression levels were observed in more advanced stages of the tumor. Furthermore, lncRNA H19 was negatively associated with patient survival time. In cell culture experiments, silencing of lncRNA H19 diminished proliferation of glioma cell lines. These effects of lncRNA H19 appeared to be intermediated by miR-675. 27981546 2016 LncRNA H19 is overexpressed in glioma tissue, is negatively associated with patient survival, and promotes tumor growth through its derivative miR-675. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc. HCC tissues, cell lines (SMMC7721, HCCLM3) down-regulated In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation. 23222811 2013 Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR etc. cell lines (HCC1937 and HCC38) up-regulated Network analysis revealed the existence of five genes related with H19,including miR-103, miR-107, let-7, miR-29b-1, and Trx. In-vitro analysis showed that suppression of H19 using siRNA reduces sphere formation capacity in both HCC1934 and iCSCL10A cell lines.In clinical studies, H19 expression was associated with hormone negativity, tumor size, and nodal status.Patients with H19 expression had significantly poor disease-free survival (DFS) and overall survival(OS). The effect of H19 expression on prognosis was the most significant in triple-negative breast cancer compared to that in other subtypes. 29693231 2018 LncRNA H19 is associated with poor prognosis in breast cancer patients and promotes cancer stemness. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR etc. breast cancer tissues differential expression Only rs2107425 near H19 was significantly associated with shorter MFS in uni- and multi-variate analysis, with the more aggressive minor allele displaying a recessive trait. 21748294 2012 Correlation of breast cancer susceptibility loci with patient characteristics, metastasis-free survival, and mRNA expression of the nearest genes. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA qPCR, Western blot, Luciferase reporter assay etc. colorectal cancer tissues, cell lines (HCT116, HT-29, SW620 and SW480) up-regulated The proliferative and invasive capacities of CRC cells were appraised through transwell,MTT and scratch assays.As a result, overexpressed H19 and down-expressed miR-29b-3p displayed close associations with the CRC patients' poor prognosis. 29754471 2018 LncRNA H19/miR-29b-3p/PGRN Axis Promoted Epithelial-Mesenchymal Transition of Colorectal Cancer Cells by Acting on Wnt Signaling. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. CRC tissues, cell lines (HCT116, SW480, 293TN) up-regulated H19 expression was upregulated in CRC tissues compared with adjacent noncancerous tissues. H19 overexpression facilitated colon cancer cell proliferation, whereas H19 knockdown inhibited cell proliferation. miR-200a bound to H19 and inhibited its expression, thereby decreasing CRC cell proliferation. H19 promotes cell proliferation by competitively binding to miR-200a and derepressing B-catenin in CRC. 28164117 2017 The lncRNA H19 Promotes Cell Proliferation by Competitively Binding to miR-200a and Derepressing B-Catenin Expression in Colorectal Cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA qPCR, Western blot etc. colorectal cancer tissues, cell lines (HCT-116 and SW-480) up-regulated overexpression of H20 is associated with decreased recurrence free survival and overall survival rates in patients with colorectal cancer,and increased viability and migration in colon cancer cells.H19 may function as a competing endogenous RNA for miR-138 and miR-200a,antagonizing their functions and thus leading to the derepression of their endogenous targets vimentin,zinc finger E-box-binding homeobox (ZEB) OL-9705-NPS 1 and ZEB2,all of which were associated with the EMT process. 28781681 2017 Overexpression of long non-coding RNA H19 is associated with unfavorable prognosis in patients with colorectal cancer and increased proliferation and migration in colon cancer cells. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN46), gastric adenocarcinomas tissues up-regulated lncRNAs H19,MEG3 and MALAT1 showed significant association with tumor stage and HOTAIR had a significant association with patient survival.H19 is a well-known oncogenic lncRNA that is involved in the reduction of p53 activity inducing proliferation in gastric cancer.In the present study,we observed a higher level of H19 which sponged out the low level expressed miR-148a leading to the overexpression of its target mRNA DNMT1.Similarly,we also observed the KLF4 overexpression due to the H19 mediated sponging of miR-148a. 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric cancer C16 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. gastric cancer tissues, cell lines (SGC7901, MKN45, MKN-28 etc.) up-regulated The results showed that overexpression of H19 promoted the features of GC including proliferation, migration, invasion and metastasis. H19 and its associated miR-675 act as oncogenes by promoting cell growth and malignant transformation in human gastric cancer. The upregulation of H19 and miR-675 in GC suggests that both H19 and miR-675 are important factors in GC tumorigenesis and metastasis. Furthermore, we showed that H19 plays additional roles mediated by separate pathways and interaction with its target gene ISM1. 24810858 2014 Overexpression of lncRNA H19 enhances carcinogenesis and metastasis of gastric cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric cancer C16 NA qPCR, RNAi, Western blot, Cell migration and invasion assay etc. gastric cancer tissues, cell lines (SGC7901, BGC823, MGC803, AGS and MKN45) up-regulated H19 expression was remarkably increased in GC tissues and cell lines compared with that in the normal control, and its up-regulation was significantly correlated to invasion depth, advanced TNM stage and regional lymph nodes metastasis in GC. The levels of H19 in gastric juice from gastric patients were significantly higher than those from normal subjects. Furthermore, knockdown of H19 expression by siRNA could inhibit cell migration and invasion in GC cells partly via regulating E-cadherin protein expression. 26774144 2016 H19 serves as a diagnostic biomarker and up-regulation of H19 expression contributes to poor prognosis in patients with gastric cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric cancer C16 NA qPCR, RNAi etc. gastric cancer tissues, cell lines (MGC-803, SGC-7901, GES-1) up-regulated The results show that lncRNA H19 is overexpressed in tumor tissues compared with adjacent normal tissues. An advanced tumor-node-metastasis stage was positively correlated with increased H19 expression, and a high H19 expression was associated with poor OS and can be regarded as an independent predictor of the OS of GC patients. The altered expression of lncRNA H19, which is induced by c-Myc, is involved in the development and progression of GC by regulating cell proliferation. 24671855 2014 c-Myc-induced, long, noncoding H19 affects cell proliferation and predicts a poor prognosis in patients with gastric cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, RNAi, Luciferase reporter assay, ISH etc. breast cancer tissues, cell lines (MDA-MB-231, SK-BR-3 and MCF-7) up-regulated BCSCs express high levels of H19, and ectopic overexpression of H19 significantly promotes breast cancer cell clonogenicity, migration and mammosphere-forming ability. Conversely, silencing of H19 represses these BCSC properties. In concordance, knockdown of H19 markedly inhibits tumor growth and suppresses tumorigenesis in nude mice. Mechanistically, we found that H19 functions as a competing endogenous RNA to sponge miRNA let-7, leading to an increase in expression of a let-7 target, the core pluripotency factor LIN28, which is enriched in BCSC populations and breast patient samples. 28102845 2017 H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, RNAi, Western blot etc. breast cancer tissues, cell lines (MCF-7, MDA-MB-231) up-regulated Quantitation of H19 lncRNA in human breast cancer tissues showed that the level of H19 lncRNA was higher in ER-positive than in ER-negative tumor tissues. These results suggest that H19 is an estrogen-inducible gene and plays a key role in cell survival and in estrogen-induced cell proliferation in MCF-7 cells, H19 expression is ER-dependent and induced by estrogen through the traditional genomic pathway of estrogen-ER interaction with the gene. 25846769 2015 H19 lncRNA mediates 17B-estradiol-induced cell proliferation in MCF-7 breast cancer cells. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 retinoblastoma C69.2 M9510/3 qPCR, Western blot etc. retinoblastoma tissues, cell lines up-regulated he results demonstrated that H19 may serve a critical oncogenic function in the progression of retinoblastoma, as lncRNA H19 levels were markedly increased in retinoblastoma cells and tissues compared with corresponding controls. In addition, patients with retinoblastoma with increased lncRNA H19 expression experienced poorer survival time compared with those with decreased lncRNA H19 levels. 29805578 2018 Long non-coding RNA H19 regulates viability and metastasis, and is upregulated in retinoblastoma H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 hepatocellular carcinoma C16 NA qRT-PCR, Western blot analysis ect. HCC tumor tissues up-regulated H19 as one of the most upregulated long noncoding RNA (lncRNA) in association with Tgfbr2 inactivation in TICs. Tgfbr2 inactivation by Ad-Cre led to a 5-fold increase of H19 expression in TICs. Accordingly, TGF-B treatment reduced H19 expression.low level of H19 mRNA expression in human HCC tissues from patients with the epithelial TGF-B gene signature in association with favorable prognosis. 30014520 2018 A novel TGF-β and H19 signaling axis in tumor-initiating hepatocytes that regulates hepatic carcinogenesis. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 malignant melanoma NA M8720/3 qPCR, Western blot, Flow cytometry, etc. melanoma tissues, cell lines (CHL-1, UACC904, A-375, 1205Lu) up-regulated the high expression of H19 in melanoma tissues was associated with advanced tumor invasion and TNM stage, distal metastasis, lymph node metastasis and shorter overall survival in patients with melanoma. 29950863 2018 lncRNA H19 predicts poor prognosis in patients with melanoma and regulates cell growth, invasion, migration and epithelial-mesenchymal transition in melanoma cells. H19antisense NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated Eight (lincRNA-VLDLR, MEG9, H19 antisense, ncR-uPAR, NEAT1 (family), LUST, UM9-5, and HOTAIR) were significantly down-regulated in HCC tumor compared to non-tumor tissues at a significance level of. 26378581 2015 Exploration of Deregulated Long Non-Coding RNAs in Association with Hepatocarcinogenesis and Survival. HANR NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, Western blot etc. hepatocellular carcinoma tissues, cell lines (Hep3B, Huh-7) up-regulated HANR was demonstrated to be up-regulated in HCC patients and HCC cell lines. Increased HANR expression in HCC predicted short survival of patients. 29055955 2017 LncRNA HANR Promotes Tumorigenesis and Increase of Chemoresistance in Hepatocellular Carcinoma HAR1A NA NA ENSG00000225978 NA NA diffuse glioma NA M8145/3 qPCR breast and ovarian cancer cell lines, glioma tissue down-regulated These results implied that these four lncRNAs might play important role in diffuse gliomas progression, particularly, PVT1 and HAR1A could be explored as promising biomarkers for diagnosis, prognosis and target therapy of diffuse gliomas.Kaplan-Meier survival curve and Cox regression analyses showed that glioma patients with high PVT1 expression or low HAR1A expression had poor survival outcome, aberrantly expressed PVT1 and HAR1A could be the independent prognosis biomarkers for glioma patients. LncRNA CYTOR was up-regulated in HCC tissues, circulating CYTOR were also highly expressed in plasma samples of HCC patients, and could serve as potential biomarker for diagnosis of HHC. 29108264 2017 lncRNAs PVT1 and HAR1A are prognosis biomarkers and indicate therapy outcome for diffuse glioma patients. HCAL NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay, RIP hepatocellular carcinoma tissues, cell lines (LO2, HepG2, PLC/PRF/5, SK-Hep-1, Huh-7, and SMMC-7721) up-regulated HCAL that was highly expressed in HCC tissues.HCAL upregulation was clinically associated with poor differentiation, intravascular cancer embolus,and decreased survival of patients with HCC.HCAL silencing significantly inhibited the growth and metastasis of HCC cells both in vitro and in vivo.HCAL directly interacted with and functioned as a sponge for microRNAs such as miR-15a, miR-196a, and miR-196b to modulate LAPTM4B expression.the presence of a novel lncRNA-miRNA-mRNA regulatory network, the HCAL-miR-15a/miR-196a/miR-196b-LAPTM4B network,in HCC and indicate that HCAL may be a potential target for treating HCC. 29246322 2017 Long Noncoding RNA HCAL Facilitates the Growth and Metastasis of Hepatocellular Carcinoma by Acting as a ceRNA of LAPTM4B. HCP5 NA 10866 ENSG00000206337 NR_040662 GRCh38_6:31400702-31477506 follicular thyroid carcinoma C73 M8330/3 RNA-seq, qPCR, RNAi etc. cell lines (FTC-133, FTC-238, Nthy-ori 3-1, HEK293T, HUVECs), FTC tissues up-regulated Overexpression of HCP5 can promote the proliferation,migration,invasiveness and angiogenic ability of FTC cells.HCP5 and alpha-2,6-sialyltransferase 2 (ST6GAL2) were co-expressed in FTC.We hypothesised that ST6GAL2 may be regulated by HCP5, which would in turn mediate the activity of FTC cells.HCP5 functions as a competing endogenous RNA (ceRNA) and acts as a sponge for miR-22-3p, miR-186-5p and miR-216a-5p, which activates ST6GAL2. 29515098 2018 LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge. HIF1A-AS2 HIF1A-AS2, 3'aHIF-1A, aHIF 100750247 ENSG00000258667 NR_045406 GRCh38_14:61715558-61751097 colorectal cancer C19.9 NA qRT-PCR, Western blot, Luciferase reporter assay, RIP human CRC tissues, Human CRC cell lines (SW620, DLD-1, HT-29, HCT116) up-regulated immunofluorescence, all those assays reflected a fact that as a ceRNA, HIF1A-AS2 could directly bind with miR-129-5p, and could positively affect cell proliferation, invasion and EMT formation by regulation of the expression of miR-129-5p and DNMT3A. 29278853 2017 LncRNA HIF1A-AS2 positively affects the progression and EMT formation of colorectal cancer through regulating miR-129-5p and DNMT3A. HIF1A-AS2 HIF1A-AS2, 3'aHIF-1A, aHIF 100750247 ENSG00000258667 NR_045406 GRCh38_14:61715558-61751097 glioblastoma NA M9440/3 RIP, RNA pull-down assay etc. glioblastoma tissues, cell lines (G2, G6, G33, G34, G35, G44, G62, G88, G146, G157, G91) up-regulated We identified hypoxia-inducible factor 1 alpha-antisense RNA 2 (HIF1A-AS2) as a subtype-specific hypoxia-inducible lncRNA, upregulated in mesenchymal GSCs. Its deregulation affects GSC growth, self-renewal, and hypoxia-dependent molecular reprogramming. Downregulation of HIF1A-AS2 led to delayed growth of mesenchymal GSC tumors, survival benefits, and impaired expression of HMGA1 in vivo. 27264189 2016 The Long Non-coding RNA HIF1A-AS2 Facilitates the Maintenance of Mesenchymal Glioblastoma Stem-like Cells in Hypoxic Niches. HIF1A-AS2 HIF1A-AS2, 3'aHIF-1A, aHIF 100750247 ENSG00000258667 NR_045406 GRCh38_14:61715558-61751097 breast cancer C50 NA qPCR, Immunohistochemistry etc. primary invasive breast cancer tissues up-regulated We found a strong positive association between HIF-1alpha and sHIF-1alpha, sHIF-1alpha and aHIF, and an inverse correlation between HIF-1alpha /sHIF-1alpha and aHIF. aHIF transcript expression was associated with poor disease-free survival in univariate and multivariate analyses in this series of high-risk primary breast carcinomas. 14580258 2003 aHIF but not HIF-1alpha transcript is a poor prognostic marker in human breast cancer. HIF2PUT EPAS1, ECYT4, HIF2A, HLF, MOP2, PASD2, bHLHe73 2034 ENSG00000116016 NA GRCh38_2:46293667-46386703 osteosarcoma NA M9180/3 qPCR etc. osteosarcoma tissues up-regulated Compared with non-cancerous bone tissues, HIF-2a mRNA and HIF2PUT expression were both significantly upregulated in osteosarcoma tissues. Interestingly, the expression levels of HIF-2a mRNA in osteosarcoma tissues were positively correlated with those of HIF2PUT. Additionally, osteosarcoma patients with HIF-2a mRNA and/or HIF2PUT over-expression more frequently had large tumor size, advanced clinical stage and positive distant metastasis. Moreover, osteosarcoma patients with HIF-2a mRNA and/or HIF2PUT over-expression had a significantly shorter overall and disease-free survival. 27623205 2016 Combined over-expression of the hypoxia-inducible factor 2a gene and its long non-coding RNA predicts unfavorable prognosis of patients with osteosarcoma. HMlincRNA717 HMlincRNA717, GACAT2, MTCL1-AS1, MTCL1AS1 100287082 ENSG00000265962 NR_120598 GRCh38_18:8695856-8707621 pancreatic cancer C25 NA qPCR etc. prostate cancer tissues down-regulated The expression of HMlincRNA717 was significantly decreased in pancreatic cancer tissues compared with paired adjacent normal tissues. It was also proved that HMlincRNA717 expression was to be associated with clinical stage, tumor size, lymph node metastasis, and distant metastasis in pancreatic cancer patients. 27338046 2016 Association of LncRNA HMlincRNA717 with prognosis in pancreatic cancer. HMlincRNA717 HMlincRNA717, GACAT2, MTCL1-AS1, MTCL1AS1 100287082 ENSG00000265962 NR_120598 GRCh38_18:8695856-8707621 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues, cell lines (A549, H157, HEK-293T) down-regulated lncRNA HMlincRNA717 expression level was significantly decreased in NSCLC tissues in comparison to adjacent non-tumor tissues. It was also proved that HMlincRNA717 expression was to be associated with NSCLC histological grade, and lymph node metastasis. In addition, survival analysis proved that down-regulated HMlincRNA717 expression was associated with poor overall survival of NSCLC patients. HMlincRNA717 expression was an independent prognostic factor for patients with NSCLC, which might be a potential prognostic biomarker and therapeutic target for NSCLC. 25674259 2015 LncRNA HMlincRNA717 is down-regulated in non-small cell lung cancer and associated with poor prognosis. HMMR-AS1 NA 101927813 ENSG00000251018 NR_109892 GRCh38_5:163483065-163494058 glioblastoma NA M9440/3 qPCR, Western blot etc. cell lines (U87, U251, A172, and U118) up-regulated We identify that an HMMR antisense lncRNA, HMMR-AS1, is hyperexpressed in GBM cell lines and stabilizes HMMR mRNA. Knockdown of HMMR-AS1 reduces HMMR expression; inhibits cell migration, invasion, and mesenchymal phenotypes; and suppresses GBM cell growth both in vitro and in vivo. Moreover, knockdown of HMMR-AS1 radiosensitizes GBM by reducing DNA repair proteins ATM, RAD51, and BMI1. Our data demonstrate a mechanism of sense-antisense interference between HMMR and HMMR-AS1 in GBM and suggest that targeting HMMR-AS1 is a potential strategy for GBM treatment. 29574252 2018 Targeting Long Noncoding RNA HMMR-AS1 Suppresses and Radiosensitizes Glioblastoma. HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 283460 ENSG00000241388 NR_024345 GRCh38_12:120941728-120980965 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated The level of HNF1A-AS was higher in tumor tissues than that in normal tissues. In addition, HNF1A-AS level was significantly associated with TNM stage and Lymph node metastasis. 27981551 2016 Long non-coding RNA HNF1A-AS1 up-regulation in non-small cell lung cancer correlates to poor survival. HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 283460 ENSG00000241388 NR_024345 GRCh38_12:120941728-120980965 colon cancer C18 NA qPCR, Luciferase reporter assay, RIP colon cancer tissues, cell lines (SW480, CaCO2, RKO, HCT8, HCT116, SW620, FHC) up-regulated HNF1A-AS1 was frequently upregulated in colon cancer tissues and associated with poor prognosis.Upregulated HNF1A-AS1 promoted colon cancer cell viability, migration and invasion both in vitro and in vivo.HNF1A-AS1 silencing impaired tumor growth and metastasis.HNF1A-AS1 functioned as an oncogene in metastasis of colon cancer in part through serving as a competing endogenous RNA to modulate miRNA-34a expression, subsequently with repression of miR-34a/SIRT1/p53 feedback loop and activation of canonical Wnt signaling pathway. 28943452 2017 Long non-coding RNA HNF1A-AS1 mediated repression of miR-34a/SIRT1/p53 feedback loop promotes the metastatic progression of colon cancer by functioning as a competing endogenous RNA. HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 283460 ENSG00000241388 NR_024345 GRCh38_12:120941728-120980965 osteosarcoma NA M9180/3 qPCR, RNAi, Western blot, MTT assay etc. osteosarcoma tissues, cell lines (HOS, SaOS2, MG63 and U2OS) up-regulated We found that HNF1A-AS1 was markedly up-regulated in OS tissues compared to their adjacent non-tumor tissues. HNF1A-AS1 expression levels were positively associated with the clinical stage, distant metastasis, and reduced overall survival of OS patients. In addition, knockdown HNF1A-AS1 expression inhibited cell proliferation, metastasis and influences the activity of the Wnt/B-catenin pathway in OS cells. 27648140 2016 Upregulation of lncRNA HNF1A-AS1 promotes cell proliferation and metastasis in osteosarcoma through activation of the Wnt/B-catenin signaling pathway. HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 283460 ENSG00000241388 NR_024345 GRCh38_12:120941728-120980965 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot, RIP etc. lung adenocarcinoma tissues, cell lines (A549, SPC-A1, H1650) up-regulated HNF1A-AS1 was significantly up-regulated in lung adenocarcinoma tissues compared with corresponding non-tumor tissues, and its expression level was significantly correlated with TNM stage, tumor size, and lymph node metastasis. Moreover, HNF1A-AS1 was determined to promote tumor proliferation and metastasis, both in vitro and in vivo, by regulating cyclin D1, E-cadherin, N-cadherin and B-catenin expression. In addition, the binding of HNF1A-AS1 to DNMT1 may explain its regulation of E-cadherin. 25863539 2015 The long non-coding RNA HNF1A-AS1 regulates proliferation and metastasis in lung adenocarcinoma. HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 283460 ENSG00000241388 NR_024345 GRCh38_12:120941728-120980965 bladder cancer C67 NA qPCR etc. bladder cancer tissues up-regulated UCB tissues showed higher HNF1A-AS1 levels than the corresponding normal tissues controls (p < 0.01). Statistical assay revealed that high HNF1A-AS1 expression was significantly correlated with histological grade (p = 0.008), tumor stage T (p = 0.003) and lymph nodes metastasis (p = 0.007). In addition, the overall survival time of patients with high HNF1A-AS1 expression was significantly shorter compared to those with low HNF1A-AS1 expression. Furthermore, multivariate analysis confirmed that relative HNF1A-AS1 expression was an independent predictor of overall survival in patients with UCB.HNF1A-AS1 expression was upregulated in UCB, and it may be a useful prognostic biomarker for patients with UCB. 29762827 2018 Upregulation of long non-coding RNA HNF1A-AS1 is associated with poor prognosis in urothelial carcinoma of the bladder HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 283460 ENSG00000241388 NR_024345 GRCh38_12:120941728-120980965 colorectal cancer C19.9 NA qPCR, Western blot, RNAi colorectal cancer tissues, cell lines (LoVo, SW620, HCT-116,SW480, HcoEpiC) up-regulated e expression of lncRNA HNF1A-AS1 was significantly upregulated in both CRC tumor tissues and CRC cell lines. lncRNA HNF1A-AS1 might be an independent prognostic factor for disease-free survival (DFS) and overall survival (OS) in patients with CRC. In addition, silencing of lncRNA HNF1A-AS1 abrogated the proliferation of CRC cells by MTS assay and clonogenic assay, arrested cell cycle at G0/G1 stage and reduced the migration and invasion in CRC cells. decreased expression of lncRNA HNF1A-AS1 suppressed the Wnt/B-catenin signaling pathway activity by downregulating the expression of B-catenin,cyclinD1, and c-myc. 29145164 2017 Long noncoding RNA HNF1A-AS1 indicates a poor prognosis of colorectal cancer and promotes carcinogenesis via activation of the Wnt/B-catenin signaling pathway. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 acute monocytic leukemia NA M9891/3 qPCR etc. bone marrow up-regulated Expression of HOTAIR in patients with acute monocytic leukemia (M5) was increased as compared to controls. In addition, the expression of downstream genes in the HOTAIR signaling pathway including EZH2, LSD1, DNMT3A and DNMT3B was significantly increased in AL patients, and showed a significant positive correlation with high expression of HOTAIR. 27748863 2016 Role of HOTAIR in the diagnosis and prognosis of acute leukemia. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 B-cell lymphoma NA M9591/3 qPCR, Western blot etc. cell lines (RCK-8, OCL-LY-10, OCL-LY-7, SU-DHL-6 and SU-DHL-4 DLBCL) up-regulated It was first found that the expression levels of HOTAIR were upregulated in DLBCL tumor tissues and cell lines, compared with normal tissues and cells. In addition, HOTAIR was significantly correlated with tumor size, clinical stage, B symptoms and International Prognostic Index scores; and higher expression levels of HOTAIR were correlated with improved prognosis. Univariate and multivariate analyses verified that HOTAIR was a key independent predictive factor for DLBCL prognosis. Furthermore, it was revealed that the knockdown of the expression of HOTAIR led to growth inhibition, cell cycle arrest and apoptosis in vitro, possibly through the phosphoinositide 3-kinase/AKT/nuclear factor-kB pathway 27122348 2016 Elevated RNA expression of long non-coding HOTAIR promotes cell proliferation and predicts a poor prognosis in patients with diffuse large B cell lymphoma HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 diffuse Large B-Cell Lymphoma NA M9680/3 qPCR Lymphoma tissues differential expression HOTAIR expression could be one of possible mechanisms for inducing H3K27me3 via EZH2-related PRC2 activation, and induced H3K27me3 may be strongly related to aggressive DLBCLs which show poor patient outcome. In Relation to Polycomb Repressive Complex Pathway Proteins and H3K27 Trimethylation 27550047 2016 Long Non-coding RNA HOTAIR Expression in Diffuse Large B-Cell Lymphoma: In Relation to Polycomb Repressive Complex Pathway Proteins and H3K27 Trimethylation HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 serous ovarian cancer C56.9 M8441/3 qPCR, RNAi etc. cell lines (A2780, Hey, SKOV3, OVCA429, OVCA433, OVCAR3) up-regulated We found that HOTAIR levels were overexpressed in SOC tissues compared with normal controls and that HOTAIR overexpression was correlated with an advanced FIGO stage and a high histological grade. HOTAIR knockdown resulted in the induction of cell cycle arrest and apoptosis through certain cell cycle-related and apoptosis-related proteins. 25796453 2015 The long non-coding RNA HOTAIR promotes the proliferation of serous ovarian cancer cells through the regulation of cell cycle arrest and apoptosis. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 esophageal cancer C15 NA qPCR, Western blot, Luciferase Reporter Assays esophageal cancer tissues, cell lines (KYSE30, KYSE150, TE-1, Eca-1, Eca-109) up-regulated High lncRNA-HOTAIR expression was associated with significantly poorer overall survival in EC. Mechanistic investigations revealed lncRNA-HOTAIR promotes the EMT by acting as a miR-148a sponge to positively regulate Snail2 expression 28441714 2017 Long non-coding RNA HOTAIR functions as miRNA sponge to promote the epithelial to mesenchymal transition in esophageal cancer HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 malignant melanoma NA M8720/3 qPCR, Western blot, RIP, RNA pull-down assay etc. malignant melanoma tissues, cell lines (A375 and A875) down-regulated HOTAIR is overexpressed in melanoma tissues and cells, especially in metastatic melanoma. High HOTAIR levels correlate with poor prognosis in melanoma patients. We also determined that HOTAIR functions as a competing endogenous RNA (ceRNA) for miR-152-3p. miR-152-3p was decreased and acted as a tumor suppressor in melanoma, and c-MET was the functional target of miR-152-3p. Furthermore, HOTAIR promotes the growth and metastasis of melanoma cells by competitively binding miR-152-3p, which functionally liberates c-MET mRNA and results in the activation of the downstream PI3k/Akt/mTOR signaling pathway. We determined that HOTAIR acts as a ceRNA to promote malignant melanoma progression by sponging miR-152-3p. 29156728 2017 Long non-coding RNA HOTAIR acts as a competing endogenous RNA to promote malignant melanoma progression by sponging miR-152-3p. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastrointestinal stromal tumor C16 M8936/0 qPCR etc. gastric cancer tissues up-regulated In this study, we identified frequent upregulation of miR-196a and lincRNA HOTAIR in high-risk gastrointestinal stromal tumors (GIST). In like manner, overexpression of HOTAIR was also strongly associated with high-risk grade and metastasis among GIST specimens. RNA interference-mediated knockdown of HOTAIR altered the expression of reported HOTAIR target genes and suppressed GIST cell invasiveness. 22258453 2012 Upregulation of miR-196a and HOTAIR drive malignant character in gastrointestinal stromal tumors. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric adenocarcinoma C16 M8140/3 qPCR etc. gastric cancer tissues up-regulated HOTAIR was significantly upregulated in GA tissues, especially in more advanced cases. High HOTAIR expression was an independent poor prognostic factor for patients with advanced GA. Further stratification analyses revealed that the association between HOTAIR expression and survival in patients with advanced GA remained significant in the subgroup of patients with TNM stages IIIA and IIIB, poorly differentiated, and smaller tumors. 26328013 2015 HOTAIR is a predictive and prognostic biomarker for patients with advanced gastric adenocarcinoma receiving fluorouracil and platinum combination chemotherapy. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 urothelial cancer NA M8120/3 microarray, qPCR, Western blot, ChIP etc. urothelial cancer tissues, cell lines (VM-CUB1 and 5637) up-regulated HOTAIR was overexpressed in approximately half of UC tissues and cell lines. Effects of HOTAIR overexpression differed between cell lines. Whereas VM-CUB1 cells acquired the expected phenotype with increased proliferation, clonogenicity, anchorage independent growth, migratory activity and epithelial-to-mesenchymal transition, 5637 cells grew more slowly displaying induction of senescence and related immune response genes. 25994132 2015 The long noncoding RNA HOTAIR has tissue and cell type-dependent effects on HOX gene expression and phenotype of urothelial cancer cells. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 acute myeloid leukemia NA M9861/3 qPCR, RNAi, Western blot, RIP etc. cell lines up-regulated We report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Clinically, AML patients with higher HOTAIR predicted worse clinical outcome compared with those with lower HOTAIR. Importantly, HOTAIR knockdown by small hairpin RNA inhibited cell growth, induced apoptosis, and decreased number of colony formation. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. 25979172 2015 Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 nasopharyngeal cancer C11 NA qPCR, ISH etc. primary NPC tissues up-regulated Quantified using qPCR, HOTAIR expression levels in fresh tissue and paraffin-embedded samples were 5.2 ~ 48.4-fold higher compared with non-cancer tissue samples. Moreover, HOTAIR expression levels increased with clinical stage progression, which was consistent with ISH findings in the paraffin-embedded tissue. Most importantly, NPC patients with higher HOTAIR levels had a poor prognosis for overall survival using univariate and multivariate analysis. In addition, HOTAIR mediated the migration, invasion and proliferation of NPC cells in vitro. 23281836 2013 Long non-coding RNA HOTAIR is an independent prognostic marker for nasopharyngeal carcinoma progression and survival. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 oral squamous cell carcinoma C06.9 M8070/3 qPCR, RNAi, MTT assay etc. cell line (Tca8113) up-regulated The expression level in tumor tissues was significantly higher than that in paracancerous tissues. Relative expression level of HOTAIR was correlated with tumor size and clinical stage. More HOTAIR was expressed in OSCC cell lines than in normal oral epithelial cells. Interfering with HOTAIR expression in Tca8113 cells significantly decelerated cell growth, arrested cell cycle, and promoted apoptosis. HOTAIR was highly expressed in OSCC tissues and facilitated the growth of OSCC cells, thus probably being an eligible molecular marker for OSCC diagnosis and prognosis determination. 26036760 2015 Expression of long noncoding RNA-HOX transcript antisense intergenic RNA in oral squamous cell carcinoma and effect on cell growth. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 endometrial cancer NA M8380/3 qPCR etc. endometrial carcinoma tissues up-regulated Our results revealed that HOTAIR expression in the EC tissues was significantly upregulated compared with normal tissues. In addition, we observed a significant association between HOTAIR expression and the EC grade and lymph node metastasis. Moreover, we found that a higher HOTAIR expression also correlated with the depth of myometrial invasion and lymphovascular space invasion. More importantly, patients with a higher HOTAIR expression showed significantly poorer overall survival than those with lower HOTAIR expression. 24285342 2014 The long non-coding RNA HOTAIR is upregulated in endometrial carcinoma and correlates with poor prognosis. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 laryngeal squamous cell cancer C32.3 NA qPCR, in vitro knockdown etc. cell line (Hep-2) up-regulated HOTAIR levels were significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues, and patients with poor histological grade or advanced clinical stage had higher HOTAIR expression. PTEN methylation was significantly reduced in Hep-2 cells depleted of HOTAIR. Taken together, these results suggest that the oncogenic role of HOTAIR in LSCC is related to promotion of PTEN methylation. 23141928 2013 Long intergenic noncoding RNA HOTAIR is overexpressed and regulates PTEN methylation in laryngeal squamous cell carcinoma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colon cancer C18 NA qPCR etc. colon cancer tissues up-regulated The expression of HOTAIR was significantly higher in colon cancer tissues than in matched tumor-adjacent normal colon tissues. HOTAIR expression was significantly higher in cases with lymph node metastasis than in those without metastasis; in lowly differentiated and undifferentiated cases than in highly and moderately differentiated cases; and in stages III + IV cases than in stagesI+ II cases. 27298568 2016 Clinical significance of HOTAIR expression in colon cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 prostate cancer C61.9 NA qPCR, RNAi, Western blot, Flow cytometry assay etc. cell line (DU145) up-regulated RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis. 26962687 2016 MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 osteosarcoma NA M9180/3 qPCR, Western blot, RNAi osteosarcoma tissue, cell line (MG63) up-regulated the expression of HOTAIR was significantly upregulated in OS tissues compared to matched adjacent normal tissues.suppression of HOTAIR in MG-63 OS cells significantly reduced migration and invasion. The silencing of HOTAIR also significantly decreased the expression of matrix metalloproteinase (MMP) 2 and MMP9, but increased E-cadherin expression through regulating the RAC a serine/threonine protein kinase-mammalian target of rapamycin signaling pathway.HOTAIR promotes OS cell growth through activation of the AKT/mTOR signaling pathway. 29285059 2017 Long noncoding RNA HOTAIR promotes the proliferation and metastasis of osteosarcoma cells through the AKT/mTOR signaling pathway. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 bladder cancer C67 NA qPCR, Western blot etc. bladder cancer tissues up-regulated Our findings indicate that HOTAIR expression has prognostic value for bladder cancer progression, recurrence, and survival and suggest that HOTAIR plays active roles in modulating the cancer epigenome, becoming an interesting candidate as a target for cancer diagnosis and therapy. The observed HOTAIR regulation by EZH2 and the possibility of modulating EZH2 activity with specific inhibitors open new possible paths to be explored in bladder cancer therapy 26457124 2015 Analysis of the Polycomb-related lncRNAs HOTAIR and ANRIL in bladder cancer HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 osteosarcoma NA M9180/3 qPCR, Transwell assay etc. Osteosarcoma tissues, cell lines (U2OS, MNNG/HOS, 143B, MG63 etc.) up-regulated HOTAIR was commonly overexpressed in osteosarcoma, which significantly correlated with advanced tumor stage, highly histological grade and poor prognosis. In vitro and in vivo experiments demonstrated that knockdown of HOTAIR could notably suppress cellular proliferation, inhibit invasion and decrease the secretion of MMP2 and MMP9 in osteosarcoma 25728753 2015 Overexpression of Long Non-Coding RNA HOTAIR Promotes Tumor Growth and Metastasis in Human Osteosarcoma HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 pancreatic cancer C25 NA qPCR, RNAi, Luciferase reporter assay, in vitro knockdown etc. cell lines (Panc1, MiaPaCa2, Panc28, L3.6pl) up-regulated We show that HOTAIR expression is increased in pancreatic tumors compared with non-tumor tissue and is associated with more aggressive tumors. Knockdown of HOTAIR (siHOTAIR) by RNA interference shows that HOTAIR has an important role in pancreatic cancer cell invasion, as reported in other cancer cell lines. HOTAIR knockdown in Panc1 and L3.6pL pancreatic cancer cells that overexpress this lincRNA decreased cell proliferation, altered cell cycle progression and induced apoptosis, demonstrating an expanded function of HOTAIR in pancreatic cancer cells compared with other cancer cell lines. HOTAIR uniquely suppressed several interferon-related genes and gene sets related to cell cycle progression in pancreatic cancer cells and tumors. 22614017 2013 HOTAIR is a negative prognostic factor and exhibits pro-oncogenic activity in pancreatic cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 head and neck squamous cell carcinoma C76.0 M8070/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell migration and invasion assay etc. HNSC tissues, cell lines (SCC25, HN4, Cal27, SCC4, HN30, HN12, HN13 and FaDu) up-regulated Knockdown of HOTAIR and HuR decreased cell viability, cellular migration and invasion. Moreover, HuR interacted and stabilized HOTAIR stability and thus promoted HOTAIR expression. Notably, HOTAIR acted as a miRNA sponge for HuR. HuR also reinforced HOTAIR sponge activity through miRNA recruitment, thus enhancing HuR expression in turn. Finally, HuR and HOTAIR levels were positively correlated and significantly up-regulated in tumours samples. 27941336 2016 A Feed-Forward Regulatory Loop between HuR and the Long Noncoding RNA HOTAIR Promotes Head and Neck Squamous Cell Carcinoma Progression and Metastasis. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 lung adenocarcinoma C34 M8140/3 qPCR, RNAi etc. NSCLC tissues, cell lines (A549, PC9, H1299, H520, HBE) up-regulated HOTAIR regulates the ratio of FOXA1 to FOXA2 and migration and invasion. HOTAIR and the ratio of FOXA1 to FOXA2 are negatively correlated. HOTAIR knockdown inhibits migration and invasion. HOTAIR is associated with LSH, and this association linked with the binding of LSH in the promoter of FOXA1, not FOXA2. Targeted inhibition of HOTAIR suppresses the migratory and invasive properties 26658322 2015 The ratio of FoxA1 to FoxA2 in lung adenocarcinoma is regulated by LncRNA HOTAIR and chromatin remodeling factor LSH HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 oral squamous cell carcinoma C06.9 M8070/3 qPCR, RNAi, Western blot etc. OSCC tissues, cell lines (TSCCA, Tca8223 etc.) up-regulated In this study, we show that HOTAIR expression increased in oral squamous cell carcinoma (OSCC) compared with non-tumor tissue and is associated with metastasis, the stage and histological differentiation. Furthermore, significant negative correlation between HOTAIR levels and E-cadherin levels was found in OSCC tissues and cell lines, and HOTAIR contributed to the regulation of E cadherin through binding to EZH2 and H3K27me3 with the E-cadherin promoter. 25901533 2015 Long non-coding RNA HOTAIR promotes tumor cell invasion and metastasis by recruiting EZH2 and repressing E-cadherin in oral squamous cell carcinoma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 esophageal squamous cell cancer NA NA qPCR, ISH etc. ESCC tissues up-regulated High expression levels of HOTAIR in ESCC patients correlated positively with clinical stage, TNM classification, histological differentiation and vital status. HOTAIR expression was found to be an independent prognostic factor in ESCC patients. ESCC patients who expressed high levels of HOTAIR had substantially lower overall 5-year survival rates than HOTAIR-negative patients. In vitro assays of ESCC cell lines demonstrated that HOTAIR mediated the proliferation, colony formation and migratory capacity of ESCC cells. 23717443 2013 Long noncoding RNA HOTAIR is a prognostic marker for esophageal squamous cell carcinoma progression and survival. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colon cancer C18 NA qPCR, RNAi, Western blot, Flow cytometry assay etc. colon cancer tissues, cell line (HCT116) up-regulated In 80 clinical colon cancer tissues, HOTAIR and miR-125a-5p levels were higher than adjacent tissues, whereas caspase 2 was lower. RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis. 26962687 2016 MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioma NA M9380/3 qPCR etc. glioma tissues up-regulated In contrast, glioma subjects with the rs12826786 CT genotype had significantly higher tumor HOTAIR RNA levels than those with the TT genotype 28083786 2017 Effects of the functional HOTAIR rs920778 and rs12826786 genetic variants in glioma susceptibility and patient prognosis. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 renal cell carcinoma C64.9 NA qPCR, RNAi, Western blot, Cell migration and invasion assay etc. RCC tissues, cell lines (786-O and ACHN) up-regulated HOTAIR expression was elevated in tissues of renal cell carcinoma compared to adjacent normal tissues, and positively correlated with metastasis. The cell migration was inhibited in scratch test and transwell assay after HOTAIR knockdown. Further researches revealed that histone demethylase JMJD3 was reduced and its target gene Snai1 expression was down-regulated after HOTAIR suppression. 28177890 2017 Long noncoding RNA HOTAIR promotes metastasis of renal cell carcinoma by up-regulating histone H3K27 demethylase JMJD3. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 renal cell carcinoma C64.9 NA Microarray, qPCR, Western blot, RNAi etc. normal renal tissues, renal cell carcinoma cell lines (ACHN, A498, Caki-1) up-regulated IGFBP2 and HOTAIR were co-expressed in clinical RCC samples. Our findings suggest that the HOTAIR-IGFBP2 axis plays critical roles in RCC metastasis and may serve as a novel therapeutic target for advanced RCC.Next, we analyzed the relationship between HOTAIR expression and patient prognosis using the Kaplan-Meier method. HOTAIR expression was significantly associated with a shorter survival in RCC patients 28931862 2017 Long non-coding RNA HOTAIR promotes cell migration by upregulating insulin growth factor-binding protein 2 in renal cell carcinoma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colon cancer C18 NA qPCR, RNAi, Western blot etc. colon cancer tissues, cell lines (SW480, HT29) up-regulated Increased HOTAIR expression was significantly correlated with the depth of tumor invasion, lymph node metastasis, organ metastasis, histological differentiation, vascular invasion and advanced tumor stage. Depletion of HOTAIR increased the expression of E-cadherin while concomitantly decreasing expression of vimentin and MMP9. Hence, HOTAIR may be another pleiotropic modulator participating in epithelial-mesenchymal transition (EMT). 24840737 2014 Long non-coding RNA HOTAIR is a powerful predictor of metastasis and poor prognosis and is associated with epithelial-mesenchymal transition in colon cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioma NA M9380/3 microarray, Western blot etc. glioblastoma tissues up-regulated HOTAIR expression was significantly higher in HGG than in low-grade glioma. Moreover, as shown in Fig. 1A, GBM demonstrated a significant increase in HOTAIR transcript levels, compared with that observed in normal tissues, LGGs, or AGs. Our data establish that HOTAIR serves as a prognostic factor for glioma patient survival, as well as a biomarker for identifying glioma molecular subtypes, a critical regulator of cell cycle progression. 24203894 2013 HOTAIR, a cell cycle-associated long noncoding RNA and a strong predictor of survival, is preferentially expressed in classical and mesenchymal glioma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. cell line (A549) up-regulated RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis. 26962687 2016 MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated The lncRNAs HOTAIR, H19 and MALAT1 were up-regulated, while PANDAR and TUG1 were down-regulated in NSCLC cancer tissues compared with the corresponding adjacent normal tissue. 28121347 2017 The use of lncRNA analysis for stratification management of prognostic risk in patients with NSCLC. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colorectal cancer C19.9 NA qPCR, RNAi etc. CRC tissues, (HEK293T, HCT116, SW480) up-regulated HOTAIR expression levels were higher in cancerous tissues than in corresponding noncancerous tissues and high HOTAIR expression correlated tightly with the presence of liver metastasis. Our findings suggest that HOTAIR expression is associated with a genome-wide reprogramming of PRC2 function not only in breast cancer but also in CRC, where upregulation of this long ncRNA may be a critical element in metastatic progression. 21862635 2011 Long noncoding RNA HOTAIR regulates polycomb-dependent chromatin modification and is associated with poor prognosis in colorectal cancers. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 pancreatic cancer C25 NA qPCR, Western blot, Luciferase reporter assay pancreatic cancer tissues, cell lines (BXPC3, CFPAC-1, Panc-1 and L3.6pl) up-regulated The long non-coding RNA, HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines, and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA. 28415631 2017 LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 bladder cancer C67 NA qPCR, Western blot etc. bladder cancer tissues, cell lines (T24, J82, BIU-87 etc.) up-regulated Ninety out of 110 specimens were detected in HOTAIR high expression. Histological grade and expression levels of HOTAIR were positively correlated with the recurrence rate. HOTAIR expression was an independent predictor of recurrence rate in multivariate Cox regression analysis. HOTAIR expression is correlated with patients' poor prognosis. 25030736 2014 Upregulation of the long noncoding RNA HOTAIR predicts recurrence in stage Ta/T1 bladder cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. cell line (HepG2) up-regulated RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis. 26962687 2016 MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated Eight (lincRNA-VLDLR, MEG9, H19 antisense, ncR-uPAR, NEAT1 (family), LUST, UM9-5, and HOTAIR) were significantly down-regulated in HCC tumor compared to non-tumor tissues at a significance level of. 26378581 2015 Exploration of Deregulated Long Non-Coding RNAs in Association with Hepatocarcinogenesis and Survival. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, in vitro knockdown etc. cell line (Bel7402) up-regulated The HOTAIR gene was significantly overexpressed in HCC tissues compared with adjacent non-tumour tissues. Patients with high HOTAIR gene expression in their tumours had an increased risk of recurrence after hepatectomy. There was also a significant correlation between HOTAIR expression and lymph node metastasis. HOTAIR lincRNA might be a potential biomarker for the existence of lymph node metastasis in HCC. 22289527 2011 Large intervening non-coding RNA HOTAIR is associated with hepatocellular carcinoma progression. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 esophageal squamous cell cancer NA NA qPCR, RNAi, in vitro knockdown etc. ESCC tissues, cell lines (TE1, TE3, TE7, TE8, KYSE30, KYSE180 etc.) up-regulated HOTAIR is upregulated in ESCC cell lines and patient samples, and promotes ESCC cell proliferation and tumour metastasis in mice. The knockdown of HOTAIR resulted in significant changes in gene expression, and data analysis suggested that HOTAIR-mediated gene regulation has a critical role in ESCC progression and is a novel epigenetic molecular target for treating ESCC patients. 24022190 2013 Long non-coding RNA HOTAIR, a driver of malignancy, predicts negative prognosis and exhibits oncogenic activity in oesophageal squamous cell carcinoma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 esophageal squamous cell cancer NA NA microarray, qPCR, RNAi, Western blot etc. ESCC tissues, cell lines (KYSE30, KYSE140, KYSE180, KYSE410, KYSE510) up-regulated It was found that there was a great upregulation of HOTAIR in ESCC compared to their adjacent normal esophageal tissues. Meanwhile, patients with high HOTAIR expression have a significantly poorer prognosis than those with low expression. Moreover, HOTAIR was further validated to promote migration and invasion of ESCC cells in vitro. 24118380 2013 HOTAIR, a prognostic factor in esophageal squamous cell carcinoma, inhibits WIF-1 expression and activates Wnt pathway. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 esophageal squamous cell cancer NA NA qPCR, RNAi etc. ESCC tissues, cell lines (KYSE30, KYSE150, KYSE450, KYSE510, KYSE180 etc.) up-regulated Notably elevated HOTAIR expression levels were observed in cancerous tissues compared to adjacent noncancerous tissues, showing a high correlation with cancer metastasis, elevated TNM stage classification, and lowered overall survival rates. Multivariate analysis revealed that HOTAIR expression is also an independent prognostic factor for comparison of TNM stage and lymph node metastasis. 24151120 2013 Upregulation of the long non-coding RNA HOTAIR promotes esophageal squamous cell carcinoma metastasis and poor prognosis. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, Western blot, RIP etc. gastric cancer tissues up-regulated we found that HOTAIR was more highly expressed in diffuse-type GC than in intestinal type. In the diffuse type, there is significant relationship between HOTAIR expression and DFS. CDH1 was downregulated in diffuse-type GC tissues and showed a negative relationship with HOTAIR. In addition, HOTAIR knockdown significantly repressed migration, invasion and metastasis both in vitro and vivo and reversed the epithelial-to-mesenchymal transition in GC cells. Moreover, it is demonstrated that HOTAIR crosstalk with microRNAs during epigenetic regulation. 26136075 2015 LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioma NA M9380/3 qPCR, Cell transfection, Western blot, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc. glioma tissues, cell lines (U87, U251, HEK 293T) up-regulated Quantitative RT-PCR demonstrated that HOTAIR expression was up-regulated in glioma tissues and cell lines. Knockdown of HOTAIR exerted tumor-suppressive function in glioma cells. Further, HOTAIR was confirmed to be the target of miR-326 and miR-326 mediated the tumor-suppressive effects of HOTAIR knockdown on glioma cell lines. Moreover, over-expressed miR-326 reduced the FGF1 expression which played an oncogenic role in glioma by activating PI3K/AKT and MEK 1/2 pathways. 26183397 2015 Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cells via modulation of miR-326. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioma NA M9380/3 qPCR, Western blot glioma tissues, cell lines (U87, U87vIII and U251) differential expression It was discovered that the 18 genes that most significantly correlated with HOTAIR expression formed a cell cycle-related mRNA network, which is positively regulated by HOTAIR. Furthermore, HOTAIR knockdown inhibited mouse intracranial GBM model formation. 28350082 2017 HOTAIR upregulates an 18-gene cell cycle-related mRNA network in glioma HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR etc. gastric cancer tissues up-regulated To further validate whether the reported HOTAIR has potential role in predict the prognosis in patients with digestive system cancer, we conducted an independent validation set including 71 gastric cancer cases by the method of qRT-PCR. For overall survival, patients with high HOTAIR expression had a significantly worse prognosis than those with low HOTAIR expression, which was consistent with the results of meta-analysis. 25968902 2015 The prognostic significance of HOTAIR for predicting clinical outcome in patients with digestive system tumors. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colorectal cancer C19.9 NA qPCR, Western blot, Luciferase report assay etc. colorectal cancer tissues, cell lines (SW480 and LOVO) up-regulated HOTAIR expression was significantly up-regulated in colorectal tissues compared with normal tissues. miR-545 expression was suppressed by HOTAIR overexpression whereas enhanced by HOTAIR silence. Suppression of EGFR expression by miR-545 mimic was abrogated by HOTAIR overexpression. HOTAIR long non-coding RNA mediates microR-545 regulating colorectal cancer cells proliferation.Although therapeutic advantage has been raised in surgery with radiation and chemotherapy, patients still face a big challenge for improving the survival rate and quality of life. 28364379 2017 MicroR-545 mediates colorectal cancer cells proliferation through up-regulating epidermal growth factor receptor expression in HOTAIR long non-coding RNA dependent. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colorectal cancer C19.9 NA qPCR, Luciferase reporter assay, Western blot, RIP colorectal cancer tissues, cell lines (CCD18CO, HCT15, CoLo205, HT29, DLD-1, and SW620) up-regulated The expressions of HOTAIR were upregulated in CRC tissue tissues compared to adjacent control tissues. lncRNA HOTAIR could regulate the progression and chemoresistance of CRC via modulating the expression levels of miR-203a-3p and the activity of Wnt/B-catenin signaling pathway.high expression of HOTAIR was associated with poorer overall survival in CRC patients 29680837 2018 LncRNA HOTAIR is a Prognostic Biomarker for the Proliferation and Chemoresistance of Colorectal Cancer via MiR-203a-3p-Mediated Wnt/Catenin Signaling Pathway. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues, cell lines (A549) up-regulated High expression of HOTAIR was detected in 17 patients and was frequently found in patients with advanced stage, lymph node metastasis or lymph-vascular invasion and short disease free interval. Furthermore, brain metastases show significantly higher HOTAIR expression compared to primary cancer tissues. HOTAIR-expressing A549 cells showed induced cell migration and anchorage independent cell growth in vitro. 23743197 2013 Large noncoding RNA HOTAIR enhances aggressive biological behavior and is associated with short disease-free survival in human non-small cell lung cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot etc. NSCLC tissues, cell lines (A549, SPC-A1,NCI-H1975 etc.) up-regulated HOTAIR was highly expressed both in NSCLC samples and cell lines compared with corresponding normal counterparts. HOTAIR upregulation was correlated with NSCLC advanced pathological stage and lymph-node metastasis. Moreover, patients with high levels of HOTAIR expression had a relatively poor prognosis. 24103700 2013 The long non-coding RNA HOTAIR indicates a poor prognosis and promotes metastasis in non-small cell lung cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR etc. cervical cancer tissues up-regulated HOTAIR and UCA1 both were significantly higher expressed in GC tumor tissues than adjacent non-tumor tissues. The results from the qRT-PCR validation in 82 newly diagnosed GC patients and the above bioinformatics results were 100% in agreement. HOTAIR and UCA1 were found to be significantly associated with overall survival. The miR-1 was downexpressed when lncRNA UCA1 was overexpressed in glioma cells.mRNA XIRP1 was found to interact with miRNA miR-133a-3p. Key miRNA miR-133a-3p was predicted to target key lncRNA HOTAIR. 29620291 2018 Integrated analysis of long non-coding RNA competing interactions revealed potential biomarkers in cervical cancer: Based on a public database. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, RNAi, Western blot, Flow cytometry assay etc. cell line (HeLa) up-regulated RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis. 26962687 2016 MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR etc. cervical cancer tissues up-regulated The results showed that HOTAIR expression in cervical cancer tissues was significantly upregulated compared with the matched nontumorous tissues. Increased HOTAIR expression was significantly correlated with FIGO stage, lymph node metastasis, depth of cervical invasion, tumor size and age, but not other clinical characteristics. Moreover, cervical cancer patients with HOTAIR higher expression have shown significantly poorer overall survival and disease-free survival than those with lower HOTAIR expression. 24748337 2014 Overexpression of long noncoding RNA HOTAIR predicts a poor prognosis in patients with cervical cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, Western Blot, Luciferase Reporter Assay cervical cancer cell lines (HeLa, CaSki, Me180, C-33A) differential expression Finally, the in vivo experiment revealed that tumor growth and metastasis could also be inhibited by HOTAIR shRNA. Our present study elucidated the regulating role of HOTAIR/miR-326 axis in cervical cancer progression and provided a new potential therapeutic strategy for cervical cancer. Although many therapeutic means such as surgery, chemotherapy, radiotherapy have been applied to cervical treatment, the prognosis and the five-year survival rate are still not satisfactory4. Previous researches had shown that HOTAIR took part in forming a complex with Polycomb repressive complex 2 (PRC2) which finally result in histone H3 lysine methylation, cancer invasion and metastasis29-31. 28893349 2017 LncRNA-HOTAIR Activates Tumor Cell Proliferation and Migration by Suppressing MiR-326 in Cervical Cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, Western blot etc. ovarian cancer tissues, cell lines (IOSE-8, A2780, SKOV-3 and SKOV-3-DDP ) up-regulated By knocking down HOXA7, HOTAIR downregulation restrained the ovarian cancer deterioration in functional experiments. Silencing of HOTAIR and HOXA7 could effectively inhibit tumor growth and increase chemosensitivity of ovarian tumors in nude mice. Downregulation of HOTAIR negatively affected the survival and activity of resistant ovarian cancer cells, and suppressed the expression of HOXA7. Silencing of HOTAIR and HOXA7 could increase the chemosensitivity of ovarian cancer cells, thus suppressing tumor development. 29455183 2018 The effect of lncRNA HOTAIR on chemoresistance of ovarian cancer through regulation of HOXA7. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, RNAi, Western blot etc. epithelial ovarian cancer tissues, cell lines (SKOV3, SKOV3.ip1 etc.) up-regulated HOTAIR expression was elevated in EOC tissues, and HOTAIR levels were highly positively correlated with the FIGO stage, the histological grade of the tumor, lymph node metastasis, and reduced overall survival and disease-free survival. The pro-metastatic effects of HOTAIR are likely partially mediated by the regulation of the expression of a number of genes involved in cell metastasis and EMT, including MMP3, MMP9, E-cadherin, vimentin, and Snail. 24662839 2014 Overexpression of long non-coding RNA HOTAIR predicts poor patient prognosis and promotes tumor metastasis in epithelial ovarian cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR hepatocellular carcinoma tissues, cell line (SMMC7221) up-regulated The silencing of HOTAIR in liver cancer cells induced the inhibition of cell proliferation and promotion of apoptosis.Several pathways such as extracellular matrix receptor interaction, focal adhesion, pathways in cancer were annotated with the HOTAIR and coexpression genes. HOTAIR might be an oncogene in HCC. It functions though promoting tumor cell growth and inhibiting apoptosis. HOTAIR may potentially be involved in HCC metastatic progression by several pathways correlated to cell adhesion.higher HOTAIR expression could significantly predict worse overall survival. 29115524 2017 High expression of long non-coding HOTAIR correlated with hepatocarcinogenesis and metastasis. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell lines (HepG2) up-regulated HOTAIR expression was detected in primary HCCs in 13 out of 64 patients. Patients with HOTAIR expression had significantly poorer prognoses and a larger primary tumor size than those without HOTAIR expression, similar to studies in breast and colorectal cancers. Moreover, introduction of human HOTAIR into liver cancer cells revealed that HOTAIR promoted more rapid proliferation compared to control cells. HOTAIR expression is associated with HCC progression, warranting further studies. 23292722 2013 Clinical significance of the expression of long non-coding RNA HOTAIR in primary hepatocellular carcinoma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR etc. breast cancer tissues differential expression A positive correlation was found between DNA methylation and HOTAIR expression. Methylation was associated with unfavorable disease characteristics, whereas no significant associations were found between HOTAIR expression and clinical or pathologic features. In multivariate, but not in univariate, Cox proportional hazard regression models, patients with high HOTAIR expression had lower risks of relapse and mortality than those with low HOTAIR expression. We found that patients with high levels of HOTAIR expression had lower risks of relapse and death than those with low expression. The results suggest that clinicopathological features and therapy treatments could modify the effect of HOTAIR. 23124417 2012 Association of large noncoding RNA HOTAIR expression and its downstream intergenic CpG island methylation with survival in breast cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA microarray, qPCR, ISH etc. breast cancer tissues up-regulated Co-expression of HOTAIR and EZH2 trended with a worse outcome. In matched primary and metastatic cancers, both HOTAIR and EZH2 had increased expression in the metastatic carcinomas. This approach offers a method to make observations on lncRNAs that may influence the cancer epigenome in a tissue-based technique. 23133536 2012 Detection of long non-coding RNA in archival tissue: correlation with polycomb protein expression in primary and metastatic breast carcinoma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, ChIP etc. cell lines (SUZ12, EZH2, PRC2 etc.) up-regulated Quantitative PCR showed that HOTAIR is overexpressed from hundreds to nearly two thousand- fold in breast cancer metastases, and HOTAIR level is sometimes high but heterogeneous among primary tumors . We next measured HOTAIR level in an independent panel of 132 primary breast tumors (stage I and II) with extensive clinical follow-up13. Indeed, nearly one third of primary breast tumors overexpress HOTAIR by over 125-fold over normal breast epithelia, the minimum level of HOTAIR overexpression observed in bona fide metastases, and high HOTAIR level is a significant predictor of subsequent metastasis and death. 20393566 2010 Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN47), gastric adenocarcinomas tissues down-regulated HOTAIR had a significant association with patient survival. 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. gastric cancer tissues, cell lines (MGC-803, SGC-7901, BGC-823, AGS) up-regulated HOTAIR upregulation was associated with larger tumor size, advanced pathological stage and extensive metastasis, and also correlated with shorter overall survival of gastric cancer patients. In particular, HOTAIR may act as a ceRNA, effectively becoming a sink for miR-331-3p, thereby modulating the derepression of HER2 and imposing an additional level of post-transcriptional regulation. 24775712 2014 Lnc RNA HOTAIR functions as a competing endogenous RNA to regulate HER2 expression by sponging miR-331-3p in gastric cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissues, gastric cell lines up-regulated The expression of HOTAIR was significantly elevated in various gastric cancer cell lines and tissues compared to normal control. Lymphovascular invasion and lymph node metastasis were more common in the high level of HOTAIR group. si-HOTAIR significantly decreased invasiveness and migration. si-HOTAIR led to differential expression of epithelial to mesenchymal transition markers. HOTAIR was involved in inhibition of apoptosis and promoted invasiveness, supporting a role for HOTAIR in carcinogenesis and progression of gastric cancer. 25063030 2014 Long non-coding RNA HOTAIR promotes carcinogenesis and invasion of gastric adenocarcinoma. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, Western blot, in vitro knockdown etc. gastric cancer tissues, cell lines (GES-1, AGS, SGC-7901, MKN-45, HGC-27 etc.) up-regulated The expression level of HOTAIR in cancer tissues was higher than that in adjacent noncancerous tissues. Expression level of HOTAIR was significantly correlated with lymph node metastasis and TNM stage. Furthermore, high expression level of HOTAIR was a predictor of poor over-all survival in GC patients. In vitro, inhibition of HOTAIR in GC cells could reduce invasiveness, as well as the expression of MMP1 and MMP3. In addition, suppression of HOTAIR could reverse EMT process. 23847441 2013 Knockdown of long non-coding RNA HOTAIR suppresses tumor invasion and reverses epithelial-mesenchymal transition in gastric cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, RNAi etc. gastric cancer tissues, cell lines (MKN74, KATO III etc.) up-regulated The expression of HOTAIR was significantly higher in cancer lesions than in adjacent non-cancerous tissues in human gastric cancers. In the diffuse type of gastric cancer, the High-HOTAIR group showed significantly more venous invasion, frequent lymph node metastases and a lower overall survival rate compared to the Low-HOTAIR group. 24130837 2013 Enhanced expression of long non-coding RNA HOTAIR is associated with the development of gastric cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, Western blot, RNAi etc cervical cancer tissues, cell lines (MRI-H196 and MRI-H186) down-regulated NRP2 was identified as a virtual target gene of miR-331-3p with a binding site of miR-331-3p,and HOTAIR was directly sponged to miR-331-3p,miR-331-3p reduced luciferase activity of wild-type of NRP2 3'UTR and HOTAIR, but not those of mutant NRP2 3'UTR and HOTAIR.MiR-331-3p down-regulated NRP2 and E7 expression levels,and further promoted cell apoptosis,while inhibited cell proliferation.Cell transfected with HPV16 E7 displayed lower levels of HOTAIR,NRP2 and P53,a higher level of miR-331-3p,over-expression of E7 further repressed cell apoptosis,while improved cell proliferation compared with control. Normal HPV (+) group exhibited a higher miR-331-3p, and lower mRNA levels of HOTAIR and NRP2 than HPV (-) group. 29130509 2018 ARFHPV E7 oncogene, lncRNA HOTAIR, miR-331-3p and its target, NRP2, form a negative feedback loop to regulate the apoptosis in the tumorigenesis in HPV positive cervical cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, Luciferase Assay etc. cervical cancer tissues, cell line (SiHa) up-regulated HOTAIR expression was significantly upregulated in both cervical cancer tissues and cell lines. HOTAIR could regulate tumorigenesis of gastric cancer in vivo and in vitro through acting as a competing endogenous RNA to sequester miR-331-3p28. the tumor-promoting role of HOTAIR in cervical cancer via sponging miR-17-5p, providing a novel therapeutic target for future treatment of cervical cancer. 29163829 2017 Long Noncoding RNA HOTAIR: An Oncogene in Human Cervical Cancer Interacting with MicroRNA-17-5p. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, RNAi, Western blot etc. cervical cancer tissues, cell lines (HeLa, ME-180, SiHa and CasKi) up-regulated HOTAIR expression was obviously increased in cervical cancer tissue. HOTAIR upregulation was associated with advanced pathological stage, histology, lymph node invasion and lymphatic metastasis, and also correlated with shorter overall survival of cervical cancer patients. Furthermore, HOTAIR overexpression promoted the proliferation, migration and invasion of cervical cancer cells, while HOTAIR knockdown inhibited cell invasion and cell viability, induced apoptosis and inhibited growth in vitro and in vivo. Moreover, HOTAIR modulated human leucocyte antigen-G (HLA-G) expression by competitively binding miR-148a. 27574106 2016 Long non-coding RNA HOTAIR modulates HLA-G expression by absorbing miR-148a in human cervical cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, RNAi, Western blot etc. cervical cancer tissues, cell lines (SiHa, HeLa, Caski) up-regulated The expression level of HOTAIR in cervical cancer tissues was higher than that in corresponding non-cancerous tissues. High HOTAIR expression correlated with lymph node metastasis, and reduced overall survival. Moreover, HOTAIR regulated the expression of vascular endothelial growth factor, matrix metalloproteinase-9 and epithelial-to-mesenchymal transition (EMT)-related genes, which are important for cell motility and metastasis. 25405331 2014 Long non-coding RNA HOTAIR is associated with human cervical cancer progression. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, Western blot, in vitro knockdown cell lines (MCF7, SKBR3, MDA-MB-231, MCF- 10A), BC tissues up-regulated The expression levels of the lncRNA HOTAIR were upregulated in BC tissues and cells.Knockdown lncRNA HOTAIR inhibited cell propagation and metastasis and facilitated cell apoptosis.MiR-20a-5p was a target of lncRNA HOTAIR and had a negative correlation with lncRNA HOTAIR.MiR-20a-5p overexpression in BC suppressed cell growth,mobility,and invasiveness and facilitated apoptosis.HMGA2 was a target of miR-20a-5p,which significantly induced carcinogenesis of BC.BC cells progression was mediated by lncRNA HOTAIR via affecting miR-20a-5p/HMGA2 in vivo.LncRNA HOTAIR affected cell growth, metastasis,and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer. 29473328 2018 LncRNA HOTAIR influences cell growth, migration, invasion, and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, Luciferase reporter assay, Western blot breast cancer tissues, cell lines (MCF-7 and T47D) up-regulated HOTAIR was able to up-regulate the expression of Bcl-w in breast cancer cells. miR-206 was capable of inhibiting the expression of Bcl-w by directly binding to the 3'UTR of Bcl-w mRNA.HOTAIR could increase the expression of Bcl-w through sequestering miR-206 at post-transcriptional level. HOTAIR-induced Bcl-w by miR-206 facilitated the proliferation of breast cancer cells.HOTAIR expression in primary breast tumors was significantly associated with worse prognosis independent of prognostic markers. 29222472 2017 Long Noncoding RNA HOTAIR Modulates MiR-206-mediated Bcl-w Signaling to Facilitate Cell Proliferation in Breast Cancer. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA Microarray, qPCR, Western blot Breast cancer tumor tissues, cell lines (MCF-7, MDA-MB-231 and HEK 293) up-regulated overexpression of JMJD6 increased HOTAIR expression and JMJD6 siRNAs suppressed it in ER+ MCF-7, triple negative MDA-MB-231 and non-breast cancer HEK 293 cells.Therefore, JMJD6 regulates HOTAIR independent of ER status.We propose that high JMJD6 expression may achieve higher levels of HOTAIR in breast tumors. Further, since high levels of HOTAIR promote metastasis and death, blocking JMJD6 may be useful in preventing such events. 29229759 2018 JMJD6 induces HOTAIR, an oncogenic lincRNA, by physically interacting with its proximal promoter. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. breast cancer tissues, cell lines (MDA-MB-453, MDA-MB-231, MCF-7 and T47D) up-regulated Ten different lncRNAs were applied in this study, which was reported to be associated with Notch-1. The level of these ten lncRNAs in breast tumors and adjacent normal tissues were evaluated, which suggested that HOTAIR and MALAT1 increased most significantly, and LUNAR1 and GAS5 decreased most significantly. 26550436 2015 Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 renal cell carcinoma C64.9 NA RNA-seq, qPCR, western blot etc. cell lines (786-O, A498, ACHN, and Caki-1) differential expression The ERB-modulated HOTAIR is able to function via antagonizing several microRNAs, including miR-138, miR-200c, miR-204, or miR-217 to impact various oncogenes, including ADAM9, CCND2, EZH2, VEGFA, VIM, ZEB1, and ZEB2, to promote RCC proliferation and invasion. 29789714 2018 Estrogen receptor B promotes renal cell carcinoma progression via regulating LncRNA HOTAIR-miR-138/200c/204/217 associated CeRNA network HOTAIRM1 HOTAIRM1, HOXA-AS1, HOXA1-AS1, NCRNA00179 100506311 ENSG00000233429 NR_038366 GRCh38_7:27095647-27100265 acute myeloid leukemia NA M9861/3 qPCR etc. bone marrow up-regulated Interestingly, HOTAIRM1 was overexpressed in NPM1-mutated AML (P < 0.001) and within this group retained its prognostic value (OR: 2.21; P = 0.01). Moreover, HOTAIRM1 expression was associated with a specific 33- microRNA signature that included miR-196b (P < 0.001). miR-196b is located in the HOX genomic region and has previously been reported to have an independent prognostic value in AML. 26436590 2016 The lincRNA HOTAIRM1, located in the HOXA genomic region, is expressed in acute myeloid leukemia, impacts prognosis in patients in the intermediate-risk cytogenetic category, and is associated with a distinctive microRNA signature. HOTAIRM1 HOTAIRM1, HOXA-AS1, HOXA1-AS1, NCRNA00179 100506311 ENSG00000233429 NR_038366 GRCh38_7:27095647-27100265 acute promyelocytic leukemia NA M9866/3 qPCR etc. bone marrow down-regulated Interestingly, HOTAIRM1 was overexpressed in NPM1-mutated AML (P < 0.001) and within this group retained its prognostic value (OR: 2.21; P = 0.01). Moreover, HOTAIRM1 expression was associated with a specific 33- microRNA signature that included miR-196b (P < 0.001). miR-196b is located in the HOX genomic region and has previously been reported to have an independent prognostic value in AML. 26436590 2016 The lincRNA HOTAIRM1, located in the HOXA genomic region, is expressed in acute myeloid leukemia, impacts prognosis in patients in the intermediate-risk cytogenetic category, and is associated with a distinctive microRNA signature. HOTAIRM1 HOTAIRM1, HOXA-AS1, HOXA1-AS1, NCRNA00179 100506311 ENSG00000233429 NR_038366 GRCh38_7:27095647-27100265 glioblastoma NA M9440/3 qPCR etc. GNS cell lines differential expression In addition, we detected 25 differentially expressed long non-coding RNAs 23046790 2012 Digital transcriptome profiling of normal and glioblastoma-derived neural stem cells identifies genes associated with patient survival HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 tongue squamous cell carcinoma C02 M8070/3 qPCR etc. tongue cancer tissues up-regulated In our study, results indicated that lncRNA HOTTIP was highly expressed in TSCC compared with adjacent non-malignant tissues and positively correlated with T stage, clinical stage, and distant metastasis in TSCC patients. 26058875 2015 Long non-coding RNA HOTTIP is correlated with progression and prognosis in tongue squamous cell carcinoma. HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 small cell lung cancer C56.9 M8441/3 microarray, qPCR, Western blot, RIP, Luciferase reporter assay etc. cell lines (H69, H446, H146, H446AR, H69AR) up-regulated HOTTIP was overexpressed in SCLC tissues, and its expression was correlated with the clinical stage and the shorter survival time of SCLC patients. Moreover, HOTTIP knockdown could impair cell proliferation, affect the cell cycle and inhibit tumor growth of mice, while HOTTIP overexpression might enhance cell proliferation and cell cycle in vitro and in vivo. Mechanistic investigations showed that HOTTIP functions as an oncogene in SCLC progression by sponging miR-574-5p and affecting the expression of polycomb group protein EZH1. 29041935 2017 A long non-coding RNA HOTTIP expression is associated with disease progression and predicts outcome in small cell lung cancer patients HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 small cell lung cancer C56.9 M8441/3 Microarray, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RNAi, RIP FFPE tissues, SCLC cell lines (H69, H69AR, H446, H446AR) up-regulated HOTTIP functioned as an oncogene in SCLC progression by binding miR-216a and abrogating its tumor-suppressive function in this setting.On the other hand,HOTTIP increased the expression of anti-apoptotic factor BCL-2,another important target gene of miR-216a,and jointly enhanced chemoresistance of SCLC by regulating BCL-2. 29367594 2018 Long non-coding RNA HOTTIP promotes BCL-2 expression and induces chemoresistance in small cell lung cancer by sponging miR-216a. HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 pancreatic cancer C25 NA qPCR, Western blot, RIP cell lines (PANC-1 and SW1990) up-regulated HOTTIP was highly expressed in PCSCs.Patients with higher HOTTIP expression had shorter disease-free survival and overall survival than those with lower expression. HOTTIP alterations affected stemness, including sphericity, tumorigenesis, and stem factors (LIN28, NANOG, OCT4, and SOX2) and markers (ALDH1, CD44, and CD133).HOTTIP mediated HOXA9 to enhance the Wnt/B-catenin pathway by binding to WDR5 in PCSCs.HOTTIP or HOXA9 alterations influenced stemness.the HOTTIP/WDR5/HOXA9/Wnt axis contributes to PCSC stemness and is a potential therapeutic target for PDAC. 28947139 2017 LncRNA HOTTIP modulates cancer stem cell properties in human pancreatic cancer by regulating HOXA9. HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 pancreatic cancer C25 NA microarray, qPCR, RNAi, Western blot etc. cell lines (Panc1, ASPC1, BxPC3 etc.) up-regulated HOTTIP is expressed in pancreatic cancer cell lines and knockdown of HOTTIP by RNA interference (siHOTTIP) in Panc1 pancreatic cancer cells decreased proliferation, induced apoptosis and decreased migration. HOTTIP functions in pancreatic cancer cells are due, in part, to regulation of some HOX genes including HOXA10, HOXB2, HOXA11, HOXA9 and HOXA1. 25912306 2015 The long non-coding RNA HOTTIP enhances pancreatic cancer cell proliferation, survival and migration. HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 pancreatic cancer C25 NA microarray, qPCR, RNAi, Western blot, Cell growth assay, Cell cycle assay etc. cell lines (PANC-1, MIA PaCa-2, Capan-2, SW1990, and BxPC-3) up-regulated Microarray analyses revealed that HOTTIP was one of the most significantly upregulated lncRNAs in PDAC tissues compared with pancreatic tissues. Quantitative PCR further verified that HOTTIP levels were increased in PDAC cell lines and patient samples compared with controls. Functionally, HOTTIP silencing resulted in proliferation arrest by altering cell-cycle progression, and impaired cell invasion by inhibiting epithelial-mesenchymal transition in pancreatic cancer. Additionally, inhibition of HOTTIP potentiated the antitumor effects of gemcitabine in vitro and in vivo. Immunohistochemistry results revealed that higher HOXA13 expression was correlated with lymph node metastasis, poor histological differentiation, and decreased overall survival in PDAC patients. 25889214 2015 The long non-coding RNA HOTTIP promotes progression and gemcitabine resistance by regulating HOXA13 in pancreatic cancer. HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 osteosarcoma NA M9180/3 qPCR, RNAi etc. osteosarcomas tissues, cell lines (MG-63, HOS) up-regulated We found that HOTTIP expression was up-regulated in OS tissues, and correlated with advanced clinical stage and distant metastasis. OS patients with high HOTTIP expression level had poorer overall survival than those with low HOTTIP expression. Multivariable Cox proportional hazards regression analysis suggested that increased HOTTIP expression was an independent prognostic factor of overall survival in OS patients. Moreover, the results of in vitro assays showed that the suppression of HOTTIP in OS cells significantly reduced cell proliferation, migration and invasion ability 26617868 2015 Long non-coding RNA HOTTIP is up-regulated and associated with poor prognosis in patients with osteosarcoma HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 gastric cancer C16 NA qPCR, RNAi etc. GC tissues, cell lines (AGS, SGC-7901, BGC-823, and MKN-28) down-regulated HOTTIP expression was remarkably increased in GC tissues and cell lines compared with that in the normal control. Clinicopathologic analysis revealed that high HOTTIP expression correlated with larger tumor size, deeper invasion depth, positive lymph node metastasis, advanced TNM stage, and shorter overall survival. Multivariate regression analysis identified HOTTIP overexpression as an independent unfavorable prognostic factor in GC patients. Moreover, HOTTIP downregulation by si-HOTTIP transfection impaired GC cell proliferation, promoted cell apoptosis, and reduced cell invasion and migration 27103834 2016 Overexpression of long noncoding RNA HOTTIP promotes tumor invasion and predicts poor prognosis in gastric cancer HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Dual-luciferase reporter assay, Cell proliferation assay etc. HCC tissues, cell lines (SMMC7721, HepG2 and Hep3B) up-regulated In the current study, we identified miR-192 and miR-204 as two microRNAs (miRNAs) suppressing HOTTIP expression via the Argonaute 2 (AGO2)-mediated RNA interference (RNAi) pathway in HCC. Interaction between miR-192 or miR-204 and HOTTIP were further confirmed using dual luciferase reporter gene assays. Consistent with this notion, a significant negative correlation between these miRNAs and HOTTIP exists in HCC tissue specimens. Interestingly, the dysregulation of the three ncRNAs was associated with overall survival of HCC patients. In addition, the posttranscriptional silencing of HOTTIP by miR-192, miR-204 or HOTTIP siRNAs could significantly suppress viability of HCC cells. On the contrary, antagonizing endogenous miR-192 or miR-204 led to increased HOTTIP expression and stimulated cell proliferation. 26710269 2015 MiRNA-192 [corrected] and miRNA-204 Directly Suppress lncRNA HOTTIP and Interrupt GLS1-Mediated Glutaminolysis in Hepatocellular Carcinoma. HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 pancreatic cancer C25 NA qPCR, Luciferase reporter assay PC cell line, PC tissues. down-regulated The current findings provided evidence that the functional rs1859168 A > C polymorphism may decrease the PC risk by down-regulating the HOTTIP expression.In addition, functional prediction of SNP revealed that rs1859168 could alter HOTTIP expression by influencing the transcription factor binding sites, and HOTTIP takes part in regulating cancer cell proliferation and survival [29, 30, 31]. In addition, functional prediction of SNP revealed that rs1859168 could alter HOTTIP expression by influencing the transcription factor binding sites, and HOTTIP takes part in regulating cancer cell proliferation and survival [29, 30, 31]. 28818070 2017 rs1859168 A>C polymorphism regulates HOTTIP expression and reduces risk of pancreatic cancer in a Chinese population. HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot etc. HCC tissues, cell lines (SNU182, SNU449, SNU423, SNU387, SNU475 etc.) up-regulated In this study we report the lncRNA HOXA transcript at the distal tip (HOTTIP) as significantly up-regulated in HCC specimens. Indeed, we observed the marked up-regulation of HOXA13 in HCC. Here, by correlating clinicopathological and expression data, we demonstrate that the levels of HOTTIP and HOXA13 are associated with HCC patients' clinical progression and predict disease outcome. 24114970 2014 Long noncoding RNA HOTTIP/HOXA13 expression is associated with disease progression and predicts outcome in hepatocellular carcinoma patients. HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 pancreatic cancer C25 NA microarray, qPCR etc. pancreatic cancer tissues, cell lines (PANC-1, BxPC-3, Capan2, MIAPaCa-2, SW1990, and AsPC-1) up-regulated Compared with the HPDE6 cells, all PC cell lines had higher HOTTIP-005, XLOC_006390, and RP11-567G11.1 expression. The most increased lncRNAs in PC tissues were HOTTIP-005, XLOC_006390, and RP11-567G11.1. Increased HOTTIP-005 and RP11-567G11.1 expression were poor prognostic factors for patients with PC. 26447755 2015 Expression profile of long non-coding RNAs in pancreatic cancer and their clinical significance as biomarkers. HOTTIP HOTTIP 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 gastric cancer C16 NA qPCR etc. GC tissues, cell lines (MGC-803, BGC-823, SGC-7901 and HGC-27) down-regulated Li et al reported that HOTTIP was upregulated in pancreatic cancer and may promote cancer cell proliferation, invasion and chemoresistance by regulating HOXA13.Survival rates, including overall survival and disease-free survival were calculated using the Kaplan-Meier method with the log-rank test applied for comparison. A receiver operating characteristic (ROC) curve was used to evaluate the diagnostic value of HOTTIP expression levels. 28693275 2017 Long non-coding RNA HOXA transcript at the distal tip as a biomarker for gastric cancer. HOTTIP HOTTIP 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 pancreatic cancer C25 NA qPCR, western blot etc. pancreatic cancer tissues, cell line CRL-2549 up-regulated It was observed that the expression levels of HOTTIP and mGluR1 were upregulated in pancreatic carcinoma tissues and pancreatic carcinoma cells, while the expression of HOTTIP was able to positively affect the expression of mGluR1. The result revealed that the overall survival of pancreatic carcinoma patients with a high expression level of HOTTIP or mGluR1 mRNA was significantly reduced in comparison with that of patients with a low expression level of HOTTIP or mGluR1 mRNA 29844833 2018 Expression levels of long non-coding RNA HOXA distal transcript antisense RNA and metabotropic glutamate receptor 1 in pancreatic carcinoma, and their prognostic values HOX NA NA NA NA NA glioma NA M9380/3 QRT-PCR, in vitro knockdown glioma tissues, glioma cell lines (U87, LN229 and U251) up-regulated The expression of HOTAIR and cell viability was found to be lowest in the sh-HOTAIR group among the three groups. The sh-HOTAIR group exhibited a higher apoptotic rate and lower number of cell migration compared with the blank and sh-NC groups. Additionally, the speed of wound healing was slower, the migration distance decreased and the survival time of nude mice was extended in the sh-HOTAIR compared to the other groups. Moreover, the sh-HOTAIR group demonstrated reduced lesion sizes and inflammation, no convulsions or hemiplegia and lesser number of satellite metastases. 28857242 2017 Down-regulation of the long noncoding RNA-HOX transcript antisense intergenic RNA inhibits the occurrence and progression of glioma. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27168619-27171915 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, Luciferase reporter assay etc. lung adenocarcinoma tissues, cell lines (A549, H1299, H1975, PC9 and SPC-A1) up-regulated Transcription factor ELK1 was demonstrated to upregulate HOXA10-AS in LAD cells through performing bioinformatics analysis and dual luciferase activity. Loss of function assays were performed in two different LAD cell lines. Silenced HOXA10-AS was proved to inhibit LAD progression by affecting cell proliferation, cell apoptosis and cell metastasis and EMT progress. Western blot analysis revealed that HOXA10-AS increased Wnt/B-catenin signaling in LAD cell lines. Finally, rescue assays were carried out to identify the biological function of HOXA10-AS-Wnt/B-catenin signaling in LAD progression. In conclusion, ELK1-induced upregulation of HOXA10-AS improved LAD progression through increasing Wnt/B-catenin signaling. 29729275 2018 ELK1-induced upregulation of lncRNA HOXA10-AS promotes lung adenocarcinoma progression by increasing Wnt/B-catenin signaling. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 laryngeal squamous cell cancer C32.3 NA Microarray, qPCR, in vitro knockdown LSCC tissues up-regulated Microarray and qRT-PCR showed that the level of HOXA11-AS was significantly higher in LSCC than that in the corresponding adjacent non-neoplastic tissues. ISH revealed that HOXA11-AS was strongly expressed in the nucleus and closely related to the T grade, neck nodal metastasis, and clinical stage. Patients with T3-4 grade, neck nodal metastasis, or advanced clinical stage presented a high HOXA11-AS expression. Kaplan-Meier analysis showed that high HOXA11-AS expression could predict a poor prognosis in LSCC patients. Furthermore, HOXA11-AS knockdown significantly inhibited the growth, migration, and invasion of LSCC cells.we speculated that HOXA11-AS might function through binding to proteins, such as transcription factors, in order to regulate the downstream genes. 29511452 2018 Expression of long non-coding RNA HOXA11-AS is correlated with progression of laryngeal squamous cell carcinoma. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 ovarian cancer C56.9 NA qPCR, Western blot etc. ovarian cancer tissues down-regulated Functional studies of ectopic expression of HOXA11-AS minor allele T in EOC cells showed decreased survival, proliferation, migration, and invasion compared to common allele A expression. Additionally, stable expression of HOXA11-AS minor allele T reduced primary tumor growth in mouse xenograft models to a greater extent than common allele A. Furthermore, HOXA11-AS expression levels were significantly lower in human EOC tumors than normal ovarian tissues, suggesting that HOXA11-AS has a tumor suppressor function in EOC which may be enhanced by the T allele 26430965 2015 A functional variant in HOXA11-AS, a novel long non-coding RNA, inhibits the oncogenic phenotype of epithelial ovarian cancer HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 osteosarcoma NA M9180/3 qPCR, Western blot etc. OS tissues, cell lines (U2OS, MG-63 and KHOS) up-regulated the expression of HOXA11-AS was upregulated in OS tissues and cell lines.The high expression of HOXA11-AS was associated with advanced clinical stage, distant metastasis and poor overall survival of OS. HOXA11-AS silencing suppressed OS cells proliferation, invasion and induced cell arrest in G0/G1 phase. HOXA11-AS acts as an endogenous sponge by directly binding miR-124-3p,and decreasing the xpression of miR-124-3p.HOXA11-AS may regulate tumor progression by affecting miR-124-3p targets, and ROCK1 expression. 28558357 2017 Long non-coding RNA HOXA11-AS functions as a competing endogenous RNA to regulate ROCK1 expression by sponging miR-124-3p in osteosarcoma. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 gastric cancer C16 NA RNA-seq, microarray, qPCR, Cell transfection, Western blot, RIP, ChIP, Luciferase reporter assay etc. gastric cancer tissues up-regulated In vitro and in vivo assays of HOXA11-AS alterations revealed a complex integrated phenotype affecting cell growth, migration, invasion, and apoptosis. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells. 27651312 2016 LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 esophageal squamous cell cancer NA NA qPCR etc. cell line (HET-1A,EC-9706,EC-10), esophageal squamous cell carcinoma tissues up-regulated The expression of HOXA11-AS is upregulated in esophageal cancer cell lines and tissues. High expression of HOXA11-AS is associated with poor prognosis of ESCC patients. 29575836 2018 Expression level and clinical significance of LncRNA HOXA11-AS in esophageal squamous cell carcinoma patients HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 serous ovarian cancer C56.9 M8441/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. SOC tissues, cell lines (OVCAR3, SKOV3, A2780, OVCA433, OVCA429, and TOV112D) up-regulated HOXA11as expression in cancer tissue was 77-fold higher than that of noncancerous tissue. Higher HOXA11as expression was significantly correlated with histological grade and preoperative CA125. HOXA11as overexpression in SOC cells led to increased cell proliferation, invasion, and migration. Moreover, HOXA11as was associated with the expression of genes involved in cell invasion, migration, and epithelial-mesenchymal transition (EMT), including VEGF, MMP-9, B-catenin, E-cadherin, Snail, Twist, and Vimentin. 27737536 2016 Long Non-coding RNA HOXA11 Antisense Promotes Cell Proliferation and Invasion and Predicts Patient Prognosis in Serous Ovarian Cancer. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 cervical cancer C53 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. cervical cancer tissues, cell lines (SiHa, HeLa, CaSki, ME-180 and C33A) up-regulated HOXA11-AS expression was significantly greater in tissues from patients with cervical cancer than in control patients. HOXA11-AS overexpression enhanced cell proliferation, migration, and tumor invasion in vitro, whereas HOXA11-AS knockdown inhibited these biologic aggressive features. In vivo xenograft experiments using the siHOXA11-AS-transfected HeLa cells revealed that HOXA11-AS strongly induced tumor growth. Furthermore, we found that HOXA11-AS knockdown decreased cancer stemness and triggered the EMT program. 27792998 2016 The long noncoding RNA HOXA11 antisense induces tumor progression and stemness maintenance in cervical cancer. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 non small cell lung cancer C34 M8046/3 qPCR etc. cell lines (A549, H460, 1299, PC9) up-regulated an up-regulated trend in HOXA11-AS level in NSCLC tissues was found compared to corresponding non-cancerous lung tissues based on qRT-PCR.Additionally, Sun39 et al. investigated the potential mechanism of HOXA11-AS in gastric cancer cells, and they found that HOXA11-AS could play an oncogenic role through the EZH2/HOXA11-AS/LSD1 complex or HOXA11-AS/miR-1297/EZH2 crosstalk. Richards43 et al. NSCLC accounts for approximately 80% of lung cancer, and currently, it still has an unsatisfactory prognosis despite the advances made in its treatments, with an overall 5-year survival rate of less than 16%5,6,7. 28717185 2017 Clinical Significance and Effect of lncRNA HOXA11-AS in NSCLC: A Study Based on Bioinformatics, In Vitro and in Vivo Verification. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, Western blot etc. cell lines (HepG2, Hep3B, Bel-7402, SMMC-7721 ) down-regulated lncRNA HOXA11-AS could promote the proliferation of HCC cells by recruiting EZH2 and suppressing the expression of the tumor suppressor DUSP5. LncRNA-HOXA11-AS is correlated with the clinicopathological features and overall survival of HCC patients. 29312625 2017 Long non-coding RNA HOXA11-AS promotes the proliferation HCC cells by epigenetically silencing DUSP5 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 colorectal cancer C19.9 NA qPCR, Western blot etc. CRC tissues, cell lines (Colo205, HCT116, Lovo, SW620, Caco-2, and SW480) up-regulated In the present study, we verified the significant upregulation of HOXA11-AS and PADI2, as well as the downregulation of miR-125a-5p, in CRC patients with liver metastasis. Overexpression and knockdown studies of HOXA11-AS or PADI2, as well as gain-/loss-of-function studies of miR-125a-5p, revealed a positive correlation between HOXA11-AS and PADI2 and a negative correlation with miR-125a-5p in the regulation of liver metastasis in CRC cell lines. In this study, HOXA11-AS expression was up-regulated in the tissues of CRC patients with liver metastasis. The knockdown and overexpression of HOXA11-AS inhibited and promoted the migration and invasion of colon cancer cells, respectively. Moreover, we confirmed that HOXA11-AS functions as a ceRNA to regulate PADI2 expression by sponging miR-125a-5p. The HOXA11-AS/miR-125a-5p/PADI2 regulatory network may represent a novel therapeutic target for liver metastasis of CRC. 29050308 2017 The lncRNA HOXA11-AS functions as a competing endogenous RNA to regulate PADI2 expression by sponging miR-125a-5p in liver metastasis of colorectal cancer. HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 glioma NA M9380/3 qPCR, Luciferase reporter assays, Western blot etc. glioma tissues, cell lines (U251, U87, LN229, SHG-44, A172) up-regulated HOXA11-AS was up-regulated in glioma tissues and cell lines, and related to overall survival.High expression of HOXA11-AS was correlated with shorter overall survival in patients with glioma. Knockdown of HOXA11-AS inhibited glioma cell proliferation, migration and invasion in vitro, and tumor growth in vivo. In addition, we demonstrated that HOXA11-AS functioned as a competing endogenous RNA (ceRNA) for miR-214-3p, which in turn positively regulated the expression of its direct target EZH2. 28946213 2017 Regulation of HOXA11-AS/miR-214-3p/EZH2 axis on the growth, migration and invasion of glioma cells HOXA13 HOXA13, HOX1, HOX1J NA ENSG00000106031 NA GRCh38_7:27193503-27200106 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot etc. HCC tissues, cell lines (SNU182, SNU449, SNU423, SNU387, SNU475 etc.) up-regulated In this study we report the lncRNA HOXA transcript at the distal tip (HOTTIP) as significantly up-regulated in HCC specimens. Indeed, we observed the marked up-regulation of HOXA13 in HCC. Here, by correlating clinicopathological and expression data, we demonstrate that the levels of HOTTIP and HOXA13 are associated with HCC patients' clinical progression and predict disease outcome. 24114970 2014 Long noncoding RNA HOTTIP/HOXA13 expression is associated with disease progression and predicts outcome in hepatocellular carcinoma patients. HOXA-AS2 HOXA-AS2, HOXA3as 285943 ENSG00000253552 NR_122069 GRCh38_7:27107777-27134302 pancreatic cancer C25 NA qPCR,RIP pancreatic cancer tissues, cell lines (AsPC-1,BxPC-3, and PANC-1) up-regulated HOXA-AS2 knockdown effectively suppressed proliferation by blocking the cell cycle transition and caused apoptosis of PC cells in vitro and in vivo. HOXA-AS2 directly interacted with enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1),which promoted PC cell growth ability. lncRNA-HOXA-AS2/EZH2/LSD1 complex may function as an oncogene in PC cell proliferation, and also provides a potential therapy target for PC.the mechanism of HOXA-AS2 in promoting PC cell proliferation and survival is more complex than we imagine. 29312501 2017 The lncRNA-HOXA-AS2/EZH2/LSD1 oncogene complex promotes cell proliferation in pancreatic cancer. HOXA-AS2 HOXA-AS2, HOXA3as 285943 ENSG00000253552 NR_122069 GRCh38_7:27107777-27134302 malignant glioma NA M9380/3 qPCR, Luciferase reporter assay, Western blot glioma tissues, cell lines (U87 and U251, HEK-293T, NHAs) up-regulated HOXA-AS2 was upregulated in glioma samples and cell lines and was positively correlated with VM. HOXA-AS2 knockdown attenuated cell viability,migration, invasion, and VM formation in glioma cells and inhibited the expression of vascular endothelial-cadherin (VE-cadherin), as well as the expression and activity of matrix metalloproteinase matrix metalloproteinase(MMP)-2 and MMP-9. HOXA-AS2 knockdown inhibited malignant glioma behaviors and VM formation via the miR-373/EGFR axis.mice in the sh-HOXA-AS2 + pre-miR-373 group had the longest survival time. 29310118 2018 Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis. HOXA-AS2 HOXA-AS2, HOXA3as 285943 ENSG00000253552 NR_122069 GRCh38_7:27107777-27134302 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Among them, AFAP1-AS1, BCAR4, H19, HOXA-AS2, MALAT1 and PVT1 were significantly up-regulated, and ADAMTS9-AS2 was significantly down-regulated in cancer tissue samples. 27596298 2016 Differentially expressed long non-coding RNAs and the prognostic potential in colorectal cancer. HOXA-AS2 HOXA-AS2, HOXA3as 285943 ENSG00000253552 NR_122069 GRCh38_7:27107777-27134302 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Cell migration and invasion assay etc. HCC tissues, cell lines (Huh7, Hep3B, SMMC-7721, and BEL-7402) up-regulated In the present study, we found that HOXA-AS2 expression was increased in HCC tissues and adjacent normal tissues and high HOXA-AS2 expression was associated with bigger tumor size, advanced tumor stage, and shorter survival time. Knockdown of HOXA-AS2 significantly inhibited HCC cell proliferation and invasion and resulted in an increase of apoptosis. 27855366 2016 HOX Antisense lincRNA HOXA-AS2 Promotes Tumorigenesis of Hepatocellular Carcinoma. HOXA-AS3 HOXA6as 100133311 ENSG00000254369 NR_038831 GRCh38_7:27129977-27155928 glioma NA M9380/3 qPCR, Western blot etc. glioma tissues, cell lines (LN229, U251, SNB19, U87 and H4) up-regulated It was shown that a novel lncRNA HOXA-AS3 was one of the most significantly upregulated lncRNAs in glioma tissues. Uni and Multivariate Cox regression analysis revealed that HOXA-AS3 was an independent prognostic factor in glioma patients. 28881797 2017 Upregulation of long noncoding RNA HOXA-AS3 promotes tumor progression and predicts poor prognosis in glioma HOXB-AS3 HOXA6as 100133311 ENSG00000254369 NR_038831 GRCh38_7:27129977-27155928 colon cancer C18 NA qPCR, Western blot etc. cell lines (SW480, SW620, HTC-116, MDA-MB-231, SK-OV-3, S18, S26, HEK293T) down-regulated Here, we discovered that the lncRNA HOXB-AS3 encodes a conserved 53-aa peptide. The HOXB-AS3 peptide, not lncRNA, suppresses colon cancer (CRC) growth. Mechanistically, the HOXB-AS3 peptide competitively binds to the ariginine residues in RGG motif of hnRNP A1 and antagonizes the hnRNP A1-mediated regulation of pyruvate kinase M (PKM) splicing by blocking the binding of the ariginine residues in RGG motif of hnRNP A1 to the sequences flanking PKM exon 9, ensuring the formation of lower PKM2 and suppressing glucose metabolism reprogramming. CRC patients with low levels of HOXB-AS3 peptide have poorer prognoses. Our study indicates that the loss of HOXB-AS3 peptide is a critical oncogenic event in CRC metabolic reprogramming. 28985503 2017 A Peptide Encoded by a Putative lncRNA HOXB-AS3 Suppresses Colon Cancer Growth HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. cell lines (A549, H1703, SK-MES-1, NCI-H1299) up-regulated HOXD-AS1 could negatively regulate the expression of miR-147a. miR-147a inhibition abrogated the effect of HOXD-AS1 knockdown on the proliferation and apoptosis of NSCLC cells. Furthermore, HOXD-AS1 positively regulated the expression of pRB (a tumor suppressor protein) in NSCLC cells. Taken together, our data indicated that HOXD-AS1 might be an oncogenic lncRNA that promotes proliferation of NSCLC and could be a therapeutic target in NSCLC. 29033588 2017 hOXD-as1 functions as an oncogenic cerna to promote nsclc cell progression by sequestering mir-147a HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 neuroblastoma NA M9500/3 microarray, qPCR, RNAi, Northern blot etc. cell line (SH-SY5Y) up-regulated One of these lncRNAs, termed HOXD-AS1, is encoded in HOXD cluster. HOXD-AS1 is overexpressed in neuroblastoma. We found that HOXD-AS1 is a subjetc to morphogenic regulation, is activated by PI3K/Akt pathway and itself is involved in control of RA-induced cell differentiation. Knock-down experiments revealed that HOXD-AS1 controls expression levels of clinically significant protein-coding genes involved in angiogenesis and inflammation, the hallmarks of metastatic cancer. 25522241 2014 HOXD-AS1 is a novel lncRNA encoded in HOXD cluster and a marker of neuroblastoma progression revealed via integrative analysis of noncoding transcriptome. HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 colorectal cancer C19.9 NA qPCR, Western blot, Luciferase reporter assay etc colorectal cancer tissues, cell lines (HCT116, CCD-112CoN) up-regulated HOXD-AS1 was upregulated in CRC tissues and cell lines, and that overexpression of HOXD-AS1 was associated with poor prognosis in patients with CRC. Furthermore, knockdown of HOXD-AS1 inhibited cell proliferation, cell invasion, epithelial mesenchymal transition and stem cell formation in vitro,as well as tumor growth and metastasis in vivo. Mechanistically, HOXD-AS1 functioned as a competing endogenous RNA for miR-217. In conclusion, the present study demonstrated that HOXD-AS1 may promote CRC progression and metastasis by competing for miR-217. In addition, HOXD-AS1 may be considered an indicator of prognosis in patients with CRC. The present study confirmed that HOXD-AS1 could act as a ceRNA for miR-217. 29749477 2018 Long non-coding RNA HOXD-AS1 promotes tumor progression and predicts poor prognosis in colorectal cancer. HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 ovarian cancer C56.9 NA qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP OC tissues, OC cell lines (Caov-3, SK-OV-3 and OVCAR-3) up-regulated HOXD-AS1 was observed to be upregulated in both OC tissues and cell lines.HOXD-AS1 was detected to positively regulate the expression of frizzled family receptor 4 (FZD4) by competitively binding to miR-608. 29416930 2018 HOXD-AS1 promotes cell proliferation, migration and invasion through miR-608/FZD4 axis in ovarian cancer. HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 liver cancer C22.0 NA Microarray, qPCR, Western blot, In vitro assays, Luciferase reporter assay Human hepatocarcinoma cell lines (SNU449, Huh28, SMMC-7721, Huh7, Hep3B), hepatocarcinoma cancerous tissues up-regulated In the current study, using gene expression profiling analysis we discovered a lncRNA HOXD-AS1 was upregulated in HCC and significantly correlated with poor prognosis of HCC patients. Meanwhile, we demonstrated that HOXD-AS1 promoted HCC metastasis by acting as a ceRNA to upregulate the expression of SOX4 and activated the expression of EZH2 and MMP2, two direct target genes of SOX4.In this study, we found that HOXD-AS1 was significantly upregulated in HCC tissues. Clinical investigation demonstrated high expression level of HOXD-AS1 was associated with poor prognosis and high tumor node metastasis stage of HCC patients, and was an independent risk factor for survival. lncRNAs also can function as competing endogenous RNAs (ceRNAs) by competitively binding miRNAs, thereby modulating the derepression of miRNAs targets. 28810927 2017 STAT3-mediated upregulation of lncRNA HOXD-AS1 as a ceRNA facilitates liver cancer metastasis by regulating SOX4. HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 melanoma NA M8720/3 qPCR, Western blot, RIP malignant melanoma tissues, cell lines (B16, A375 and A2508, HEMn) up-regulated lncRNA HOXD-AS1 expression was remarkably higher in melanoma tissues. Increased expression of lncRNA HOXD-AS1 correlated with poor survival of melanoma patients.upregulated lncRNA HOXD-AS1 expression dramatically promoted cell proliferation and invasion of melanoma. lncRNA HOXD-AS1 knockdown notably reduced tumor growth.lncRNA HOXD-AS1 could epigenetically suppress the expression of RUNX3 via binding to EZH2. Downregulation of RUNX3 attenuated the proliferation and invasion-inhibiting effects induced by lncRNA HOXD-AS1 knockdown in melanoma cells. 29312805 2017 LncRNA HOXD-AS1 promotes melanoma cell proliferation and invasion by suppressing RUNX3 expression. HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 epithelial ovarian cancer C56.9 NA qPCR, Luciferase reporter assay, Western blot epithelial ovarian cancer tissues, cell lines (SKOV3, HO8910, ES-2, and CAOV3, IOSE80) up-regulated the expression of HOXD-AS1 was upregulated in EOC tissues and cell lines. High HOXD-AS1 expression was correlated with advanced FIGO stage, lymph node metastasis, and poor overall survival in EOC patients. HOXD-AS1 promoted cell proliferation, invasion, and epithelial-mesenchymal transition (EMT) via activating Wnt/B-catenin signaling in EOC cells.miR-133a-3p was a direct downstream target of HOXD-AS1 in EOC. HOXD-AS1 promoted cell proliferation, invasion, and EMT process through sponging miR-133a-3p in EOC cells. 29239819 2017 LncRNA HOXD-AS1 promotes epithelial ovarian cancer cells proliferation and invasion by targeting miR-133a-3p and activating Wnt/B-catenin signaling pathway. HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 osteosarcoma NA M9180/3 qPCR, Western blot, in vitro knockdown OS tissues, OS cell lines (MG63, 143B, U2OS, SaOS) up-regulated the expression level of HOXD-AS1 was significantly upregulated in OS tissues and cells.in vitro assays confirmed that knockdown of HOXD-AS1 suppressed cell proliferation, colony formation, migration, and invasion, and promoted cell cycle arrest at G1 stage and apoptosis in OS cells. in vivo assays confirmed that knockdown of HOXD-AS1 significantly decreased tumor growth in xenograft mice, and decreased tumor size and weight. Importantly, we also showed that knockdown of HOXD-AS1 significantly reduced signal transducer and activator of transcription 3 and its target protein (CyclinD1, Bcl-2, and MMP-2) expression in vitro and in vivo. Moreover, overexpression of STAT3 could reverse the suppression of proliferation ability induced by sh-HOXD-AS1 in U2OS cells. 29571260 2018 Knockdown of long non-coding RNA HOXD-AS1 inhibits the progression of osteosarcoma. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 epithelial ovarian cancer C56.9 NA qPCR, Western blotting etc. cell lines (A2780, OVCAR3) up-regulated HULC expression was examined in EOC, borderline and benign ovarian tumors, and normal ovarian tissues by RT-PCR. Ovarian cancer cell phenotypes, as well as autophagy-associated proteins were examined after HULC overexpression or downregulation by plasmid or small interfering RNA (siRNA) transfection, respectively. LncRNA-protein interactions were examined by ribonucleoprotein immunoprecipitation (RIP) assays. We found that HULC expression levels were higher in EOC tissues than normal samples. HULC overexpression induced cell proliferation, migration, invasion, whereas reduced cell apoptosis in vitro and induced tumor growth in vivo. In contrast, downregulation of HULC by siRNA transfection reduced cell proliferation, migration and invasion, and induced cell apoptosis and autophagy. Our results showed that HULC overexpression reduced ATG7, LC3-II and LAMP1 expression, while inducing SQSTM1 (P62) and ITGB1 expression. HULC downregulation had the opposite effects. 29022892 2017 The lncRNA HULC functions as an oncogene by targeting ATG7 and ITGB1 in epithelial ovarian carcinoma HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 cervical cancer C53 NA qPCR etc. cervical cancer tissues up-regulated HULC expression was high in cervical cancer. Also, the high HULC expression was significantly associated with the FIGO stage, lymph node metastasis and depth of cervical invasion. 27775802 2016 Expression of lncRNA HULC in cervical cancer and its correlation with tumor progression and patient survival. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 diffuse large B-cell lymphoma NA M9680/3 qPCR, Western blot etc. lymph node tissues up-regulated Firstly, we found that HULC was remarkably overexpressed in both DLBCL tissues and cell lines. Moreover, we illustrated that HULC was closely related to DLBCL characteristics, such as Ann Arbor stages, B symptoms, CHOP-like treatment, rituximab and IPI. Importantly, we verified that HULC was an key predictive factor for DLBCL diagnosis and prognosis from sizable samples through the long time follow-ups. Furthermore, we reveal that the HULC knockdown could significantly arrest cell proliferation and induce apoptosis by repressing cyclin D1 and Bcl-2 in DLBCL cells. 27044827 2016 Long noncoding RNA HULC predicts poor clinical outcome and represents pro-oncogenic activity in diffuse large B-cell lymphoma HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 breast cancer C50 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. TNBC tissues, cell lines (MDA-MB-231, MDA-MB-468, BT549, BT483) up-regulated HULC expression was increased in TNBC tissues and cell lines and associated with malignant status and poor prognosis of TNBC patients. Furthermore, silencing TNBC expression effectively suppressed TNBC cells metastasis through MMP-2 and MMP-9. 27986124 2016 Long Noncoding RNA Highly Up-regulated in Liver Cancer Predicts Unfavorable Outcome and Regulates Metastasis by MMPs in Triple-negative Breast Cancer. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 pancreatic cancer C25 NA qPCR, RNAi etc. pancreatic cancer tissues, cell lines (MIAPace-2, CFPAC-1, PANC-1, AsPC-1 etc.) up-regulated The higher expression of HULC was significantly correlated with large tumor size, advanced lymph node metastasis and vascular invasion. Multivariate analyses revealed that HULC expression served as an independent predictor for overall survival. Further experiments revealed that HULC knockdown significantly repressed cell proliferation of PC in vitro. 25412939 2014 Long noncoding RNA HULC is a novel biomarker of poor prognosis in patients with pancreatic cancer. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 osteosarcoma NA M9180/3 qPCR, Luciferase reporter assay, Western blot cell lines (MG63, hFOB1.19, OS-732) up-regulated Suppression of HULC in osteosarcoma cells inhibited cell viability,migration,invasion, and promoted apoptosis. HULC functioned as an endogenous sponge for miR-122,and its silence functioned through upregulating miR-122.Furthermore,overexpression of miR-122 inactivated PI3K/AKT, JAK/STAT, and Notch pathways by downregulation of HNF4G. high levels of HULC were associated with low survival rates in osteosarcoma patients. 28688193 2017 Knockdown of lncRNA HULC inhibits proliferation, migration, invasion, and promotes apoptosis by sponging miR-122 in osteosarcoma. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 prostate cancer C61.9 NA qPCR, Western blot, RNAi cell lines (PC3, LNCaP, DU145, RWPE-1) down-regulated In PC3 and LNCaP cells under irradiation, survival rate and cell cycle were decreased and apoptosis was increased by HULC knockdown. HULC knockdown arrested PC3 cells at G0/G1 phase.DU-145 was sensitive to irradiation, and resistance to irradiation of DU-145 cells was enhanced by HULC overexpression.HULC knockdown enhanced the sensitivity of PC3 xenografts to irradiation.HULC knockdown improved sensitivity of PCa cells to irradiation both in vivo and in vitro. HULC suppressed Beclin-1 phosphorylation, thereby reduced autophagy, involving the mTOR pathway.the irradiationinduced decrease of survival rate in PCa cells and alteration of survival rate induced by irradiation were further augmented by HULC knockdown but reduced by HULC overexpression. 29694502 2018 LncRNA HULC mediates radioresistance via autophagy in prostate cancer cells. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 osteosarcoma NA M9180/3 qPCR etc. osteosarcoma tissues up-regulated Our data demonstrated that higher levels of expression of HULC were associated with lower survival rates in OS patients, both in terms of overall and event-free survival. Elevated HULC expression was associated with poor clinical outcomes among the OS patients, which suggests that HULC could be a potential prognostic biomarker in OS. 27253450 2016 High Expression of HULC Is Associated with Poor Prognosis in Osteosarcoma Patients. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, ChIP, RNA pull-down assay etc. CRC tissues, cell lines (DLD1, HCT116, LOVO, RKO, LS174T, HCT8, HR28348, HT29, SW620, and SW480) up-regulated HULC expression is also over-expressed in CRC, and its increased level is associated with poor prognosis and shorter survival. Knockdown of HULC impaired CRC cells proliferation, migration and invasion, and facilitated cell apoptosis in vitro, and inhibited tumorigenicity of CRC cells in vivo. Mechanistically, HULC could simultaneously interact with EZH2 to repress underlying targets NKD2 transcription. In addition, rescue experiments determined that HULC oncogenic function is partly dependent on repressing NKD2. 27496341 2016 Long noncoding RNA HULC promotes colorectal carcinoma progression through epigenetically repressing NKD2 expression. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 prostate cancer C61.9 NA qPCR, Western blot, Luciferase reporter assay etc. cell lines (LNCaP, PC3,DU145,RWPE-1), PCa tissues up-regulated HULC expression was upregulated in PCa tissues and cell lines compared to adjacent non-tumor tissues and the normal prostate cell line RWPE-1. High HULC expression was positively associated with advanced clinicopathologic features and poor overall survival (OS) for PCa patients.HULC inhibition suppressed PCa cell growth and metastasis both in vitro and in vivo.Furthermore, HULC knockdown reduced N-cadherin and vimentin expression and increased E-cadherin expression in PCa cells.LncRNA HULC might play oncogenic roles in PCa progression, which provided a novel therapeutic strategy for PCa patients.lncRNA HULC enhanced epithelial mesenchymal transition to promote tumorigenesis and metastasis of hepatocellular carcinoma via the miR-200a-3p/ZEB1. 29765457 2018 High lncRNA HULC expression is associated with poor prognosis and promotes tumor progression by regulating epithelial-mesenchymal transition in prostate cancer. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 osteosarcoma NA M9180/3 qPCR etc. osteosarcoma tissues, cell lines (MG-63, U2OS, SAOS-2 etc.) up-regulated In the present study, we demonstrated that HULC was significantly up-regulated in osteosarcoma tissues and cell lines compared with normal controls, and over-expression of HULC was correlated with clinical stage and distant metastasis. Moreover, higher HULC expression was associated with shorter overall survival of osteosarcoma patients.e, decreased expression of HULC markedly suppressed osteosarcoma cell proliferation, migration, and invasion. 26045809 2015 Increased expression of lncRNA HULC indicates a poor prognosis and promotes cell metastasis in osteosarcoma. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RIP etc. cell lines (HepG2, Hep3B) up-regulated HULC promoted the growth of HCC cells through elevating COX-2 protein. knockdown of USP22 or COX-2 attenuated HULC-mediated abnormal growth of HCC cells.HULC promoted the survival of HepG2 and Hep3B cells in a dosedependent manner.We previous revealed that three miRNAs (miR-6825e5p, miR-6845e5p and miR-6886e3p) were involved in HULC mediated USP22 and Sirt1 upregulation 28634076 2017 lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues up-regulated The increased expression of HULC in HCC tissue may represent a good prognostic biomarker for curatively resected HCC. Terefore, in combination with other tumor prognostic factors, the determination of the expression levels of these lncRNAs may lead to a more accurate prediction of HCC prognosis. 29170515 2017 Prognostic Value of Long NonCoding RNA HULC and MALAT1 Following the Curative Resection of Hepatocellular Carcinoma. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. cell lines (HepG2, SNU-449, and SK-Hep-1) up-regulated Sp1, Sp3 and Sp4 transcription factors regulate HULC and other lncRNAs in HCC cells. Sp proteins and HULC regulate HCC cell proliferation, survival, migration/invasion. Knockdown of Sp1 and HULC inhibit HCC cancer cell migration and invasion 26317792 2015 Specificity protein (Sp) transcription factors and metformin regulate expression of the long non-coding RNA HULC. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot etc. HCC tissues, cell lines (Huh-6, Huh-7, HepG2, BEL-7402, MHCC-97H, Sk-Hep1, SMMC-7721 etc.) up-regulated We found that HULC was aberrantly up-regulated in HCC tissues and associated with TNM stage, intrahepatic metastases, HCC recurrence, and postoperative survival. HULC depletion inhibited the growth and metastasis of HCC cell lines in vitro and in vivo. Moreover, HULC contributes to ZEB1-induced epithelial-mesenchymal transition (EMT), a requirement for tumor invasion and metastasis that plays a key role in cancer progression. 27285757 2016 LncRNA HULC enhances epithelial-mesenchymal transition to promote tumorigenesis and metastasis of hepatocellular carcinoma via the miR-200a-3p/ZEB1 signaling pathway. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, RIP, RNA pull-down assay etc. HCC tissues, cell lines (HepG2 and SMMC-7721) up-regulated We validated the markedly increased expression levels of HULC in hepatocellular carcinoma tissues compared to their adjacent noncancerous tissues. Furthermore, up-regulation of HULC was correlated with grading and overall survival. Meanwhile, HULC could promote cell proliferation, migration, and invasion in vitro and inhibit cisplatin-induced apoptosis. Moreover, we show that HULC specifically binds to Y-box binding protein 1 (YB-1) protein both in vitro and in vivo. 28027578 2017 Long noncoding RNA HULC modulates the phosphorylation of YB-1 through serving as a scaffold of extracellular signal-regulated kinase and YB-1 to enhance hepatocarcinogenesis. IGF2-AS IGF2-AS, IGF2-AS1, IGF2AS, PEG8 51214 ENSG00000099869 NM_016412 GRCh38_11:2140501-2148666 non small cell lung cancer C34 M8046/3 qPCR, Western blot non-small cell lung cancer tissues, cell lines (A549, H23, H226, SW900, H441, H510A, H596, SK-MES-1, H920 and H1299) down-regulated IGF2AS is downregulated in both NSCLC human tumors and NSCLC cell lines, as well as in stage III or IV tumors. Downregulated IGF2AS was significantly correlated with NSCLC patients’ short overall survival. 28471495 2017 Prognostic implication and functional role of long noncoding RNA IGF2AS in human non-small cell lung cancer ILF3-AS1 XLOC_013222 NA ENSG00000267100 NA GRCh38_19:10651862-10653844 melanoma NA M8720/3 qPCR, RIP etc. breast cancer tissues, non-small cell lung cancer tissues up-regulated lncRNA ILF3-AS1 is upregulated in melanoma tissues and cell lines, and correlated with poor prognosis of melanoma patients. Functional experiments showed that knockdown of ILF3-AS1 inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues.Moreover,inhibition of miR-200b/a/429 abrogates the biological roles of ILF3-AS1 knockdown on melanoma cell proliferation, migration and invasion. 28935763 2017 Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration and invasion via negatively regulating miR-200b/a/429 in melanoma INTS7 INTS7, C1orf73, INT7 NA ENSG00000143493 NA GRCh38_1:211940399-212035542 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues up-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. ITGB2-AS1 NA 100505746 ENSG00000227039 NR_038311 GRCh38_21:44921051-44929678 breast cancer C50 NA Western blot, Flow cytometry, etc. cell lines (MDA-MB-231, MCF-7) down-regulated The results of biological function experiments showed that ITGB2-AS1 could promote the migration and invasion of breast cancer. Furthermore, ITGB2-AS1 increased the mRNA and protein expression of ITGB2. LncRNA ITGB2-AS1 could promote the migration and invasion of breast cancer cells by up-regulating ITGB2.higher expression group had a poorer overall survival rate. 29941860 2018 LncRNA ITGB2-AS1 Could Promote the Migration and Invasion of Breast Cancer Cells through Up-Regulating ITGB2. JPX JPX, DCBALD06, ENOX, LINC00183, NCRNA00183 554203 ENSG00000225470 NR_024582 GRCh38_X:73944184-74070408 glioma NA M9380/3 qPCR glioma tissues down-regulated Expression of lncRNAs MEG3, JPX, RNCR3, and ZFAS1 significantly differed between low and high malignancy grade. MEG3, JPX, RNCR3, and ZFAS1 showed significant decrease with tumour malignant progression. Expression of certain lncRNAs seems to be associated with patient's age at the time of diagnosis as correlation analysis showed moderate negative association for MEG3, ZFAS1, and RNCR3. 29138748 2017 Identifying Novel Glioma-Associated Noncoding RNAs by Their Expression Profiles KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 10984 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 non small cell lung cancer C34 M8046/3 qPCR etc. cell line (A549) up-regulated Bioinformatics analysis and qRT-PCR indicated that KCNQ1OT1 expression was higher in stage I LC patients (P<0.01), and survival analysis showed that high expression of KCNQ1OT1 in LC patients was associated with better prognosis (P<0.05). qRT-PCR showed a negative correlation between KCNQ1OT1 and Ki67 expression and tumor size (P<0.01), which indicated that KCNQ1OT1 is associated with tumor growth in LC. There was no significant correlation between KCNQ1OT1 level and lymph node metastasis (P>0.05). KCNQ1OT1 overexpression significantly inhibited cell proliferation and tumor growth in vitro and in vivo (P<0.05). 29504267 2018 Overexpression of long non-coding RNA KCNQ1OT1 is related to good prognosis via inhibiting cell proliferation in non-small cell lung cancer. KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 10984 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 melanoma NA M8720/3 Microarray, qPCR, Western blot etc. melanoma tissues, cell lines (HACAT, A375, A875 and MuM-2C) up-regulated KCNQ1OT1 expression is up-regulated in melanoma tissues and cells.KCNQ1OT1 promoted cell proliferation and metastasis in melanoma.By directly bindin to miR-153,KCNQ1OT1 acted as a competing endogenous RNA (ceRNA) to de-repress MET expression. 29667930 2018 KCNQ1OT1 promotes melanoma growth and metastasis. KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 10984 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 10984 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (Huh-7, SMMC-7721, Hep3B, MHCC97-H and MHCC97-L, LO2, 293T), HCC tissues up-regulated The ectopic high expression of KCNQ1OT1 was associated with liver cirrhosis,a larger tumor size, an advanced TNM stage,and a worse overall survival and tumor-free survival. KCNQ1OT1 exerted its effects partly by relying on the microRNA-504 (miR-504)mediated regulation of cyclin-dependent kinase 16 (CDK16),in addition to the regulation of the glycogen synthase kinase 3B (GSK3B)/B-catenin/Bcl-2 signaling pathway. The present study revealed the functions and mechanisms of action of lncRNA KCNQ1OT1 regarding its role in promoting the growth of HCC.KCNQ1OT1 may prove to be a potential therapeutic target for human HCC. 29532864 2018 Long non-coding RNA KCNQ1OT1 mediates the growth of hepatocellular carcinoma by functioning as a competing endogenous RNA of miR-504. KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 10984 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 acute myeloid leukemia NA M9861/3 qPCR peripheral blood up-regulated The expression of LncRNA KCNQ1OT1 was associated with NCCN risk grade and survival status in patients with AML. The median overall survival time was significantly shorter in patients with high expression of LncRNA KCNQ1OT1 than that in patients with low expression(P<0.05). 29950199 2018 [Expression and Clinical Significance of LncRNA KCNQ1OT1 in Patients with Acute Myeloid Leukemia]. KRT18P55 KRT18P55 NA ENSG00000265480 NA GRCh38_17:28275986-28317783 gastric cancer C16 NA qPCR etc. cell lines (GES-1, SGC-7901, MGC-803, BGC-823, AGS, HG27 etc.) up-regulated A significant upregulation was observed in GC cell lines and tissue samples. This finding was consistent with the results of 29 pairs of GC tissue samples from TCGA. Additionally, we indicated that the increased expression of KRT18P55 was related to the progression of intestinal type, which was also supported by results of independent GC cohorts from TCGA. However, we did not find significant difference in prognosis between patients with high and low expression of KRT18P55. Finally, KRT18P55 showed potential diagnostic value for GC with an area under the receiver operating characteristic curve of 0.733. 26855593 2016 Upregulated long intergenic noncoding RNA KRT18P55 acts as a novel biomarker for the progression of intestinal-type gastric cancer LeXis NA NA NA NA NA osteosarcoma NA M9180/3 qPCR, Western blot etc. OS tissues, cell lines (Nhost, KHOS, 143b, LM7, U2OS, and MG-63) up-regulated LeXis expression was upregulated in OS tissues. Increased LeXis expression was significantly correlated with high tumor stage, large tumor size, and poor prognosis. LeXis increased CTNNB1 expression by functioning as a ceRNA of CTNNB1 against miR-199a.Moreover, LeXis increased CTNNB1 expression by functioning as a ceRNA of CTNNB1 against miR-199a. The 5-year survival rate of patients with OS having distant metastases is approximately 30% . 28744406 2017 Long noncoding RNA LeXis promotes osteosarcoma growth through upregulation of CTNNB1 expression. LINC00092 LINC00092, NCRNA00092 100188953 ENSG00000225194 NR_024129 GRCh38_9:96019732-96027965 ovarian cancer C56.9 NA microarray, qPCR, RNAi, RNA pull-down assay etc. ovarian cancer tissues, cell lines (SKOV-3 and A2780) up-regulated CXCL14-high CAFs mediated upregulation of LINC00092 in ovarian cancer cells, the levels of which also correlated with poor prognosis in patients. Mechanistic studies showed that LINC00092 bound a glycolytic enzyme, the fructose-2,6-biphosphatase PFKFB2, thereby promoting metastasis by altering glycolysis and sustaining the local supportive function of CAFs. 28087599 2017 Long Noncoding RNA LINC00092 Acts in Cancer-Associated Fibroblasts to Drive Glycolysis and Progression of Ovarian Cancer. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 colon cancer C18 NA qPCR, Western blot, Luciferase reporter assay, RIP etc. colon cancer tissues, cell lines (Hct116, SW1417, SW620, Caco2, SW480, HT29, HCT8 and NCM460) up-regulated We showed that loss of epithelial characteristics and simultaneous gain of mesenchymal features correlated with CYTOR expression. Knockdown of CYTOR attenuated colon cancer cell migration and invasion. Conversely, ectopic expression of CYTOR induced an EMT program and enhanced metastatic properties of colon cancer cells. Mechanistically, the binding of CYTOR to cytoplasmic B-catenin impeded casein kinase 1 (CK1)-induced B-catenin phosphorylation that enabled it to accumulate and translocate to the nucleus. Reciprocally, B-catenin/TCF complex enhanced the transcription activity of CYTOR in nucleus, thus forming a positive feed-forward circuit. Moreover, elevated CYTOR, alone or combined with overexpression of nuclear B-catenin, was predictive of poor prognosis. Our findings suggest that CYTOR promotes colon cancer EMT and metastasis by interacting with B-catenin, and the positive feed-forward circuit of CYTOR-B-catenin might be a useful therapeutic target in antimetastatic strategy. 29606502 2018 A Positive Feed-Forward Loop between LncRNA-CYTOR and Wnt/B-Catenin Signaling Promotes Metastasis of Colon Cancer. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 tongue squamous cell carcinoma C02 M8070/3 qPCR tongue squamous cell carcinoma tissues up-regulated Quantitative Real time PCR (qRT-PCR) results indicated that LINC00152 was highly expressed in 15 primary TSCC biopsies when compared with 14 adjacent non-tumor tongue squamous cell epithelium samples. Kaplan-Meier analysis demonstrated that increased LINC00152 expression contributed to both poor overall survival (p = 0.006) and disease-free survival (p = 0.007) of TSCC patients. 28367232 2017 Upregulated long non-coding RNA LINC00152 expression is associated with progression and poor prognosis of tongue squamous cell carcinoma LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues up-regulated Further validation in a larger cohort including 205 ESCC patients, 82 patients suffering from esophagus dysplasia and 210 healthy controls confirmed that increased Linc00152, CFLAR-AS1 and POU3F3 might be potential biomarkers for predicting the early progress. We also revealed that circulating levels of three lncRNAs were associated with poor post-surgery prognosis of ESCC patients. 27855375 2016 Three Circulating LncRNA Predict Early Progress of Esophageal Squamous Cell Carcinoma. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 glioblastoma NA M9440/3 qPCR, Western blot etc. glioblastoma tissues, cell lines (NHAs, U87,U251, LN229, A172, and U118) up-regulated LINC00152 expression level was upregulated in glioblastoma tissues and cell lines. Overexpression of LINC00152 promoted the U87 and LN229 cell proliferation and invasion. Moreover, overexpression of LINC00152 suppressed the E-cadherin expression, where ectopic expression of LINC00152 promoted the N-cadherin, Vimentin, and Snail expression. Overexpression of LINC00152 suppressed the miR-107 expression in the U87 cell and enhanced the HMGA2 expression,which is a direct target gene of miR-107. In addition, we showed that the miR-107 expression was downregulated in the glioblastoma tissues and cell lines.Interesting, the expression of LINC00152 was negatively related with miR-107 expression in the glioblastoma tissues. Furthermore, LINC00152 promoted the glioblastoma cell proliferation and invasion through inhibiting miR-107 expression. 29671226 2018 LncRNA LINC00152 promoted glioblastoma progression through targeting the miR-107 expression. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, RNAi, Cell proliferation assay etc. ccRCC tissues, cell lines (786O, Caki-2, A498, ACHN, Caki-1) up-regulated Linc00152 expression was significantly up-regulated in cancerous tissues and cell lines compared with normal counterparts, and high Linc00152 expression was closely associated with advanced TNM stage. Further experiments demonstrated that overexpression of Linc00152 can significantly promote cell proliferation and invasion, inhibit cell cycle arrest in G1 phase and dramatically decrease apoptosis in both 786O and Caki-2 cell lines, whereas the opposite results were observed with attenuated Linc00152 expression. 27186403 2016 Long non-coding RNA Linc00152 is a positive prognostic factor for and demonstrates malignant biological behavior in clear cell renal cell carcinoma. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 lung cancer C34 NA qPCR, microarray etc. lung cancer tissues, cell lines up-regulated Our study indicates LINC00152 plays an important role in lung tumor growth and is potentially a diagnostic/prognostic marker. LINC00152 overexpression caused by histone acetylation. 28592840 2017 Overexpression of LINC00152 correlates with poor patient survival and knockdown impairs cell proliferation in lung cancer LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 lung adenocarcinoma C34 M8140/3 qPCR etc. lung adenocarcinoma tissues, cell lines (H1299, H1975, A549 and H1650) up-regulated Linc00152 was upregulated in lung adenocarcinoma. Linc00152 independently predicts poor prognosis and promotes tumor progression in lung adenocarcinoma. Linc00152 needs to be considered as a potential molecular target in future cancer pharmacology. Overexpression of Linc00152 in lung cancer cells stimulated proliferation, tumor cell invasion and migration. Knockdown of Linc00152 inhibited cell growth and cell invasion and migration.Kaplan-Meier and Cox proportional hazards analyses were used to analyze the overall survival (OS) and disease-free survival (DFS) rates. 28819405 2017 Linc00152 promotes Cancer Cell Proliferation and Invasion and Predicts Poor Prognosis in Lung adenocarcinoma. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay etc. glioma tissues, cell lines (U87, U251 and HEK) up-regulated Linc00152 was up-regulated in glioma tissues as well as in GSCs. Knockdown of linc00152 inhibited cell proliferation, migration and invasion, while promoted GSC apoptosis. Linc00152 regulated the malignant behavior of GSCs by binding to miR-103a-3p, which functions as a tumor suppressor.In addition, knockdown of linc00152 down-regulated forebrain embryonic zinc finger protein 1 (FEZF1),a direct target of miR-103a-3p which played an oncogenic role in GSCs.FEZF1 elevated promoter activities and up-regulated expression of the oncogenic gene cell division cycle 25A (CDC25A).CDC25A over-expression activated the PI3K/AKT pathways, which regulated the malignant behavior of GSCs.Linc00152 knockdown combined with over-expressed miR-103a-3p suppressed tumor growth and manifested high survival in nude mice. 28651608 2017 Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 colorectal cancer C19.9 NA qPCR tumors tissues, CRC cell line (HCT-116) up-regulated A cell culture under hypoxic conditions revealed several lncRNAs,such as LINC00152, whose levels were increased in the cytoplasm of colorectal cancer cells.A database study indicated that LINC00152 shares microRNA-binding sites, such as miR-138 and miR-193, with HIF1,thus suggesting that LINC00152 could possibly function as a competing endogenous RNA that can augment Hif1 translation in the cytoplasm of hypoxic colorectal cancer cells. 29345294 2017 Hypoxia stimulates the cytoplasmic localization of oncogenic long noncoding RNA LINC00152 in colorectal cancer. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (SMMC-7721, Hep3B, HCCLM3 and HepG2), HCC tissues down-regulated The results indicated that the expression level of LINC00152 was positively correlated with tumor size (OR=5.19, 95% CI: 2.33-11.52, p<.0001), TNM stage (OR=3.12, 95% CI: 1.77-5.51, p<.0001) and lymph node metastasis (OR=3.41, 95% CI: 2.13-5.48, p<.00001). Moreover, elevated LINC00152 could predict unfavorable OS with pooled HR of 1.66 (95% CI: 1.29-2.13, p<.0001) and poor DFS (HR=2.13, 95% CI: 1.39-3.25, p=.0005) in cancer patients. CONCLUSION: LINC00152 was correlated with advanced clinicopathological features and poor prognosis as a novel predictive biomarker in various cancers. 29617624 2018 Long noncoding RNA LINC00152 as a novel predictor of lymph node metastasis and survival in human cancer: a systematic review and meta-analysis. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 gastric cancer C16 NA Microarray, qPCR, Western blot, RNAi etc. gastric cancer tissues, cell lines (MGC-803, AGS, SGC-7901, BGC-823 and GES-1) up-regulated LINC00152 was proven to have a higher expression level in GC tissues than in the adjacent normal tissues.GC cells proliferation was inhibited after LINC00152 was down-regulated.LINC00152 inhibited the expression of miR-193a-3p,which negatively regulated MCL1 In addition,GC cells proliferation was inhibited by cell transfection with shRNA-MCL1,and enhanced by transfection with miR-193a-3p mimics. Our study suggested that LINC00152 was overexpressed in GC tissues,and it down-regulated miR-193a-3p to enhance miR-193a-3p expression thereby promoting GC cells proliferation.Furthermore,an interesting discovery is that LINC00152 works as a competing endogenous RNA (ceRNA) through sponging miR-193a-3p and shares the identical responsive elements of miR-193a-3p with some signaling pathway factor like erb-b2 receptor tyrosine kinase 4 (ERBB4). 29339419 2018 LINC00152 down-regulated miR-193a-3p to enhance MCL1 expression and promote gastric cancer cells proliferation. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 glioblastoma C22.0 M8170/3 qPCR, Western blot analysis, RNA-seq U87 cells, brain tumors and normal brain tissue up-regulated LINC00152/CYTOR is upregulated in glioblastoma multiforme (GBM) and aggressive wild-type IDH1/2 grade II/III gliomas and upregulation associates with poor patient outcomes.LINC00152 and its homolog MIR4435-2HG associate with aggressive tumors and promote cellular invasion through a mechanism that requires the structural integrity of a hairpin structure. 29991527 2018 LINC00152 Promotes Invasion Through a 3'-hairpin Structure and Associates with Prognosis in Glioblastoma. LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 colorectal cancer C19.9 NA qPCR, Western blot, etc. 80 human CRC tissue samples, 40 non?cancerous tissue samples. CRC cell lines (SW480, SW620 , LoVo). down-regulation Collectively, these findings demonstrate the critical role of lnc00152 in tumor growth and progression in CRC, and identify a novel therapeutic target associated with CRC development and progression. Kaplan?Meyer overall survival curves display higher lnc00152 levels in patients with colorectal cancer (CRC) with lower survival times (log?rank test, P=0.047). However, further clarifications of the systemic correlation between miRNAs and lncRNAs are required. 29956750 2018 Long non?coding RNA 00152 functions as a competing endogenous RNA to regulate NRP1 expression by sponging with miRNA?206 in colorectal cancer. LINC00161 LINC00161, C21orf100, NCRNA00161 118421 ENSG00000226935 NR_026552 GRCh38_21:28539318-28540355 hepatocellular carcinoma C22.0 M8170/3 qPCR, in vitro knockdown etc. hepatocellular carcinoma tissues, cell lines (HepG2, Hep3B, Huh7 and SMMC7721) up-regulated The result showed that the expression level of LINC00161 was significantly higher in HCC tissues. Further analysis indicated that HCC patients with higher LINC00161 expression have shorter survival. 28915581 2017 Up-regulation of LINC00161 correlates with tumor migration and invasion and poor prognosis of patients with hepatocellular carcinoma LINC00174 NA 285908 ENSG00000179406 NR_026873 GRCh38_7:66376044-66493566 colorectal cancer C19.9 NA qPCR, Luciferase reporter assay etc. lung tissues, cell lines (DLD1, HCT116, LOVO, RKO, LS174T, HCT8, HR28348, HT29, SW620, SW480 and NCM460) up-regulated increased expression of LINC00174 in CRC tissues and cells in comparison to their corresponding controls.Moreover,the aberrant overexpression of LINC00174 indicated the poor prognosis of CRC patients.Silence of LINC00174 was able to repress CRC cell growth in vitro and in vivo.We first reported that transcription factor STAT1 mediated LINC00174 expression in CRC. In addition, rescue assay was performed to further confirm that LINC00174 contributed to CRC progression by regulating miR-1910-3p/TAZ signal pathway. Taken together, our study discovered the oncogenic role of LINC00174 in clinical specimens and cellular experiments,showing the potential LINC00174/miR-1910-3p/TAZ pathway. 29729381 2018 STAT1-mediated upregulation of lncRNA LINC00174 functions a ceRNA for miR-1910-3p to facilitate colorectal carcinoma progression through regulation of TAZ. LINC00176 NA NA NA NA GRCh38_20:64034344-64039962 hepatocellular carcinoma C22.0 M8170/3 RNA-seq, Microarray, qPCR liver tissue, HCC cell lines (Huh7 and HepG2) up-regulated Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185. Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185. In Linc00176-depleted HCC, these miRNAs were released from Linc00176 and downregulated their target mRNAs. 28869604 2017 Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs. LINC00222 C6orf181, dJ354J5.2, NCRNA00222 387111 ENSG00000203801 NR_033376 GRCh38_6:108751654-108769942 lung adenocarcinoma C34 M8140/3 PCR, Western blot analysis The human lung adenocarcinoma cell lines (SPC-A-1 and LTEP-a-2), lung adenocarcinoma tissues and adjacent non-tumor lung tissues down-regulated LINC00222 is downregulated in lung adenocarcinoma tissues. Enforced expression of LINC00222 significantly inhibited the proliferation, migration and invasive ability of lung adenocarcinoma cells, and also induced apoptosis. Furthermore, overexpression of LINC00222 enhanced the activity of glycogen synthase kinase-3B (GSK3B), which is a key element of the Wnt signaling pathway. 29990868 2018 Long non-coding RNA LINC00222 regulates GSK3β activity and promotes cell apoptosis in lung adenocarcinoma. LINC00261 LINC00261, ALIEN, C20orf56, DEANR1, HCCDR1, NCRNA00261, onco-lncRNA-17 140828 ENSG00000259974 NR_001558 GRCh38_20:22547671-22578642 non small cell lung cancer C34 M8046/3 qPCR non-small cell lung cancer tissues down-regulated the LINC00261 expression level in NSCLC tissues was suppressed compared with that in adjacent normal lung tissues.Low expression of LINC00261 was found to significantly correlate with TNM stage, lymph node status, and distant metastasis.low LINC00261 expression level was associated with poorer overall survival.low expression of LINC00261 was an independent adverse prognostic factor of NSCLC. 29272004 2017 Decreased expression of long non-coding RNA LINC00261 is a prognostic marker for patients with non-small cell lung cancer: a preliminary study. LINC00261 LINC00261, ALIEN, C20orf56, DEANR1, HCCDR1, NCRNA00261, onco-lncRNA-17 140828 ENSG00000259974 NR_001558 GRCh38_20:22547671-22578642 hepatocellular carcinoma C22.0 M8170/3 qRT-PCR, Western blot, in vitro knockdown HCC tissues, HCC cell lines (SMCC-7721, MHCC97L and MHCC97H) down-regulated LINC00261 was frequently lower in HCC tissues compared to adjacent normal tissues. Decreased LINC00261 expression associated with lager tumor size, TNM stage (III-IV) and poor overall survival time of HCC patients. The functional assays demonstrated that overexpression of LINC00261 in HCC cells inhibited cell proliferation, cell colony formation, cell invasion and EMT process in vitro. Moreover, we also demonstrated that upregulation of LINC00261 significantly inhibited Notch signaling by downregulating Notch1 and Hes-1 expression in HCC cells. 29278875 2018 LINC00261 suppresses cell proliferation, invasion and Notch signaling pathway in hepatocellular carcinoma. LINC00261 LINC00261, ALIEN, C20orf56, DEANR1, HCCDR1, NCRNA00261, onco-lncRNA-17 140828 ENSG00000259974 NR_001558 GRCh38_20:22547671-22578642 gastric cancer C16 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. primary GC tissues, cell lines (MGC803, BGC823, MKN28, MKN45, and SGC7901) down-regulated LINC00261 was downregulated in GC cell lines and cancerous tissues, as compared with normal gastric epithelial cells and adjacent noncancerous tissue samples. Low LINC00261 expression was correlated with deeper tumor invasion, higher tumor stage, and lymphatic metastasis. Univariate and multivariate analyses indicated that low LINC00261 expression predicted poor prognosis. Ectopic expression of LINC00261 impaired cell migration and invasion, leading to the inhibition of metastasis in vitro and in vivo. Knockdown of LINC00261 expression promoted cell migration and invasion in vitro. Overexpression of LINC00261 was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin, and Vimentin expression. 27439973 2016 Decreased expression of the long noncoding RNA LINC00261 indicate poor prognosis in gastric cancer and suppress gastric cancer metastasis by affecting the epithelial-mesenchymal transition. LINC00271 LINC00271, C6orf217, NCRNA00271 100131814 ENSG00000231028 NR_026805 GRCh38_6:135497801-135716055 papillary thyroid cancer NA M8260/3 qPCR etc. primary PTC tissues down-regulated The results suggested LINC00271 was significantly downregulated in PTC compared with the level in the adjacent normal tissues 27833134 2016 Long intergenic non-coding RNA 271 is predictive of a poorer prognosis of papillary thyroid cancer. LINC00319 NA 284836 ENSG00000188660 NR_026960 GRCh38_21:43446601-43453893 lung cancer C34 NA qPCR, Western blot cell lines (PAa, Agi Y-83a, A549, HBE, Anip-973) up-regulated linc00319 increased the proliferation and invasion of A549 cells,and suppressed cell apoptosis.linc00319 promotes cell proliferation and invasion in lung cancer cells by directly binding with and downregulating the tumor suppressor miR-32.High level of HOTAIR was demonstrated to be correlated with invasion,metastasis,and poor survival in lung cancer patients. 28800794 2017 Long Intergenic Noncoding RNA 319 (linc00319) Promotes Cell Proliferation and Invasion in Lung Cancer Cells by Directly Downregulating the Tumor Suppressor MiR-32. LINC00319 NA 284836 ENSG00000188660 NR_026960 GRCh38_21:43446601-43453893 lung adenocarcinoma C34 M8140/3 qPCR, Luciferase reporter assay etc. lung adenocarcinoma tissues, cell lines (H157, 95D, SPC-A-1, A549, SK-LU-1, Calu-3, HCC-78, H1299 and H1975) up-regulated We observed that increased expression of LINC00319 in lung adenocarcinoma tissues and cells in comparison to their corresponding controls.Moreover,the aberrant overexpression of LINC00319 indicated the poor prognosis of lung adenocarcinoma patients.Silence of LINC00319 was able to repress lung adenocarcinoma cell growth in vitro.Rescue assay was performed to further confirm that LINC00319 contributed to lung adenocarcinoma progression by regulating miR-450b-5p/EZH2 signal pathway.Taken together, our study discovered the oncogenic role of LINC00319 in clinical specimens and cellular experiments,showing the potential LINC00319/miR-450b-5p/EZH2 pathway. 29408583 2018 Long intergenic non-protein coding RNA 319 aggravates lung adenocarcinoma carcinogenesis by modulating miR-450b-5p/EZH2. LINC00324 C17orf44,NCRNA00324 284029 ENSG00000178977 NR_026951 GRCh38_7:8220642-8224043 gastric cancer C16 NA qPCR, Western blot, RIP, etc. gastric cancer tissues, cell lines (SGC7901, BGC823, MGC803, AGS, GES-1) up-regulated The overexpression of LINC00324 was correlated with advanced TNM stage, larger tumor size, and lymph node metastasis as well as poor prognosis. LINC00324 could combine with the RNA-binding protein (RBP) human antigen R (HuR) and thus stabilize the expression of FAM83B. 29915327 2018 Long intergenic non-coding RNA 00324 promotes gastric cancer cell proliferation via binding with HuR and stabilizing FAM83B expression. LINC00339 LINC00339, HSPC157, NCRNA00339 29092 ENSG00000218510 NR_023918 GRCh38_1:22024558-22031223 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR, Cell proliferation assay etc. PDAC tissues, cell lines (AsPC-1, BxPC-3, Capan-2, CFPAC-1, HPAC, MIA PaCa-2, PANC-1 and SW1990) down-regulated The qRT-PCR results showed that CRNDE, NR_036488, ENSG00000244649, AFAP1-AS and UCA1 expression was significantly increased and ENSG00000218510 expression was remarkably decreased in PDAC tissues compared with paired normal pancreatic tissues. Consistent with the findings in PDAC tissues, CRNDE, NR_036488, ENSG00000244649, AFAP1-AS1 and UCA1 expression was dramatically enhanced and ENSG00000218510 reduced in all or most of 8 PDAC cell lines in relative to the nonmalignant HPDE6-C7 cells or hTERT-HPNE cells at the RNA level. 27628540 2016 Analysis of long non-coding RNA expression profiles in pancreatic ductal adenocarcinoma. LINC00339 LINC00339, HSPC157, NCRNA00339 29092 ENSG00000218510 NR_023918 GRCh38_1:22024558-22031223 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (U87,U251), glioma tissues up-regulated Knockdown of LINC00339 inhibited glioma cell proliferation, migration, invasion, and tube formation,meanwhile downregulating the expression of VM-related molecular MMP-2 and MMP-14.TWIST1 upregulated the promoter activities of MMP-2 and MMP-14. 29499931 2017 Long Non-coding RNA LINC00339 Stimulates Glioma Vasculogenic Mimicry Formation by Regulating the miR-539-5p/TWIST1/MMPs Axis. LINC00339 LINC00339, HSPC157, NCRNA00339 29092 ENSG00000218510 NR_023918 GRCh38_1:22024558-22031223 non small cell lung cancer C34 M8046/3 qPCR, Western blot, RIP, Luciferase reporter assays,etc. NSCLC tissues, cell lines (SK-MES-1, Calu-3, A549, H460, NHBE) up-regulated Results showed that LINC00339 was significantly up-regulated in NSCLC tissue and cells, which indicated the poor prognosis of NSCLC patients. LINC00339 silencing inhibited the proliferation and invasion, accelerated the apoptosis, and suppressed the tumor growth of NSCLC cells in vitro and in vivo. LINC00339 promoted the NSCLC progression via FOXM1 via targeting miR-145. 29906749 2018 Long non-coding RNA LINC00339 facilitates the tumorigenesis of non-small cell lung cancer by sponging miR-145 through targeting FOXM1. LINC00342 LINC00342, NCRNA00342 150759 ENSG00000232931 NR_103734 GRCh38_2:95807118-95816215 non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. NSCLC tissues, cell line (A549) up-regulated LINC00342 was significantly up-regulated in NSCLC tissues compared with normal tissues. We confirmed the over-expression of LINC00342 in a cohort of NSCLC patients and found LINC00342 expression level was positively correlated with lymph node metastasis and TNM stages. 27299310 2016 Analysis of Long Non-Coding RNA Expression Profiles in Non-Small Cell Lung Cancer. LINC00460 NR_034119 728192 ENSG00000233532 NR_034119 GRCh38_13:106374477-106384315 nasopharyngeal cancer C11 NA RNA-seq, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown tissues, NPC cell lines (SUNE-1, CNE-1, HNE-1, CNE-2, C666-1 and HONE-1) up-regulated LINC00460 was markedly increased in NPC tissues and cells compared to their corresponding controls. Silencing LINC00460 was able to suppress NPC cell growth in vitro while overexpressing LINC00460 reversed this process. LINC00460 contributed to the progression of NPC through regulating miR-149-5p/IL6 signal pathway. 28987345 2017 LncRNA-LINC00460 facilitates nasopharyngeal carcinoma tumorigenesis through sponging miR-149-5p to up-regulate IL6. LINC00460 NR_034119 728192 ENSG00000233532 NR_034119 GRCh38_13:106374477-106384315 non small cell lung cancer C34 M8046/3 qPCR etc. lung cancer tissues, cell lines (A549, H1299, H1975, H460, PC9 and SPC-A1) up-regulated we found that the expression of the lncRNA linc00460 is significantly upregulated in NSCLC tumors and associated with poor prognosis for NSCLC patients, implying that linc00460 is important for lung cancer development.Functional studies through gain- and loss-of-function strategies showed that linc00460 promotes cell migration and invasion through inducing epithelial-mesenchymal transition in lung cancer cells, whereas it has no effect on cell proliferation. The mechanism investigations through RNA pull-down assay and mass spectrometry identified that hnRNP K physically interacts with linc00460, and it also participates in cell migration and invasion. 29409808 2018 Long non-coding RNA linc00460 promotes epithelial-mesenchymal transition and cell migration in lung cancer cells. LINC00460 NR_034119 728192 ENSG00000233532 NR_034119 GRCh38_13:106374477-106384315 esophageal squamous cell cancer NA NA RNA-seq, Microarray, qRT-PCR, in vitro knockdown ESCC tissues, Human esophageal cancer cell lines (KYSE150, KYSE180, KYSE450, KYSE70, KYSE140 and TE3) up-regulated A novel three-lncRNA signature, comprised of RP11-366H4.1.1 (ENSG00000248370), LINC00460 (ENSG00000233532) and AC093850.2 (ENSG00000230838), was identified. The signature classified patients into high-risk and low-risk groups with different overall survival (OS) and disease-free survival (DFS). The signature indicates that patients in the high-risk group show poor OS and DFS, whereas patients with a low-risk group show significantly better outcome. The independence of the signature was validated by multivariable Cox regression analysis. 29409459 2018 A three-lncRNA signature predicts overall survival and disease-free survival in patients with esophageal squamous cell carcinoma. LINC00460 NR_034119 728192 ENSG00000233532 NR_034119 GRCh38_13:106374477-106384315 colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues down-regulated The expression of all 18 candidate lncRNAs was evaluated by RT-qPCR, using 80 pairs of CRC and control tissue samples. Among these, eight lncRNAs (MALAT-1, NR_029373, NR_046321, NR_034119, GAS5, BANCR, NR_026817 and PCAT-1) were found significantly dysregulated in CRC tumor tissues compared with controls. 27591862 2016 Identification of long noncoding RNAs as potential novel diagnosis and prognosis biomarkers in colorectal cancer. LINC00470 C18orf2 56651 ENSG00000132204 NR_023925 GRCh38_18:1254383-1408344 glioblastoma NA M9440/3 qPCR, RNAi, Western blot etc. cell line (U251 and U87) up-regulated LINC00470 was a positive regulator for AKT activation in GBM. LINC00470 bound to FUS and AKT to form a ternary complex, anchoring FUS in the cytoplasm to increase AKT activity. Higher pAKT activated by LINC00470 inhibited ubiquitination of HK1, which affected glycolysis, and inhibited cell autophagy. Furthermore, higher LINC00470 expression was associated with GBM tumorigenesis and poor patient prognosis. 29866190 2018 A cytoplasmic long noncoding RNA LINC00470 as a new AKT activator to mediate glioblastoma cell autophagy. LINC00472 LINC00472, C6orf155 79940 ENSG00000233237 NR_121612 GRCh38_6:71344344-71420769 breast cancer C50 NA qPCR, Cell proliferation assay, Cell migration assay etc. cell lines (MCF7 and SKBR3) down-regulated Our qPCR results showed that high LINC00472 expression was associated with less aggressive breast tumors and more favorable disease outcomes. Patients with high expression of LINC00472 had significantly reduced risk of relapse and death compared to those with low expression. Cell culture experiments showed that up-regulation of LINC00472 expression could suppress breast cancer cell proliferation and migration. 25865225 2015 Prognostic and predictive values of long non-coding RNA LINC00472 in breast cancer. LINC00472 LINC00472, C6orf155 79940 ENSG00000233237 NR_121612 GRCh38_6:71344344-71420769 lung adenocarcinoma C34 M8140/3 RNA-seq, qPCR etc. LUAD tissues down-regulated The results showed that CHIAP2, LINC00472, LINC00961 and MGC27382 were downregulated in LUAD tumor tissues when compared with adjacent non-tumor lung tissues, while AFAP1-AS1, CHIAP2 and FER1L4 were upregulated in LUAD tumor tissues. 27826625 2016 Integrated analysis of long non-coding RNA-associated ceRNA network reveals potential lncRNA biomarkers in human lung adenocarcinoma. LINC00473 LINC00473, C6orf176, bA142J11.1 90632 ENSG00000223414 NR_026860 GRCh38_6:165908802-165988048 cervical cancer C53 NA qPCR, Western blotting etc. cell lines (SiHa, HeLa, Caski, C4-1, C-33a) up-regulated LINC00473 promoted cell proliferation and inhibited cell apoptosis in cervical cancer cells in vitro. Moreover, we found that LINC00473 enhanced the growth of cervical cancer cells in vivo. Mechanistic investigation showed that LINC00473 directly interacted with ILF2 and suppressed its degradation. Finally, we demonstrated that miR-34a reduced the stability of LINC00473. These fndings may have important implications for developing novel therapeutic strategies for cervical cancer.Patients with higher LINC00473 levels had shorter overall survival time than those with lower LINC00473 levels. 29218240 2017 The long noncoding RNA LINC00473, a target of microRNA 34a, promotes tumorigenesis by inhibiting ILF2 degradation in cervical cancer LINC00473 LINC00473, C6orf176, bA142J11.1 90632 ENSG00000223414 NR_026860 GRCh38_6:165908802-165988048 lung cancer C34 NA microarray, qPCR, RNA-ISH, FISH etc. lung cancer tissues up-regulated We discovered that LINC00473 is consistently the most highly induced gene in LKB1-inactivated human primary NSCLC samples and derived cell lines. Elevated LINC00473 expression correlated with poor prognosis, and sustained LINC00473 expression was required for the growth and survival of LKB1-inactivated NSCLC cells. Mechanistically, LINC00473 was induced by LKB1 inactivation and subsequent cyclic AMP-responsive element-binding protein (CREB)/CREB-regulated transcription coactivator (CRTC) activation. We determined that LINC00473 is a nuclear lncRNA and interacts with NONO, a component of the cAMP signaling pathway, thereby facilitating CRTC/CREB-mediated transcription 27140397 2016 cAMP/CREB-regulated LINC00473 marks LKB1-inactivated lung cancer and mediates tumor growth LINC00473 LINC00473, C6orf176, bA142J11.1 90632 ENSG00000223414 NR_026860 GRCh38_6:165908802-165988048 wilms tumor C64.9 M8960/3 qRT- PCR, Western blot, Luciferase reporter assay Wilms tumour tissues, Wilms tumour cell line (SK-NEP-1) up-regulated the expression of LINC00473 was elevated in tumour tissues than that in relative normal tissues. Higher LINC00473 levels correlated to higher stage and unfavourable histology Wilms tumour. Mechanistically, knockdown of LINC00473 inhibited cell vitality and induced Bcl-2-dependent apoptosis and G1/S arrest via CDK2 and cyclin D1.Moreover,LINC00473 harboured binding sites for miR-195 and limited miR-195 availability in a dose-dependent manner.Forced expression of miR-195 impaired tumour survival and metastasis, which, however,could be restored by LINC00473. Furthermore, IKKa was the downstream of LINC00473/miR-195 signals and could be directly targeted by miR-195 to participate LINC00473-induced tumour progression. 29159834 2017 LINC00473 antagonizes the tumour suppressor miR-195 to mediate the pathogenesis of Wilms tumour via IKKa. LINC00473 LINC00473, C6orf176, bA142J11.1 90632 ENSG00000223414 NR_026860 GRCh38_6:165908802-165988048 mucoepidermoid carcinoma C73 M8430/3 Microarray, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RNAi etc. cell lines (UM-HMC3A and UM-HMC3B, H3118, MEC, H292), mucoepidermoid carcinoma tissue down-regulated In this study, we investigated the role of LINC00473 in mediating CRTC1-MAML2 oncogenic activity in human MEC. We found that LINC00473 transcription was significantly induced in human CRTC1-MAML2-positive MEC cell lines and primary MEC tumors, and was tightly correlated with the CRTC1-MAML2 RNA level. LINC00473 induction was dependent on the ability of CRTC1-MAML2 to activate CREB-mediated transcription. Depletion of LINC00473 significantly reduced the proliferation and survival of human MEC cells in vitro and blocked the in vivo tumor growth in a human MEC xenograft model. RNA in situ hybridization analysis demonstrated a predominantly nuclear localization pattern for LINC00473 in human MEC cLINC00473 depletion resulted in differential expression of genes important in cancer cell growth and survival. LINC00473 likely regulates gene expression in part through its ability to bind to a cAMP signaling pathway component NONO, enhancing the ability of CRTC1-MAML2 to activate CREB-mediated transcription. 29353885 2017 CRTC1-MAML2 fusion-induced lncRNA LINC00473 expression maintains the growth and survival of human mucoepidermoid carcinoma cells LINC00511 LINC00511, LCAL5, onco-lncRNA-12 400619 ENSG00000227036 NR_033876 GRCh38_17:72323123-72640472 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, Luciferase reporter assay, Western blot, RIP pancreatic cancer, cell lines (PANC-1, MIA PaCa-2, Capan-2, SW1990, ASPC-1, BxPC-3) up-regulated The aberrant up-regulation of linc00511 was detected in PDAC cell lines and patient specimens compared with controls.An increase in linc00511 expression indicates the adverse clinical pathological characteristics and poor prognosis. linc00511 depletion in PDAC cells decreased proliferation,migration, invasion and endothelial tube formation.linc00511 could up-regulate VEGFA via its competing endogenous RNA (ceRNA) activity on hsa-miR-29b-3p. 28984028 2017 Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa-miR-29b-3p in pancreatic ductal adenocarcinoma. LINC00511 LINC00511, LCAL5, onco-lncRNA-12 400619 ENSG00000227036 NR_033876 GRCh38_17:72323123-72640472 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, RNA pull-down assay etc. NSCLC tissues, cell lines (A549, SK-MES-1, H1299, 95D, H460, H520, H1975, H157, SK-LU-1, and SPC-A-1) up-regulated Herein, we identified LINC00511 as an oncogenic lncRNA by driving tumorigenesis in NSCLC. We found LINC00511 was upregulated and associated with oncogenesis, tumor size, metastasis, and poor prognosis in NSCLC. Moreover, LINC00511 affected cell proliferation, invasiveness, metastasis, and apoptosis in multiple NSCLC cell lines. Mechanistically, LINC00511 bound histone methyltransferase enhancer of zeste homolog 2 ((EZH2, the catalytic subunit of the polycomb repressive complex 2 (PRC2), a highly conserved protein complex that regulates gene expression by methylating lysine 27 on histone H3), and acted as a modular scaffold of EZH2/PRC2 complexes, coordinated their localization, and specified the histone modification pattern on the target genes, including p57, and consequently altered NSCLC cell biology. 27845772 2016 Long Intergenic Noncoding RNA 00511 Acts as an Oncogene in Non-small-cell Lung Cancer by Binding to EZH2 and Suppressing p57. LINC00514 NA 283875 ENSG00000262152 NR_033861 GRCh38_16:2988961-2994509 neuroendocrine prostate cancer NA NA RNA-seq, Microarray, qPCR etc. neuroendocrine prostate cancer tissues up-regulated Top candidate lncRNAs FENDRR, H19, LINC00514, LINC00617, and SSTR5-AS3 identified in this study are implicated in the development of NEPC. 29757368 2018 The long noncoding RNA landscape of neuroendocrine prostate cancer and its clinical implications. LINC00628 NA 127841 ENSG00000280924 NR_027022 GRCh38_1:204368431-204369719 breast cancer C50 NA qPCR, Western blot, Cell proliferation assay, Cell migration and invasion assay etc. breast cancer tissues, cell lines (LCC9, MDA-MB-231, LCC2 and MCF-7) down-regulated The relative expression level of LINC00628 in breast cancer tissues and cell lines were significantly decreased. The overexpression of LINC00628 suppressed breast cancer cells proliferation, invasion and migration. Further, with the overexpression of LINC00628, cell cycle was arrested in G0/G1 phase in breast cancer cells and cell apoptosis was promoted. The relative expression of Caspase-3 and Bax protein were significantly increased and the relative expression of Bcl-2 protein was significantly decreased after transfection with LINC00628. 28165561 2017 Long non-coding RNA LINC00628 suppresses the growth and metastasis and promotes cell apoptosis in breast cancer. LINC00665 NA 100506930 ENSG00000232677 NR_038278 GRCh38_19:36313067-36331718 hepatocellular carcinoma C22.0 M8170/3 RNA-seq, qPCR etc. hepatocellular carcinoma tissues up-regulated Overexpression of LINC00665 in patients with HCC was significantly associated with gender, tumor grade, stage, and tumor cell type. Overexpression of LINC00665 in patients with HCC was significantly associated with overall survival (OS) (HR=1.47795%; CI: 1.046-2.086). Bioinformatics analysis identified 469 related genes and further analysis supported a hypothesis that LINC00665 regulates pathways in the cell cycle to facilitate the development and progression of HCC through ten identified core genes: CDK1, BUB1B, BUB1, PLK1, CCNB2, CCNB1, CDC20, ESPL1, MAD2L1, and CCNA2. 29728556 2018 Expression of the Long Intergenic Non-Protein Coding RNA 665 (LINC00665) Gene and the Cell Cycle in Hepatocellular Carcinoma Using The Cancer Genome Atlas, the Gene Expression Omnibus, and Quantitative Real-Time Polymerase Chain Reaction. LINC00668 NA 400643 ENSG00000265933 NR_034100 GRCh38_18:6919496-6929966 oral squamous cell carcinoma C06.9 M8070/3 RNAi, Western blot, qPCR, Luciferase reporter assays, RNA pull-down assays OSCC tissues, cell lines (SCC4, SCC9, SCC1, SCC25, TU183, HSU3, FADU, OEC-M1, SNU1041, and SCC15) up-regulated LINC00668 is up-regulated in human primary OSCC tissues.We first demonstrated that LINC00668 expression was up-regulated, which was correlated with tumor progression, and miR-297 down-regulated in OSCC tissues and cells. Importantly, LINC00668 expression was negatively correlated with miR-297 expression in OSCC tissues. Loss-of-function of LINC00668 revealed that LINC00668 functioned as a ceRNA for miR-297 to facilitate VEGFA expression, promoting OSCC progression. Finally, we confirmed that LINC00668 promoted OSCC activity through VEGFA signaling.In conclusion, these results suggest that LINC00668 promotes OSCC tumorigenesis via miR-297/VEGFA axis, which may provide a new target for the diagnosis and therapy of OSCC disease. 28564590 2017 Long intergenic non-coding RNA 668 regulates VEGFA signaling through inhibition of miR-297 in oral squamous cell carcinoma. LINC00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 100499467 NA NR_036488 GRCh38_17:72403322-72592804 pancreatic ductal adenocarcinoma C25.3 M8500/3 RNA-seq, qPCR, Western blot cell lines (PANC-1 PANC1, BxPC3, MiaPaCa2 and Aspc1,) up-regulated We generated a catalogue of PDA-associated lncRNAs. Systems biology and experimental functional analysis of two epithelial lncRNAs (LINC00673 and FAM83H-AS1) suggest they regulate the transcriptional profile of pancreatic tumour samples and PDA cell lines.We also detected lncRNAs located in proximity to GATA6 and FOXA2, both important transcription factors involved in pancreas development. PDA is characterised by high penetrance mutations in four genes (KRAS, TP53, CDKN2A and SMAD4).We performed a similar analysis and identified five candidate lncRNAs within loci that harboured somatic SNP variants associated with increased risk of PDA 29440233 2018 Comprehensive characterisation of compartment-specific long non-coding RNAs associated with pancreatic ductal adenocarcinoma. LINC00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 100499467 NA NR_036488 GRCh38_17:72403322-72592804 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay, Western blot, RNAi hepatocellular carcinoma tissues, cell lines (HCCLM3, MHCC97L,HepG2, Hep3B and Huh7,THLE-3, L-02) up-regulated LINC00673 was upregulated in HCC cancerous tissue. LINC00673 overexpression is associated with poor prognosis and low survival rate. LINC00673 silencing inhibited the proliferation,invasion and epithelial-mesenchymal transition (EMT) of HCC cells in vitro. miR-205 targeted 3'-UTR of LINC00673.miR-205 could reverse the effect of LINC00673 on HCC cells.LINC00673 silencing reduced the tumor volume and weight. 29312806 2017 Long non-coding RNA LINC00673 promotes hepatocellular carcinoma progression and metastasis through negatively regulating miR-205 LINC00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 100499467 NA NR_036488 GRCh38_17:72403322-72592804 tongue squamous cell carcinoma C02 M8070/3 qPCR, RNAi, Cell migration and invasion assay, ISH etc. TSCC tissues, cell lines (Tca8113 and Cal27) up-regulated LINC00673 was significantly upregulated in TSCC samples. Then we examined LINC00673 expression in 202 TSCC tissue specimens, LINC00673 is highly expressed in a significant proportion of human TSCC biopsies and correlates with poor prognosis. Knockdown LINC00673 significantly inhibited the cell invasion and migration capability in TSCC cells. 28039470 2017 Overexpression long non-coding RNA LINC00673 is associated with poor prognosis and promotes invasion and metastasis in tongue squamous cell carcinoma. LINC00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 100499467 NA NR_036488 GRCh38_17:72403322-72592804 gastric cancer C16 NA qPCR, Western blot, RIP etc. gastric cancer cell lines (MKN45, AGS, MKN-28 ,Sgastric cancer-7901) down-regulated RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) proved that LINC00673 suppressed KLF4 expression by interacting with EZH2 and DNMT1 in GC cells. Moreover, we confirmed that LINC00673 promoted cell proliferation and invasion by partly repressing KLF4 expression in GC. Taken together, these results indicated that LINC00673 may be a prognostic biomarker and therapeutic target for GC patients.Higher LINC00673 expression predicted poor disease-free survival (DFS) and overall survival (OS) in GC patients. 29221147 2017 Long noncoding RNA LINC00673 epigenetically suppresses KLF4 by interacting with EZH2 and DNMT1 in gastric cancer LINC00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 100499467 NA NR_036488 GRCh38_17:72403322-72592804 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. cell lines (BEAS-2B, A549, H1975, H596, H520, H1650, H1703 and HEK-293) up-regulated high linc00673 expression was associated with poor prognosis of NSCLC patients.Linc00673 acted as a ceRNA by sponging miR-150-5p and regulated ZEB1 expression indirectly. linc00673 modulated cell proliferation, migration, invasion and EMT by sponging miR-150-5p and regulating ZEB1 expression indirectly. the inhibition of linc00673 significantly attenuated the tumorigenesis ability of A549 cells in vivo. Linc00673 is associated with poor survival in NSCLC patients. 28697764 2017 Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p. LINC00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 100499467 NA NR_036488 GRCh38_17:72403322-72592804 breast cancer C50 NA RNA-seq, qPCR breast cancer tissues up-regulated We identified lnc00673 (ERRLR01) as a marker of overall survival (OS) in breast cancer patients.ERRLR01 levels were elevated in triple-negative breast cancer (TNBC) as compared with Luminal-A,Luminal-B, and HER2 breast cancer subtypes. ERRLR01 levels were also inversely correlated with breast cancer survival across all breast cancer patients.OS in ERa-tumors correlated with negative overall survival,while in ERa+ tumors,ERRLR01 correlated with positive outcomes.This suggests ERRLR01 is modulated by hormone signaling in breast cancer.ERRLR01 correlated with distinct pathways including epithelial development and cellular differentiation. 28795861 2017 linc00673 (ERRLR01) is a prognostic indicator of overall survival in breast cancer. LINC00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 100499467 NA NR_036488 GRCh38_17:72403322-72592804 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR, Cell proliferation assay etc. PDAC tissues, cell lines (AsPC-1, BxPC-3, Capan-2, CFPAC-1, HPAC, MIA PaCa-2, PANC-1 and SW1990) up-regulated The qRT-PCR results showed that CRNDE, NR_036488, ENSG00000244649, AFAP1-AS and UCA1 expression was significantly increased and ENSG00000218510 expression was remarkably decreased in PDAC tissues compared with paired normal pancreatic tissues. Consistent with the findings in PDAC tissues, CRNDE, NR_036488, ENSG00000244649, AFAP1-AS1 and UCA1 expression was dramatically enhanced and ENSG00000218510 reduced in all or most of 8 PDAC cell lines in relative to the nonmalignant HPDE6-C7 cells or hTERT-HPNE cells at the RNA level. 27628540 2016 Analysis of long non-coding RNA expression profiles in pancreatic ductal adenocarcinoma. LINC00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 100499467 NA NR_036488 GRCh38_17:72403322-72592804 melanoma NA M8720/3 qPCR, Flow cytometry assay, RNA pull-down assay etc. cell lines (A375, HEK293T) up-regulated Increased expression of this lncRNA, SLNCR1, mediates melanoma invasion through a highly conserved sequence similar to that of the lncRNA SRA1. Using a sensitive technique we term RATA (RNA-associated transcription factor array), we show that the brain-specific homeobox protein 3a (Brn3a) and the androgen receptor (AR) bind within and adjacent to SLNCR1's conserved region, respectively. SLNCR1, AR, and Brn3a are specifically required for transcriptional activation of matrix metalloproteinase 9 (MMP9) and increased melanoma invasion. 27210747 2016 The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region. LINC00704 MANCR NA ENSG00000231298 NA GRCh38_10:4650185-4678154 thyroid cancer C73.9 NA qPCR, Western blot, etc. cell lines (BHT101, BCPAP) down-regulated Downregulation of LINC00704 could significantly impair thyroid cancer cells proliferation, colony formation, inhibit cell-cycle progression and cell invasion, and induce cell apoptosis. 29923329 2018 Identification of differential expressed lncRNAs in human thyroid cancer by a genome-wide analyses. LINC00857 LINC00857 439990 ENSG00000237523 NR_038464 GRCh38_10:80207710-80219657 lung cancer C34 NA microarray, qPCR, RNAi etc. lung cancer tissues, cell lines (H1299, H838 and SK-LU-1) down-regulated LINC00857, a top deregulated lncRNAs, was overexpressed in tumors and significantly associated with poor survival in LUAD. knockdown of LINC00857 with siRNAs decreased tumor cell proliferation, colony formation, migration and invasion in vitro, as well as tumor growth in vivo. Overexpression of LINC00857 increased cancer cell proliferation, colony formation and invasion. Mechanistic analyses indicated that LINC00857 mediates tumor progression via cell cycle regulation. 26862852 2016 Non-coding RNA LINC00857 is predictive of poor patient survival and promotes tumor progression via cell cycle regulation in lung cancer LINC00857 LINC00857 439990 ENSG00000237523 NR_038464 GRCh38_10:80207710-80219657 gastric cancer C16 NA qRT-PCR, Western blot analysis GC cell lines (AGS, BGC-823, MKN-45 and SGC-7901) and a gastric epithelial cell line (GES-1) GC tissues and adjacent non-tumor tissues up-regulated LINC00857 was increased in GC tissues compared with adjacent non-tumor tissues.LINC00857 knockdown induced by specific small interfering RNAs significantly inhibited GC cell proliferation in vitro. the results indicated that LINC00857 knockdown suppressed GC cell proliferation through deregulating the cell cycle, resulting in the downregulation of cyclin D1 and cyclin E1. 30008909 2018 Long non-coding RNA LINC00857 promotes gastric cancer cell proliferation and predicts poor patient survival. LINC00880 AK311218 339894 ENSG00000243629 NR_034007 GRCh38_3:157081667-157123004 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated To identify lncRNAs that are critical to lung carcinogenesis, we selected three lncRNAs, CAR intergenic 10 (hereafter, CAR10), AK311218, and RP11-480I12.3, from the most up-regulated lncRNAs in the HPR NSCLCs (Table S3) and tested their expression by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The expression of these lncRNAs was consistent with the microarray analysis. 27322209 2016 Long non-coding RNA stabilizes the Y-box-binding protein 1 and regulates the epidermal growth factor receptor to promote lung carcinogenesis. LINC00959 NA NA NA NA GRCh38_10:130063896-130110817 colorectal cancer C19.9 NA qPCR, Western blot, RNAi etc. human colon cancer cell lines (HCT116, SW480) down-regulated In vitro, LINC00959 knockdown enhanced colon cancer cell proliferation, invasion, and migration; upregulated N-cadherin and vimentin; and downregulated E-cadherin and Caspase-3. LINC00959 overexpression produced the opposite effects. These data suggest that LINC00959 inhibits tumor cell invasion and migration by suppressing epithelial-mesenchymal transition and promotes apoptosis through Caspase-3. LINC00959 may be a tumor suppressor and useful prognostic biomarker in CRC.Survival analysis for LINC00959 expression in 116 CRC patients from the OncoLnc database. (P=0.0218) 29228592 2017 Long non-coding RNA LINC00959 predicts colorectal cancer patient prognosis and inhibits tumor progression. LINC00961 SPAAR, LINC00961, SPAR， lin-RECK-3 NA ENSG00000235387 NA GRCh38_9:35909483-35937153 non small cell lung cancer C34 M8046/3 qPCR, Western blot NSCLC tissue, cell lines (SPC-A1, A549, PC9, NCI-H1299, NCI-H1975, SK-MES-1, 16HBE) down-regulated Decreased LINC00961 was associated with NSCLC patients advanced clinical stage, lymph node metastasis, and shorter survival time. LSD1 could directly bind to LINC00961 promoter regions and epigenetically repress its transcription in NSCLC cells.Ectopic overexpression of LINC00961 inhibits NSCLC cell migration,invasion in vitro and metastasis in vivo. LINC00961 could act as a tumor suppressor partially via affecting B-catenin expression. Collectively, decreased LINC00961 might play a key role in NSCLC progression, and may serve as a novel prognostic marker in human NSCLC. 29156520 2017 Long noncoding RNA LINC00961 inhibits cell invasion and metastasis in human non-small cell lung cancer. LINC00961 SPAAR, LINC00961, SPAR， lin-RECK-3 NA ENSG00000235387 NA GRCh38_9:35909483-35937153 non small cell lung cancer C56.9 NA PCR, Western blot analysis Human NSCLC cell lines (A549 and H226) lung cancer tissues( LUAD tumor and LUSC tumor tissues) compared with the peri‐tumor tissues and the healthy normal controls down-regulated it was significantly reduced in human non-small cell lung cancer (NSCLC) tissues. upregulation of LINC00961 repressed proliferating cell nuclear antigen expression and increased Bax expression, indicating that it acts as an important pro-apoptosis gene. Conversely, inhibition of LINC00961 induced proliferating cell nuclear antigen expression and restrained Bax protein levels. 30010215 2018 Long noncoding RNA LINC00961 inhibits cell proliferation and induces cell apoptosis in human non-small cell lung cancer. LINC00968 NA 100507632 ENSG00000246430 NR_038236 GRCh38_8:56496246-56559823 non small cell lung cancer C34 M8046/3 qPCR, Western blot, in vitro knockdown etc. cell line (BEAS-2B, A549, H1299, SPCA1 and H358), LUAD tumor tissues up-regulated LINC00968 was significantly increased in LUAD tissues, LUSC tissues and NSCLC cells compared to their corresponding controls. Inhibition of Additionally, downregulation of LINC00968 induced apoptosis capacity of A549 cell. Apoptosis-related proteins BCL-2 were decreased and BAX was increased by knockdown of LINC00968, respectively. Meanwhile we observed that Wnt signaling pathway was involved in the LINC00968-induced NSCLC progression. Finally, in vivo tumor xenografts were established using A549 cells to detect the function of LINC00968 in NSCLC tumorigenesis. Silencing LINC00968 greatly inhibited NSCLC tumor progression, which was consistent with the in vitro tests. In conclusion, we have uncovered that LINC00968 could be regarded as a novel prognostic biomarker and therapeutic target in NSCLC diagnosis and treatment. 28926089 2017 Long non-coding RNA LINC00968 acts as oncogene in NSCLC by activating the Wnt signaling pathway. LINC00968 NA 100507632 ENSG00000246430 NR_038236 GRCh38_8:56496246-56559823 osteosarcoma NA M9180/3 qPCR, Western blot, etc. cell lines (U2OS, MG63, Saos-2, SW1353, 143-B, hFOB) up-regulated overexpression of LINC00968 promoted osteosarcoma cell survival and cell colony formation ability in Saos-2 and 143-B cells. In addition, LINC00968 was able to induce osteosarcoma cell migration and invasion through up-regulating MMP-2 and MMP-9 protein levels. Knockdown of LINC00968 inactivated PI3K/AKT/mTOR signaling pathway in vitro. 29904919 2018 LINC00968 functions as an oncogene in osteosarcoma by activating the PI3K/AKT/mTOR signaling. LINC01060 NA 401164 ENSG00000249378 NR_033869 GRCh38_4:188400736-188681051 pancreatic cancer C25 NA microarray, RIP, etc. pancreatic cancer tissues, cell lines (PANC-1, MIA-PaCa-2, ASPC-1, SW1990, BXPC-3, CFPAC-1, Panc 03.27, HPDE) down-regulated Lower Linc01060 expression in pancreatic cancer tissues was significantly associated with a poor prognosis. Linc01060 inhibited pancreatic cancer proliferation and invasion in vitro and in vivo. These data demonstrate that Linc01060 plays a key role in suppressing pancreatic cancer progression by regulating vinculin expression. 29913236 2018 Loss of Linc01060 induces pancreatic cancer progression through vinculin-mediated focal adhesion turnover. LINC01088 NA 100505875 ENSG00000249307 NR_038342 GRCh38_4:78971748-79308798 ovarian cancer C56.9 NA Microarray, RT-qPCR, Western blot, Luciferase reporter assay malignant epithelial ovarian tumor tissue, human ovarian cancer cell line A2780 down-regulated the expression of long intergenic non-coding RNA 1088 (LINC01088) was clearly reduced in benign epithelial ovarian tumor tissues compared to matched normal ovarian tissues. This was shown by global cDNA gene chip scanning and real-time qPCR, and validated in 42 clinical specimens.Furthermore, we found that LINC01088 inhibited the growth of ovarian cancer xenografts in nude mice.Correlation analysis between LINC01088 and mircoRNAs (miRNAs) conducted using primary clinical samples and RNA co-precipitation experiments revealed that miR-24-1-5p was one of the targets of LINC01088. Overexpression of miR-24-1-5p facilitated cell proliferation both in vitro and in vivo, however, LINC01088 could partially reverse the cell proliferation induced by miR-24-1-5p. 29440672 2018 LINC01088 inhibits tumorigenesis of ovarian epithelial cells by targeting miR-24-1-5p. LINC01089 LINC01089, LIMT 338799 ENSG00000212694 NR_002809 GRCh38_12:121795267-121803906 breast cancer C50 NA microarray, qPCR, RNAi, Cell migration and invasion assay etc. cell lines (MCF10A, MDA-MB-231) down-regulated Functional analyses of this group uncovered LINC01089 (here renamed LncRNA Inhibiting Metastasis; LIMT), a highly conserved lncRNA, which is depleted in basal-like and in HER2-positive tumors, and the low expression of which predicts poor patient prognosis. Interestingly, EGF rapidly downregulates LIMT expression by enhancing histone deacetylation at the respective promoter. We also find that LIMT inhibits extracellular matrix invasion of mammary cells in vitro and tumor metastasis in vivo. 27485121 2016 LIMT is a novel metastasis inhibiting lncRNA suppressed by EGF and downregulated in aggressive breast cancer. LINC01089 LINC01089, LIMT 338799 ENSG00000212694 NR_002809 GRCh38_12:121795267-121803906 astrocytoma NA M9400/3 qPCR etc. astrocytoma tissues up-regulated Our analysis ultimately generated a list of 7 lncRNAs that were differentially expressed in astrocytomas in comparison to the NAT samples. Among these lncRNAs, ENST00000244906, ENST00000545440, NR_002809 and ENST00000436616 were shown to be upregulated by a factor greater than twofold, whereas 3 lncRNAs, XLOC_010967, BC002811 and ASO1937, were shown to be downregulated by a factor greater than twofold. 26252651 2016 The Use of Three Long Non-Coding RNAs as Potential Prognostic Indicators of Astrocytoma. LINC01133 NA 100505633 ENSG00000224259 NR_038849 GRCh38_1:159961218-159984750 colorectal cancer C19.9 NA qPCR colorectal cancer tissues down-regulated LINC01133 was significantly down-regulated in CRC tissues compared to normal tissue samples. Moreover, Kaplan-Meier survival analysis revealed that high LINC01133 expression predicted significantly better overall survival (p = 0.0093). 28537675 2017 Downregulation of long non-coding RNA LINC01133 is predictive of poor prognosis in colorectal cancer patients LINC01133 NA 100505633 ENSG00000224259 NR_038849 GRCh38_1:159961218-159984750 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, RIP, Flow cytometry assay, Cell proliferation assay etc. NSCLC tissues, cell lines (PC9, SPC-A1, NCI-H1975, H1299, and A549) up-regulated Here, we found that LINC01133 expression is up-regulated in NSCLC tissues, and its' over-expression is associated with patients poor prognosis and short survival time. LINC01133 knockdown decreased NSCLC cells proliferation, migration, invasion and induced cell cycle G1/S phase arrest and cell apoptosis. Mechanistic investigations showed that LINC01133 could interact with EZH2, LSD1 and recruit them to KLF2, P21 or E-cadherin promoter regions to repress their transcription. Furthermore, rescue experiments demonstrated that LINC01133 oncogenic function is partly through regulating KLF2. 26840083 2016 Long non-coding RNA LINC01133 represses KLF2, P21 and E-cadherin transcription through binding with EZH2, LSD1 in non small cell lung cancer. LINC01133 NA 100505633 ENSG00000224259 NR_038849 GRCh38_1:159961218-159984750 lung squamous cell carcinoma C34 M8070/3 microarray, qPCR, RNAi etc. NSCLC tissues, cell lines (H1703) up-regulated Quantitative real-time polymerase chain reaction assay confirmed that LINC01133 was upregulated in LSCC but not in the LAD samples. LSCC patients. LINC01133 may promote invasion of LSCC cell. 25908174 2015 A novel long noncoding RNA LINC01133 is upregulated in lung squamous cell cancer and predicts survival. LINC01133 NA 100505633 ENSG00000224259 NR_038849 GRCh38_1:159961218-159984750 esophageal squamous cell cancer NA NA qRT-PCR ect. ESCC cell lines (KYSE-140, KYSE-150, KYSE-180, KYSE-30, KYSE-410, KYSE-510, KYSE-520, EC-18, and HKESC1) and an immortalized esophageal epithelial cell line (NE-1), ESCC tissues and paired normal tissues down-regulated LINC01133 expression levels were frequently lower in ESCC tissues and cell lines than in paired normal tissues and an immortalized esophageal epithelial cell line, respectively. LINC01133 was an independent protective factor and had an anti-tumor effect in the early stage of ESCC development.drinking status in our cohort impaired the predictive accuracy of LINC01133 for patients with ESCC 30007982 2018 Predictive Value of LINC01133 for Unfavorable Prognosis was Impacted by Alcohol in Esophageal Squamous Cell Carcinoma. LINC01207 NA NA NA NA GRCh38_4:164754131-164803795 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot, RIP, ChIP etc. NSCLC tissues, cell lines (A549) up-regulated LINC01207 was significantly up-regulated in LAD tissues compared with paired non-tumor tissues, while there was no significant differences between LSCC tissues and adjacent non-tumor tissues. The expression level of LINC01207 was associated with TNM stage of LAD patients, and higher LINC01207 level indicated advanced TNM stage and shorter survival. 26693067 2015 The long noncoding RNA LINC01207 promotes proliferation of lung adenocarcinoma. LINC01287 TCONS_l2_00027522 103724390 ENSG00000234722 NR_125776 GRCh38_7:153399920-153413963 hepatocellular carcinoma C16 NA qRT-PCR， Western blot assay， ChIP， Luciferase reporter assay HCC cell lines (HepG-2, Huh7, Bel7402 and Hep3B) and the normal liver epithelial cell line LO2, HCC tissues and matched normal tissue up-regulated the expression of LINC01287 was increased in HCC cell lines, as well as tissues. Knockdown of LINC01287 decreased HCC cell growth and invasion both in vitro and in vivo. LINC01287 can negatively regulate miR-298 expression by acting as a ceRNA. miR-298 directly targeted STAT3 and inhibited its expression. LINC01287 exerted its function via the miR-298/STAT3 axis in HCC. Interestingly, STAT3 elevated LINC01287 expression via c-jun, which bound to the LINC01287 promoter. A feedback loop was also discovered between LINC01287 and the miR-298/STAT3 axis. 30001751 2018 LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells. LINC01296 DUXAP9, LINC01296, FLJ39632, lncRNA-CTD903 NA ENSG00000225210 NA GRCh38_14:19062316-19131167 gastric cancer C16 NA qPCR, Western blot gastric cancer tissues, cell lines (SGC-7901, BGC-823, MGC-803, and MKN-45,GES-1) up-regulated LINC01296 was up-regulated in GC tissue and correlated with poor prognosis.LINC01296 knockdown significantly inhibited GC tumor growth. LINC01296 sponged miR-122,LINC01296 was positively correlated with MMP-9 expression, while miR-122 was negatively correlated to it. Overall,results indicate that LINC01296 acts as oncogenic lncRNA in GC carcinogenesis, suggesting the LINC01296/miR-122/MMP-9 regulatory pathway in GC tumorigenesis.GC patients with high LINC01296 levels had poor overall survivals than that with low LINC01296 level. 29091895 2017 Long intergenic noncoding RNA 01296 aggravates gastric cancer cells progress through miR-122/MMP-9. LINC01296 DUXAP9, LINC01296, FLJ39632, lncRNA-CTD903 NA ENSG00000225210 NA GRCh38_14:19062316-19131167 colon cancer C18 NA qPCR, RIP etc. colon carcinoma tissues, cell lines(CCD841a, SW480, DLD-1, HCT116, SW620, Caco-2 and HT29) up-regulated LINC01296 was upregulated in CC cancerous tissues and cell lines compared to adjacent normal tissue and normal liver cell lines. Besides, LINC01296 overexpression was associated with poor prognostic and lower survival rate.Moreover, LINC01296 silencing inhibited the proliferation, invasion of CC cells in vitro detected by epithelialmesenchymal transition (EMT). Bioinformatics analysis revealed that miR-21a targeted 3'-UTR of LINC01296. Rescue experiments confirmed that miR-21a could reverse the function of LINC01296 on CC cells.The expression of LINC01296 and mir-21a is negatively correlated in CC. 29673421 2018 Long noncoding RNA LINC01296 harbors miR-21a to regulate colon carcinoma proliferation and invasion. LINC01296 DUXAP9, LINC01296, FLJ39632, lncRNA-CTD903 NA ENSG00000225210 NA GRCh38_14:19062316-19131167 prostate cancer C61.9 NA qPCR, Western blot prostate cancer tissues, cell lines (22Rv1 and LNCaP) up-regulated LINC01296-expression level was higher in prostate cancer tissues and prostate cancer cells than in adjacent nontumor tissues and immortalized normal prostate stromal WPMY1 cells. Multivariate analysis showed that LINC01296 expression was an independent predictor of biochemical recurrence-free survival in prostate cancer. 28392705 2017 Long noncoding RNA LINC01296 is associated with poor prognosis in prostate cancer and promotes cancer-cell proliferation and metastasis LINC01296 DUXAP9, LINC01296, FLJ39632, lncRNA-CTD903 NA ENSG00000225210 NA GRCh38_14:19062316-19131167 breast cancer C16 NA qRT-PCR, Western blot assays, ect. BC cells (MCF7, MDA-MB-231, SKBR3, BT-20, T47D, MDA-MB-436), and normal mammary epithelial cells (MCF10A), BC tissues and matched adjacent non-tumorous tissue up-regulated LINC01296 is up-regulated in both BC tissue samples and cells. silencing of LINC01296 inhibited BC cell growth in vitro and in vivo. Also, cell apoptosis was enhanced after LINC01296 silenced. Moreover, cell migration and invasion potential were both abrogated in the si-LINC01296 groups. 29981416 2018 Overexpression of long noncoding RNA LINC01296 indicates an unfavorable prognosis and promotes tumorigenesis in breast cancer. LINC01296 DUXAP9, LINC01296, FLJ39632, lncRNA-CTD903 NA ENSG00000225210 NA GRCh38_14:19062316-19131167 hepatoblastoma C22.0 M8970/3 Microarray, Western blot HB liver tissues down-regulated Our results showed decreased proliferation and migration activities of HB cells overexpressing LINC01314. Moreover, mechanistic investigations revealed that LINC01314 overexpression inhibited nuclear translocation of YAP, by inducing MST1 expression and promoting phosphorylation of LATS1 and YAP, consequently downregulating the expression of cell cycle regulatory proteins (MCM7 and cyclin D1). 29571247 2018 Comprehensive analysis and experimental verification of LINC01314 as a tumor suppressor in hepatoblastoma. LINC01420 NBDY, LINC01420, NoBody 550643 ENSG00000204272 NA GRCh38_X:56729241-56818380 nasopharyngeal cancer C11 NA qPCR, RNAi, Cell migration and invasion assay, ISH etc. NPC tissues, cell lines (HNE1, HK-1, HNE2 and 5-8F) up-regulated The expression level of LINC01420 in NPC tissues were higher than nasopharyngeal epithelial (NPE) tissues. Moreover, NPC patients with high LINC01420 expression level showed poor overall survival. Knockdown LINC01420 inhibited NPC cell migration and invasion in vitro. 28123602 2017 High Expression of LINC01420 indicates an unfavorable prognosis and modulates cell migration and invasion in nasopharyngeal carcinoma. LINC01503 lnc-PPP2R4-5 100506119 ENSG00000233901 NR_120685 GRCh38_9:129332300-129359538 squamous cell carcinoma NA M8070/3 RNA-seq, Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RNAi, RIP non-tumor esophageal tissues, cell lines (OE33 and FLO-1, TE7, TE5 and KYSE510, KYSE30 ) up-regulated High levels in SCCs correlated with shorter survival times of patients. The transcription factor TP63 bound to the super enhancer at the LINC01503 locus and activated its transcription. Expression of LINC01503 in ESCC cell lines increased their proliferation, colony formation, migration, and invasion. Knockdown of LINC01503 in SCC cells reduced their proliferation, colony formation, migration, and invasion, and the growth of xenograft tumors in nude mice. Expression of LINC01503 in ESCC cell lines reduced ERK2 dephosphorylation by DUSP6, leading to activation of ERK signaling via MAPK. 29454790 2018 Increased Expression of the Long Non-Coding RNA LINC01503, Regulated by TP63, in Squamous Cell Carcinoma and Effects on Oncogenic Activities of Cancer Cell Lines. LINC01638 NA 105372978 ENSG00000233521 NA GRCh38_22: 27221349-27224727 breast cancer C16 NA qRT-PCR, Western blot assay, ChIP, Luciferase reporter assay, RIP cell lines (MCF-10A, T47D, MCF7, BT474, SKBR3, ZR-75-30, ZR-75-1, MDA-MB-231, BT549, and HCC1937), fresh breast tumor and adjacent non-cancerous breast tissue up-regulated LINC01638 is highly expressed in TNBC tissues and cells.Mechanistically, LINC01638 interacts with c-Myc to prevent SPOP-mediated c-Myc ubiquitination and degradation. C-Myc transcriptionally enhances MTDH (metadherin) expression and subsequently activates Twist1 expression to induce EMT. Analysis of the epithelial marker E-cadherin and mesenchymal markers Vimentin and EMT-associated transcription factor Twist1 revealed that LINC01638 knockdown increased E-cadherin and reduced Vimentin and Twist1 expression at the mRNA (Fig. 2g) and protein (Fig. 2h) levels in MDA-MB-231 and BT549 cells, whereas LINC01638 overexpression showed an inverse effect in T47D cells (Fig. 2g, h). 30002443 2018 LINC01638 lncRNA activates MTDH-Twist1 signaling by preventing SPOP-mediated c-Myc degradation in triple-negative breast cancer. LINC01793 NA 101927285 ENSG00000222030 NR_110219 GRCh38_2:59217708-59279400 gastric cancer C16 NA qRT-PCR, ect. gastric cancer cells, Gastric cancer tissues and paracancerous tissues up-regulated LINC01793 was overexpressed in gastric cancer tissues compared to paracancerous tissues. Moreover, LINC01793 overexpression in gastric cancer was closely related to patients with poor prognosis. GSEA analysis found that LINC01793 was closely related to apoptosis, cell cycle, invasion and metastasis of gastric cancer cells. 29978448 2018 Overexpression of lncRNA LINC01793 acts as a potential predictor for progression and poor prognosis of gastric cancer. LINC02163 NA 107986389 ENSG00000251026 NA GRCh38_5:104079911-104105,403 gastric cancer C16 NA qPCR, Western blot, etc. Gastric cancer cell lines, normal gastric epithelial cell line. up-regulated To the best of our knowledge, our findings provided the first evidence that LINC02163 functioned as an oncogene in GC. LINC02163 may be a candidate prognostic biomarker and a target for new therapies in GC patients.GC patients with high LINC02163 expression had shorter disease-free survival and the over-all survival rate than those with low LINC02163 expression.The miR-593-3p/FOXK1 axis mediated LINC02163’s effect on GC. 29893595 2018 LINC02163 regulates growth and epithelial-to-mesenchymal transition phenotype via miR-593-3p/FOXK1 axis in gastric cancer cells. LINC02454 NA 105369807 ENSG00000256268 NR_146529 GRCh38_12:65602869-65612997 papillary thyroid cancer NA M8260/3 Microarray, etc. 318 papillary thyroid carcinoma (PTC) tissues, 35 normal thyroid gland tissues. Differential expression According to multivariate Cox analysis, the combination of two DEGs (METTL7B and KCTD16) and two DElncRNAs (LINC02454 and LINC02471) could predict the outcome in a more exact way. In conclusion, top DEGs and DElncRNAs could raise diagnosis of PTC in indeterminate FNAB specimens, and some could function as molecule biomarkers for tumor progression and prognosis. The prognostic role of these factors was examined via Kaplan-Meier method, and the log-rank test was conducted to contradistinguish survival time. 29968931 2018 Role of differentially expressed genes and long non-coding RNAs in papillary thyroid carcinoma diagnosis, progression, and prognosis. LINC02471 AC079630.2 105369734 ENSG00000223914 NR_146526 GRCh38_12:40156113-40211419 papillary thyroid cancer NA M8260/3 Microarray, etc. 318 papillary thyroid carcinoma (PTC) tissues, 35 normal thyroid gland tissues Differential expression According to multivariate Cox analysis, the combination of two DEGs (METTL7B and KCTD16) and two DElncRNAs (LINC02454 and LINC02471) could predict the outcome in a more exact way. In conclusion, top DEGs and DElncRNAs could raise diagnosis of PTC in indeterminate FNAB specimens, and some could function as molecule biomarkers for tumor progression and prognosis. The prognostic role of these factors was examined via Kaplan-Meier method, and the log-rank test was conducted to contradistinguish survival time. 29968931 2018 Role of differentially expressed genes and long non-coding RNAs in papillary thyroid carcinoma diagnosis, progression, and prognosis. linc-GPR65-1 NA 8477 ENSG00000140030 NA GRCh39_14:88005124-88014811 gastric cancer C16 NA qPCR, Western blot, in vitro knockdown etc. cell lines (GES-1, MKN-28, SGC-7901, HGC-27, NCI-N87, AGS, and BGC-823), gastric cancer tissues up-regulated Linc-GPR65-1 was significantly up-regulated in 50 gastric cancer tissues compared to the corresponding normal tissues. In addition, increased linc-GPR65-1 expression was associated with TNM stage (P = 0.037), tumor size (P = 0.024), distal metastasis (P = 0.023), and poor prognosis of gastric cancer patients. Moreover, functional assays indicated that decreased linc-GPR65-1 expression inhibited the aggressive phenotypes of gastric cancer cells, and enhanced linc-GPR65-1 expression resulted in the opposite phenomenon. These data showed that linc-GPR65-1, regulating the PTEN-AKT-slug signaling pathway, might act as a tumor promoter and serve as a novel target for gastric cancer prevention and therapy. 29336198 2018 Long non-coding RNA GPR65-1 is up-regulated in gastric cancer and promotes tumor growth through the PTEN-AKT-slug signaling pathway. linc-ITGB1 ITGB1, CD29, FNRB, GPIIA, MDF2, MSK12, VLA-BETA, VLAB NA ENSG00000150093 NA GRCh38_10:32900319-33005792 breast cancer C50 NA qPCR etc. breast carcinoma tissues down-regulated lincITGB1 levels were lower in tumor tissues of BC patients in comparison to adjacent non-cancerous breast tissues (p < 0.001). Linc-ITGB1 expression was significantly associated with lymph node metastasis, pathological differentiation and TNM stage (all p < 0.05). linc-ITGB1 be a potential biomarker in the prognosis of BC.The present study aimed to determine the relationship between linc-ITGB1 expression and clinicopathological features and survival. 28829502 2017 Expression of long non-coding RNA linc-ITGB1 in breast cancer and its influence on prognosis and survival. linc-POU3F3 POU3F3, BRN1, OTF8, brain-1, oct-8 NA ENSG00000198914 NA GRCh38_2:104855511-104858574 esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues up-regulated Further validation in a larger cohort including 205 ESCC patients, 82 patients suffering from esophagus dysplasia and 210 healthy controls confirmed that increased Linc00152, CFLAR-AS1 and POU3F3 might be potential biomarkers for predicting the early progress. We also revealed that circulating levels of three lncRNAs were associated with poor post-surgery prognosis of ESCC patients. 27855375 2016 Three Circulating LncRNA Predict Early Progress of Esophageal Squamous Cell Carcinoma. linc-POU3F3 POU3F3, BRN1, OTF8, brain-1, oct-8 NA ENSG00000198914 NA GRCh38_2:104855511-104858574 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN49), gastric adenocarcinomas tissues down-regulated We observed the association of Linc-POU3F3 overexpression in gastric tumors from patients with non-vegetarian diet habit. 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. linc-POU3F3 POU3F3, BRN1, OTF8, brain-1, oct-8 NA ENSG00000198914 NA GRCh38_2:104855511-104858574 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, etc. hepatocellular carcinoma tissues, cell lines (Li-7, HepG2, SNU-449, Bel-7402) up-regulated linc-POU3F3 expression significantly promoted tumor cell proliferation, migration and invasion. In addition, linc-POU3F3 expression was negatively correlated with POU3F3 mRNA and protein expressions in hepatocellular carcinoma tissues, and negatively regulated POU3F3 mRNA and protein expressions in hepatocellular carcinoma cells.Patients with linc-POU3F3 high-expression have shorter survival time than those with lowexpression of linc-POU3F3. 29906746 2018 Linc-POU3F3 is overexpressed in hepatocellular carcinoma and regulates cell proliferation, migration and invasion. lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 102800311 NA NA NA glioma NA M9380/3 qPCR, Western blot etc. cell lines (SMMC7721, U251MG) down-regulated In this work, we found that X-ray irradiation or hypoxia treatment elevated lincRNA-p21 expression in SMMC7721 hepatoma and U251MG glioma cells.High lincRNA-p21 levels were associated with poor cancer-specific survival in patients. F.. However, tumor cells can express a wide range of transcription factors, such as hypoxia-inducible factor-1a (HIF-1a).found that LincRNA-p21 was downregulated in non-small-cell lung cancer tissue, but no association was observed with TP53 mutational status. 28689810 2017 LincRNA-p21 knockdown enhances radiosensitivity of hypoxic tumor cells by reducing autophagy through HIF-1/Akt/mTOR/P70S6K pathway. lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 102800311 NA NA NA non small cell lung cancer C34 M8046/3 qPCR, RNAi etc. NSCLC tissues, cell lines (NCI-H23, NCI-H1299, HCC-44) down-regulated LincRNA-p21 was down-regulated in tumor tissue, but no association was observed with TP53 mutational status. To explain the poor outcome of patients with high lincRNA-p21 expression, we studied the role of lincRNA-p21 in angiogenesis in vitro and observed a global downregulation in the expression of angiogenesis-related genes when lincRNA-p21 was inhibited. 27496652 2016 LincRNA-p21 Impacts Prognosis in Resected Non-Small Cell Lung Cancer Patients through Angiogenesis Regulation. lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 102800311 NA NA NA gastric cancer C16 NA qPCR, Western blot etc. GC tissues, cell lines (MGC-803, MKN-45, BGC-823, MKN-28, SGC-7901, GES-1) down-regulated p21 was significantly reduced in gastric cancer tissues (p<0.001) compared with that in normal tissues and this lower level of lincRNA-p21 was significantly correlated with higher invasion depth grade (p=0.024), more distant metastasis (p=0.009) and advanced TNM stage (p=0.011).The high incidence rate and relative low survival rate makes gastric cancer a significant threat to human health. 28969031 2017 Down regulation of lincRNA-p21 contributes to gastric cancer development through Hippo-independent activation of YAP. lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 102800311 NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot etc. HCC tissues down-regulated We demonstrated that lincRNA-p21 acted as a tumor suppressive lncRNA in human hepatocellular carcinoma. We firstly found the downregulation of lincRNA-p21 level in human hepatocellular carcinoma tissues, and showed that low expression of lincRNA-p21 was associated with high disease stage and predicted poor survival.We showed that lincRNA-p21 knockdown promoted proliferation and colony formation of HepG2, Huh7 and Bel-7042 cells in vitro, while lincRNA-p21 overexpression obtained oppose results.We demonstrated that ER stress accounted for lincRNA-p21 effects on apoptosis, proliferation and in vivo growth of hepatocellular carcinoma. 26305675 2015 LincRNA-p21 activates endoplasmic reticulum stress and inhibits hepatocellular carcinoma lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 102800311 NA NA NA prostate cancer C61.9 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. prostate cancer tissues, cell lines (LNCaP, DU145 and PC3) down-regulated LincRNA-p21 was found to be down-regulated in human prostate cancer, and low levels of lincRNA-p21 correlated with high disease stage and prediction of poor survival. We further showed that lincRNA-p21 inhibited prostate cancer cell proliferation and colony formation in vitro and reduced rate of prostate cancer cell population growth in vivo. Study of mechanisms involved revealed that lincRNA-p21 promoted apoptosis and induced expression of p53 downstream genes by regulating p53 binding to their promoters. 27976428 2017 Long intragenic non-coding RNA lincRNA-p21 suppresses development of human prostate cancer. lincRNA-VLDLR VLDLR-AS1, linc-VLDLR, lincRNA-VLDLR 401491 ENSG00000147852 NR_015375 GRCh38_9:2422702-2643359 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated Eight (lincRNA-VLDLR, MEG9, H19 antisense, ncR-uPAR, NEAT1 (family), LUST, UM9-5, and HOTAIR) were significantly down-regulated in HCC tumor compared to non-tumor tissues at a significance level. 26378581 2015 Exploration of Deregulated Long Non-Coding RNAs in Association with Hepatocarcinogenesis and Survival. linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 prostate cancer C61.9 NA qPCR, microarray etc. cell lines (Du145, 22RV1) down-regulated lncRNA-ROR and Oct4 mRNA both contain miR-145 binding sites, and Oct4 and lncRNA-ROR directly compete for microRNA binding. Curcumin induced high miR-145 expression and inhibited the expression of lncRNA-ROR. The tumorigenicity of curcumin- treated HuPCaSCs in nude mice was significantly reduced. In summary, reducing the expression of endogenous lncRNA-ROR could effectively increase the available concentration of miR-145 in HuPCaSCs, where miR-145 prevents cell proliferation by decreasing Oct4 expression. In particular, we hypothesized that lncRNA-ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Oct4. Thus, curcumin suppresses the proliferation, in vitro invasion, and tumorigenicity of HuPCaSCs through ceRNA effect of miR-145 and lncRNA-ROR caused. 28843521 2017 Curcumin suppresses proliferation and in vitro invasion of human prostate cancer stem cells by ceRNA effect of miR-145 and lncRNA-ROR linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 gallbladder cancer C23.9 NA qPCR, RNAi, Western blot etc. GBC tissues, cell lines (SGC-996, GBC-SD, Noz) up-regulated We found that LncRNA-ROR expression level was upregulated in gallbladder cancer tissues and was significantly associated with tumor sizes and lymph node metastasis. High expression of LncRNA-ROR was significantly associated with poor prognosis in gallbladder cancer patients. Moreover, knockdown of LncRNA-ROR inhibited cell proliferation, migration, and invasion. The epithelial-mesenchymal transition (EMT) phenotype induced by TGF-B1 was reversed after LncRNA-ROR knocking down in SGC-996 and Noz cells. 27449039 2016 Overexpression of LncRNA-ROR predicts a poor outcome in gallbladder cancer patients and promotes the tumor cells proliferation, migration, and invasion. linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 renal cell carcinoma C64.9 NA qPCR, Western blot renal cell carcinoma tissue, cell lines (Caki.1, Caki.2, HK.2) up-regulated lncRNA ROR was found to be expressed at high levels in RCC tissues and cell lines. Patients with RCC exhibiting high expression levels of lncRNA ROR had shorter survival rates,compared with those with low expression levels of lncRNA ROR.The knockdown of lncRNA ROR resulted in a decrease of cell proliferation and increase of apoptosis in vitro. The suppression of lncRNA ROR also induced an increase in the expression of p53 and a decrease in the expression of c-Myc in vitro.lncRNA ROR was expressed at high levels in RCC tissue and cell lines, and was associated with the proliferation ability of RCC cells. 29039528 2017 lncRNA ROR promotes the proliferation of renal cancer and is negatively associated with favorable prognosis. linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 lung cancer C34 NA qPCR Liver Cancer tissues up-regulated Our findings indicate that linc-ROR plays an oncogenic role in NSCLC development and may function as a prognostic and predictive biomarker for NSCLC. Cox regression analyses were performed to explore the effect of lincROR as an independent predictor of survival. Fu et al21 reported that linc-ROR promotes pancreatic cancer cell proliferation and invasiveness by sponging some different miRNAs. 29028092 2017 Long non-coding RNA ROR is a novel prognosis factor associated with non-small-cell lung cancer progression. linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 pancreatic cancer C25 NA qPCR, RNAi, Western blot, Northern blot, Flow cytometry assay, FISH etc. pancreatic cancer tissues up-regulated Compared with adjacent non-tumor tissues, ROR was up-regulated in most tumor tissues. Knockdown of ROR by RNA interference in PCSCs inhibited proliferation, induced apoptosis and decreased migration. Moreover, ROR silencing resulted in significantly decreased tumourigenicity of PCSCs in nude mice than controls. In particular, ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Nanog. 26636540 2016 ROR functions as a ceRNA to regulate Nanog expression by sponging miR-145 and predicts poor prognosis in pancreatic cancer. linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. cell lines (HepG2 and SMMC-7721) up-regulated linc-ROR promotes HCC metastasis via induction of epithelial-mesenchymal transition (EMT).linc-ROR was significantly upregulated in radioresistant HCC cells.Knockdown of linc-ROR reduces in vitro and in vivo radiosensitivity of parental HCC cells by reducing DNA repair capacity, while ectopic expression of linc-ROR enhances radiosensitivity of radioresistant HCC cells.Further mechanistic investigations revealed that lincRNA-ROR exerted its biological effects by acting as a competing endogenous RNA (ceRNA) for miR-145 to regulate RAD18 expression, thereby promoting DNA repair. 29559320 2018 Long non-coding RNA ROR promotes radioresistance in hepatocelluar carcinoma cells by acting as a ceRNA for microRNA-145 to regulate RAD18 expression. linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 pancreatic cancer C25 NA qPCR, RIP etc. cell lines (PANC-1, SW1990) up-regulated linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family. 28580169 2017 Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 esophageal squamous cell cancer NA NA qRT-PCR, Western blot, RIP ESCC tumor tissues, EC cell lines (EC109 and EC9706) up-regulated ROR expression in ESCC tumor tissues was significantly higher than in the adjacent tissues.The survival rate of ESCC patients with high ROR expression levels was lower than that of patients with low ROR expression levels.ROR overexpression could downregulate miR-145 by up to 50% was proven by RIP,DLR assay,and qRT-PCR.FSCN1 was a downstream target of ROR/miR-145.Transwell assays were used to show that overexpression of ROR enhanced migration and invasion behavior of ESCC and miR-145 hindered these effects. 29430188 2018 LincRNA-ROR promotes metastasis and invasion of esophageal squamous cell carcinoma by regulating miR-145/FSCN1. linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 lung cancer C34 NA qPCR, Western blot lung cancer tissues, cell line (A549) up-regulated Here, qRT-PCR analysis revealed that p53 and ROR were upregulated while miR-145 was downregulated in non-small cell lung cancer (NSCLC) tissues and LCSCs compared to their paired adjacent normal tissues and lung cancer cells (LCCs). Besides, high p53 level, low miR-145 level, and high ROR level were associated with poor prognosis in NSCLC. 28516515 2017 Interaction of lincRNA ROR and p53/miR-145 correlates with lung cancer stem cell signatures linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN48), gastric adenocarcinomas tissues down-regulated LINCROR could sponge the miR-148a, miR-145 and miR-21 and can act as ceRNA modulating the miRNA-mediated post-transcriptional regulation of EGFR, KLF4, DNMT1 and AGO4 . The downregulation of LINCROR when its target miR-145 abundantly expressed.In addition, we observed the expression level LINCROR directly correlated with the overexpression of the miR-145. This relationship has been already reported in colon cancer and shown to be involved in overall survival. Our results suggest that reduced LINCROR/high miR-145 might be associated with better prognosis. LINCROR is an active member associated with reprogramming and stemness-related transcription factors. Downregulation of LINCROR by miR-145 might impair the cancer stemness by deregulation of another transcription factor KLF4 . 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase report assay etc. HCC tissues, cell lines (HH, HCCLM3, MHCC97-H, HepG2 and SMMC-7721) up-regulated linc-ROR was upregulated in HCC tissues and high linc-ROR expression level predicted poor prognosis.ROR was upregulated in HCC tissues and high linc-ROR expression level predicted poor prognosis. ROR and ZEB2 interact with miR-145 by functioning as competing endogenous RNAs (ceRNAs).The disease-free survival (DFS) and over survival (OS) curves were plotted using the Kaplan-Meier method. 28680141 2017 The lincRNA-ROR/miR-145 axis promotes invasion and metastasis in hepatocellular carcinoma via induction of epithelial-mesenchymal transition by targeting ZEB2. linc-UFC1 UFC1, HSPC155 NA ENSG00000143222 NA GRCh38_1:161152776-161158856 cervical cancer C53 NA qPCR, western blot, RIP etc. cervical cancer tissues, cell lines (Hela and Siha) up-regulated Here, it was demonstrated that linc-UFC1 expression was significantly increased in cervical cancer tissues, and its overexpression was associated with the poor survival of patients with cervical cancer. 29790665 2018 Long noncoding RNA UFC1 is activated by E2F1 and exerts oncogenic properties by functioning as a ceRNA of FOXP3 LINK-A LINC01139, LINK-A, LINKA 339535 ENSG00000215808 NR_015407 GRCh38_1:238480384-238486023 breast cancer C50 NA Cell transfection, Fluorescence quenching assay, Lipid-RNA pulldown assay etc. TNBC tissues, cell lines (MDA-MB-231, MDA-MB-468, MCF-10A) differential expression LINK-A directly interacts with the AKT pleckstrin homology domain and PIP3 at the single-nucleotide level, facilitating AKT-PIP3 interaction and consequent enzymatic activation. LINK-A-dependent AKT hyperactivation leads to tumorigenesis and resistance to AKT inhibitors. Genomic deletions of the LINK-A PIP3-binding motif dramatically sensitized breast cancer cells to AKT inhibitors. 28218907 2017 The LINK-A lncRNA interacts with PtdIns(3,4,5)P3 to hyperactivate AKT and confer resistance to AKT inhibitors. LINP1 NA 108570035 ENSG00000223784 NR_138480 GRCh38_10:6737382-6739026 cervical cancer C53 NA qPCR, RIP cervical cancer tissues up-regulated 29527968 2018 LINP1 facilitates DNA damage repair through non-homologous end joining (NHEJ) pathway and subsequently decreases the sensitivity of cervical cancer cells to ionizing radiation. LL22NC03-N64E9.1 NA NA NA NA GRCh38_22:15796959-15798346 lung cancer C34 NA qPCR, etc. lung cancer tissues, cell lines (BEAS-2B, A549, H1703, H292) up-regulated LL22NC03-N64E9.1, promoted proliferation of lung cancer cells in vitro, was highly expressed in lung cancer tissues and was associated with increased overall survival (OS), tumor size, and tumor stage in patients with lung cancer. 29935018 2018 A Novel Long Noncoding RNA (lncRNA), LL22NC03-N64E9.1, Promotes the Proliferation of Lung Cancer Cells and is a Potential Prognostic Molecular Biomarker for Lung Cancer. Lnc01614 NA NA NA NA NA gastric cancer C16 NA qPCR, Western blot, in vitro knockdown etc. cell lines (BGC-823, SGC-7901, AGS, MKN28, GES-1), gastric cancer tissue up-regulated Compared with patients with low expression of lnc01614, patients with high expression of lnc01614 had higher tumor staging, greater lymph node metastasis and distant metastasis rates, and lower overall survival rate. In comparison with the negative control si-NC group, cell proliferation, invasion and migration abilities in lnc01614 knockdown expression group (si-lnc01614) were significantly decreased. Si-lnc01614 group exhibited increased E-cadherin expression, and significantly reduced vimentin and snail expression. 29565488 2018 Long noncoding RNA Lnc01614 promotes the occurrence and development of gastric cancer by activating EMT pathway. lncARSR NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot hepatocellular carcinoma tissues, cell lines (SMMC-7721,HepG2) up-regulated lncARSR is upregulated in HCC, associated with large tumor size and advanced BCLC stage, and indicts poor prognosis. overexpression of lncARSR enhances doxorubicin resistance of HCC cells in vitro and in vivo.while knockdown of lncARSR increases sensitivity of HCC cells to doxorubicin in vitro and in vivo. lncARSR physically associates with PTEN mRNA, promotes PTEN mRNA degradation, decreases PTEN expression, and activates PI3K/Akt pathway. the effects of lncARSR overexpression on doxorubicin resistance could be reversed by PI3K/Akt pathway inhibitor, and lncARSR knockdown-induced doxorubicin sensitivity could be reversed by PTEN depletion. Taken together,upregulated lncARSR promotes doxorubicin resistance in HCC via modulating PTEN-PI3K/Akt pathway, and implied that lncARSR may serve as a promising prognostic biomarker and therapeutic target for HCC chemo-resistance.high expression of lncARSR indicates poorer recurrence-free and overall survival. 28464252 2017 Long Noncoding RNA lncARSR Promotes Doxorubicin Resistance in Hepatocellular Carcinoma via Modulating PTEN-PI3K/Akt Pathway. lncARSR NA NA NA NA NA renal cell carcinoma C64.9 NA qPCR, Western blot, RIP, ChIP, RNA pull-down assay etc. RCC tissues, cell lines (A498, 769P, Ketr-3, Caki-1, Caki-2) up-regulated Here we show that long non-coding RNA lncARSR is upregulated in primary renal T-ICs and associated with a poor prognosis of clear cell RCCs (ccRCC). Knockdown of lncARSR attenuates the self-renewal, tumorigenicity and metastasis of renal T-ICs. 27886176 2016 A feed-forward loop between lncARSR and YAP activity promotes expansion of renal tumour-initiating cells. lncBRM NA NA NA NA NA ovarian cancer C56.9 NA qPCR, Western blot, RIP, Luciferase reporter assay etc. OC tissues, cell lines (A2780, TOV112D, HO-8910, OVCAR-3, SKOV3) up-regulated lncBRM expression was signifcantly increased in OC tissues. Upregulation of lncBRM expression was correlated with histological grade, FIGO stages, lymph node metastasis and poor prognosis of patients with OC. Functional assays showed that lncBRM positively regulated cell proliferation, migration and invasion in OC. Moreover, lncBRM upregulated Sox4 by competitively binding miR-204. Together, lncBRM functions as an oncogene in OC and can be a promising therapeutic target for OC treatment. 29218242 2017 Long noncoding RNA lncBRM facilitates the proliferation, migration and invasion of ovarian cancer cells via upregulation of Sox4 lncCAMTA1 NA 110841581 ENSG00000237436 NR_149049 GRCh38_1:6783892-6784843 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RNAi, Western blot, Cell proliferation assay etc. HCC tissues, cell lines (SMMC-7721, HCCLM3, HepG2, Hep3B, and Huh7) up-regulated High lncCAMTA1 expression in HCC indicates poor clinical outcome. In vitro and in vivo functional experiments showed that overexpression of lncCAMTA1 promotes HCC cell proliferation, CSC-like properties, and tumorigenesis. Conversely, depletion of lncCAMTA1 inhibits HCC cell proliferation, CSC-like properties, and tumorigenesis. Furthermore, CAMTA1 is required for the effects of lncCAMTA1 on HCC cell proliferation and CSC-like properties, and the expression of lncCAMTA1 and CAMTA1 is significantly negatively correlated in HCC tissues. 27669232 2016 Long Noncoding RNA lncCAMTA1 Promotes Proliferation and Cancer Stem Cell-Like Properties of Liver Cancer by Inhibiting CAMTA1. lnc-CYP4A22-2/3 NA NA NA NA NA clear cell renal cell carcinoma C64.9 M8005/0 microarray, qPCR etc. ccRCC tissues up-regulated lnc-ZNF180-2 levels were similar in localized ccRCC and normal renal tissue, but we observed a significant increase of lnc-ZNF180-2 expression in advanced ccRCC tissue. Furthermore, lnc-ZNF180-2 expression levels were an independent predictor of progression-free survival, cancer-specific survival and overall survival in ccRCC patients. We also observed that lnc-CYP4A22-2/3 expression levels allowed discrimination of ccRCC and normal renal tissue. In conclusion, lncRNAs are involved in renal carcinogenesis, and quantification of lnc-ZNF180-2 may be useful for the prediction of ccRCC patients outcome following nephrectomy. 26609485 2015 The long non-coding RNA lnc-ZNF180-2 is a prognostic biomarker in patients with clear cell renal cell carcinoma. lnc-DILC TFDP1, DILC, DP1, DRTF1, Dp-1 7027 ENSG00000198176 NA GRCh38_13:113584721-113641470 liver cancer C22.0 NA microarray, Luciferase reporter assay etc. HCC tissues down-regulated Depletion of lnc-DILC markedly enhanced LCSC expansion and facilitated HCC initiation and progression, whereas ectopic expression of lnc-DILC dramatically inhibited LCSC expansion. Mechanistically, lnc-DILC inhibited the autocrine IL-6/STAT3 signaling. The putative binding locus of lnc-DILC within IL-6 promoter was confirmed by pull down assay. Consistently, the oligoribonucleotide mimics and an oligodeoxynucleotide decoy of lnc-DILC abrogated the effects on IL-6 transcription, STAT3 activation and LCSC expansion triggered by lnc-DILC depletion and lnc-DILC overexpression. Moreover, our data suggested that lnc-DILC mediated the crosstalk between TNF-a/NF-kB signaling and IL-6/STAT3 cascade. Clinical investigation demonstrated the reduction of lnc-DILC in patient HCCs, and suggested the correlation between lnc-DILC levels and IL-6, EpCAM or CD24 expression. Decreased lnc-DILC expression in HCCs predicts early recurrence and short survival of patients, highlighting its prognostic value 26812074 2016 Long non-coding RNA DILC regulates liver cancer stem cells via IL-6/STAT3 axis lncFOXO1 NA NA NA NA NA breast cancer C50 NA microarray, qPCR, Western blot, ChIP, CCK-8 assay etc. breast cancer tissues, cell lines (MCF-7, BT-549, MB-231, MB-453 and MB-415) down-regulated lncFOXO1 is significantly decreased in breast cancer tissues and cell lines and downregulation of lncFOXO1 expression associates with poorer overall survival. Functional assays demonstrated its suppressive role in breast cancer in vivo and in vitro. Mechanistically, lncFOXO1 suppressed the growth of breast cancer by increasing FOXO1 transcription. Moreover, we found that lncFOXO1 associated with BRCA-1-associated protein 1 (BAP1) and regulates its binding and the level of mono-ubiquitinated H2A at K119 (ubH2AK119) at FOXO1 promoter. 28339037 2017 The long non-coding RNA lncFOXO1 suppresses growth of human breast cancer cells through association with BAP1. lncGPR107 LncGPR107 401554 ENSG00000196979 NR_135124 GRCh38_9:130140610-130144219 liver cancer C22.0 NA qPCR, Western blot, ChIP, etc. liver cancer tissues up-regulated LncGPR107 drove the self-renewal of liver TICs through GPR107. LncGPR107 participated in the transcriptional regulation of GPR107 in cis, through recruiting SRCAP remodeling complex to GPR107 promoter. the expression pattern of GPR107 was associated with liver tumor clinical characteristics, including metastasis, relapse and prognosis. 29925408 2018 LncGPR107 drives the self-renewal of liver tumor initiating cells and liver tumorigenesis through GPR107-dependent manner. lncHERG LOC644794 NA NA NA GRCh38_7:66904120-66906297 glioblastoma NA M9440/3 qPCR, Luciferase reporter assay etc. GBM cell lines (U87, U251, LN229) up-regulated LncHERG knockdown impaired cell proliferation, migration and invasion while inhibition of miR-940 in the meantime reversed this trend.In conclusion,our study highlights the essential role of lncHERG in glioblastoma by acting as a competing endogenous RNA of miR-940, which may serve as a new prognostic biomarker in glioblastoma. 29296221 2017 Long noncoding RNA lncHERG promotes cell proliferation, migration and invasion in glioblastoma lnc-HOST2 CERNA2, HOST2, lncRNA-HOST2 642934 NR_134505 NA osteosarcoma NA M9180/3 qRT-PCR, Western blot osteosarcoma tissues, cell lines (U2OS, MG-63, and KHOS) up-regulated The expression levels of lnc-HOST2 in osteosarcoma tissues were significantly higher than those in corresponding noncancerous bone tissues (p < 0.01). Statistical assay indicated that the expression level of lnc-HOST2 was positively correlated with tumor stage (p = 0.003) and distant metastasis (p = 0.000).down-regulation of lnc-HOST2 suppressed proliferation and induced cell apoptosis in osteosarcoma cells. Notably, we confirmed that up-regulation of lnc-HOST2 led to Bcl-2 downregulation and Bax upregulation in osteosarcoma cells. 29509239 2018 Prognostic value of long non-coding RNA HOST2 expression and its tumor-promotive function in human osteosarcoma. Lnc-IL7R NA NA ENSG00000168685 NA GRCh38_5:35852695-35879603 cervical intraepithelial neoplasia NA M8077/2 qPCR, Western blot, RNAi etc. cervical intraepithelial neoplasia tissues, cell lines (Hela and SiHa) up-regulated We here investigated the clinical role of inflammation-related LncRNA-IL7R (Lnc-IL7R) in healthy cervical tissue (n=15), CIN 1/2/3 (n=35), cervical cancer (n=70), and clarified its function via knockdown in vitro and in vivo. The results showed that the expression of Lnc-IL7R was increased from normal tissues to neoplastic lesions and cervical cancer. Patients with high expression of Lnc-IL7R had poor prognosis with short overall survival time, and cox regression analysis revealed that Lnc-IL7R could be independent prognostic factor for cervical cancer. These data indicated that Lnc-IL7R predicts a poor clinical outcome of cervical cancer patients, and knockdown of Lnc-IL7R is amenable to the treatment of cervical cancer. 29720427 2018 Up-regulation of inflammation-related LncRNA-IL7R predicts poor clinical outcome of patients with cervical cancer. lnc-JPH1-7 NA NA NA NA NA head and neck squamous cell carcinoma C76.0 M8070/3 qPCR, RNAi etc. cell lines (UMSCC-10B, UMSCC-22B, HN-1, HN-12, HN-30, SCC-4, Cal-27 etc.) up-regulated We found that elevated lnc-JPH1-7 levels in HNSCCs associated not only with poor prognosis, methyltransferase KMT2D (MLL1) mutation, and concurrent TP53 mutation and 3p deletion, but also significantly correlated to advanced tumor stage. Furthermore, higher median lnc-JPH1-7 expression was observed among HPVnegative patients and patients reporting history of smoking. 27323410 2016 The non-coding landscape of head and neck squamous cell carcinoma. lnc-KCTD6-3 FAM3D-AS1, lnc-KCTD6-3 105377108 ENSG00000244383 NR_134853 GRCh38_3:58607080-58634440 pharyngeal cancer C14 NA RNA-seq, qPCR etc. cell lines (HN-1, HN-30) down-regulated We confirmed the dysregulation of these noncoding RNAs in head and neck cancer cell lines derived from different anatomic sites, and determined that ectopic expression of the two lncRNAs inhibited key EMT and stem cell genes and reduced cellular proliferation and migration. 25904139 2015 Transcriptome sequencing uncovers novel long noncoding and small nucleolar RNAs dysregulated in head and neck squamous cell carcinoma. lnc-KCTD6-3 FAM3D-AS1, lnc-KCTD6-3 105377108 ENSG00000244383 NR_134853 GRCh38_3:58607080-58634440 tongue cancer C02 NA RNA-seq, qPCR etc. cell lines (UMSCC-10B, HN-12) down-regulated We confirmed the dysregulation of these noncoding RNAs in head and neck cancer cell lines derived from different anatomic sites, and determined that ectopic expression of the two lncRNAs inhibited key EMT and stem cell genes and reduced cellular proliferation and migration. 25904139 2015 Transcriptome sequencing uncovers novel long noncoding and small nucleolar RNAs dysregulated in head and neck squamous cell carcinoma. lnc-KCTD6-3 FAM3D-AS1, lnc-KCTD6-3 105377108 ENSG00000244383 NR_134853 GRCh38_3:58607080-58634440 laryngeal cancer C32 NA RNA-seq, qPCR etc. cell lines (UMSCC-22B) down-regulated We confirmed the dysregulation of these noncoding RNAs in head and neck cancer cell lines derived from different anatomic sites, and determined that ectopic expression of the two lncRNAs inhibited key EMT and stem cell genes and reduced cellular proliferation and migration. 25904139 2015 Transcriptome sequencing uncovers novel long noncoding and small nucleolar RNAs dysregulated in head and neck squamous cell carcinoma. lnc-LCE5A-1 NA NA NA NA NA pharyngeal cancer C14 NA RNA-seq, qPCR etc. cell lines (HN-1, HN-30) down-regulated We confirmed the dysregulation of these noncoding RNAs in head and neck cancer cell lines derived from different anatomic sites, and determined that ectopic expression of the two lncRNAs inhibited key EMT and stem cell genes and reduced cellular proliferation and migration. 25904139 2015 Transcriptome sequencing uncovers novel long noncoding and small nucleolar RNAs dysregulated in head and neck squamous cell carcinoma. lnc-LCE5A-1 NA NA NA NA NA tongue cancer C02 NA RNA-seq, qPCR etc. cell lines (UMSCC-10B, HN-12) down-regulated We confirmed the dysregulation of these noncoding RNAs in head and neck cancer cell lines derived from different anatomic sites, and determined that ectopic expression of the two lncRNAs inhibited key EMT and stem cell genes and reduced cellular proliferation and migration. 25904139 2015 Transcriptome sequencing uncovers novel long noncoding and small nucleolar RNAs dysregulated in head and neck squamous cell carcinoma. lnc-LCE5A-1 NA NA NA NA NA laryngeal cancer C32 NA RNA-seq, qPCR etc. cell lines (UMSCC-22B) down-regulated We confirmed the dysregulation of these noncoding RNAs in head and neck cancer cell lines derived from different anatomic sites, and determined that ectopic expression of the two lncRNAs inhibited key EMT and stem cell genes and reduced cellular proliferation and migration. 25904139 2015 Transcriptome sequencing uncovers novel long noncoding and small nucleolar RNAs dysregulated in head and neck squamous cell carcinoma. lncMAPK6 NA NA ENSG00000069956 NA GRCh38_15:51952106-52067372 liver cancer C22.0 NA Luciferase reporter assay etc. liver cancer tissues up-regulated MAPK6 was the most highly expressed MAPK component in liver cancer and liver TICs and lncMAPK6 participated in the transcriptional regulation of MAPK6in cis. This work revealed the importance role of MAPK signaling in liver TIC self-renewal and added a new layer for liver TIC and MAPK6 expression regulation. 29764463 2018 LncMAPK6 drives MAPK6 expression and liver TIC self-renewal. lnc-MX1-1 NA NA NA NA NA prostate cancer C61.9 NA microarray, qPCR, RNAi etc. prostate cancer tissues, cell lines (VCaP, LNCaP, 22Rv1, PC3, DU145) up-regulated In the present study, we identified that lncRNA lnc-MX1-1 is over-expressed in prostate cancer tissues compared with their adjacent normal prostate tissues by gene expression array profiling. The expression of lnc-MX1-1 in 60 prostate cancer cases was determined by real-time quantitative PCR and the correlations between lnc-MX1-1 expression and patients' clinical features were further analyzed. 26797523 2016 Long non-coding RNA lnc-MX1-1 is associated with poor clinical features and promotes cellular proliferation and invasiveness in prostate cancer. lncNRON NRON，NCRNA00194 641373 ENSG00000253079 NR_045006 GRCh38_9:126408041-126408410 hepatocellular carcinoma C22.0 M8170/3 qPCR, western blot HCC tissues, cell lines (QGY-7703, HepG2, BEL-7404, Hep3B, SMMC-7721 and MHCC97) down-regulated We observed that lncNRON was downregulated in HCC tumour tissues; low lncNRON expression was associated with poor tumour differentiation and the presence of vascular tumour thrombus, which tended to result in poor clinical outcomes, as demonstrated by the recurrence rate and survival curves. 29772429 2018 Long non-coding RNA NRON is downregulated in HCC and suppresses tumour cell proliferation and metastasis lncPARP1 lncPARP1 105373113 ENSG00000225518 NR_146920 GRCh38_1: 226083639-226090292 hepatocellular carcinoma C22.0 M8170/3 qPCR, western blot etc. hepatocellular carcinoma tissue, cell lines (SMMC-7721, HepG2, Huh7, SK-Hep-1, PLC/PRF/5, and Bel-7402) up-regulated Here, we identified a novel oncogenic lncRNA termed as lncPARP1, which was significantly up-regulated in HCC. Increase in lncPARP1 expression was associated with age, a-fetoprotein (AFP) levels, tumor size, recurrence, and poor prognosis of HCC patients. 29776974 2018 The long noncoding RNA lncPARP1 contributes to progression of hepatocellular carcinoma through up-regulation of PARP1 lnc-PCTST NA NA NA NA NA pancreatic cancer C25 NA qRT-PCR, Western blot assay, ect. The normal human pancreatic ductal cell line (hTERT-HPNE), Human pancreatic cancer cell lines (PANC-1, MiaPaCa-2, BxPC-3 and AsPC-1) and 293T cells, PC and non-tumor tissues down-regulated lnc-PCTST expression is down-regulated in pancreatic cancer tissues. Also, lnc-PCTST has shown to be negatively correlated with transforming acidic coiled-coil 3 (TACC-3) expression.lnc-PCTST overexpression in pancreatic cancer cell lines inhibited cell proliferation and invasion in vitro, and tumorigenesis in vivo, but did not altered cell migration. Additionally, TACC-3 knockdown simulated the inhibiting effect of lnc-PCTST overexpression on pancreatic cancer cell lines, and the impaired proliferation, invasion effect and E-cadherin, vimentin expression on lnc-PCTST over-expressed cell lines can be rescued by overexpressed TACC-3. Significantly, the expression of lnc-PCTST was closely associated with its genomic neighboring gene TACC-3 and inhibited its promoter activity. 29978472 2018 Long non-coding RNA lnc-PCTST predicts prognosis through inhibiting progression of pancreatic cancer by downregulation of TACC-3. LncRNA00673 NA NA NA NA NA colorectal cancer C19.9 NA qPCR CRC tissue, Human CRC cell lines (HT-29, LOVO, SW480, HCT-116, RKO, HCT-8, HCT-15, DLD1) up-regulated The expression level of lncRNA00673 is up-regulated in CRC tissues and cells, which is related to the degree of malignancy and poor prognosis.knockdown of lncRNA0673 could inhibit the proliferation of CRC cells. 29461596 2018 Association of the upregulation of LncRNA00673 with poor prognosis for colorectal cancer. lncRNA-422 NA NA NA NA NA colorectal cancer C19.9 NA qPCR cell lines (NCM460, SW480, HCT116, DLD-1, HT29, and SW620) down-regulated lncRNA-422(ENST00000415820) significantly downregulated in the tissues and serum of CRC patients, and is closely associated with the poor prognosis. lncRNA-422 overexpression inhibited cell proliferation, migration, and invasion. Knockdown of lncRNA-422 promoted tumorigensis.lncRNA-422 acts as a tumor suppressor by PI3K/AKT/mTOR pathway in CRC.CRC patients with high expression of lncRNA-422 had a significantly longer survival time than those with low lncRNA-422 expression. 29050940 2017 Long non-coding RNA-422 acts as a tumor suppressor in colorectal cancer lncRNA625 NA NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR, RNAi, Western blot, Cell migration and invasion assay etc. ESCC tissues, cell lines (KYSE150, KYSE450, KYSE510) up-regulated We identified lncRNA625 as a novel regulator of ESCC cell proliferation, invasion and migration. ESCC patients with high lncRNA625 expression had significantly shorter survival time than those with low expression. LncRNA625 also showed specific prognostic value for patients with metastatic ESCC. Finally, we identified E1A-binding protein p300 (EP300) as a downstream executor of lncRNA625-induced transcriptional responses. 28194033 2017 Integrative analyses of transcriptome sequencing identify novel functional lncRNAs in esophageal squamous cell carcinoma. lncRNA-AK098783 NA NA NA NA GRCh38_10:86948677-86949657 colorectal cancer C19.9 NA Microarray, qPCR etc. colorectal cancer tissues, cell lines (CaCO2, HCT116, Lovo, SW480, SW620) up-regulated lncRNA-AK098783 expression level was frequently higher in cancerous tissues than corresponding noncancerous tissue. Higher AK098783 expression was significantly correlated with shortened overall survival (P < 0.001) and distant metastasis (P < 0.001). 29590393 2018 Long non-coding RNA expression profiles reveals AK098783 is a biomarker to predict poor prognosis in patients with colorectal cancer. lncRNA-ATB LOC109207222 109207222 NA NA NA colon cancer C18 NA qPCR etc. colon cancer tissues up-regulated LncRNA-ATB was upregulated in colon cancer tissues compared with adjacent mucosa. LncRNA-ATB levels were also higher in metastatic cancer tissues. Among the three highly invasive colon cancer cell lines, lncRNA-ATB levels were relatively higher with concurrent low levels of E-cad compared with levels in the three low-invasive cell lines. LncRNA-ATB expression correlated with pN stage and AJCC stage. Striking differences were observed in overall survival and disease-free survival in cases with both high lncRNA-ATB expression and low E-cad expression. Reduction of lncRNA-ATB increased expression of epithelial markers E-cad, ZO-1, and decreased expression of mesenchymal markers ZEB1 and N-cadherin (N-cad), and significantly influenced colon cancer cell progression. Plasma lncRNA-ATB was upregulated in colon cancer patients one month after surgery. 26487301 2015 LncRNA-ATB mediated E-cadherin repression promotes the progression of colon cancer and predicts poor prognosis lncRNA-ATB LOC109207222 109207222 NA NA NA colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated High lncRNA-ATB expression was significantly associated with greater tumor size, depth of tumor invasion, lymphatic invasion, vascular invasion, and lymph node metastasis. Patients of the high-lncRNA-ATB expression group had significantly poorer outcomes than those of the low-expression group. Additionally, levels of lncRNA-ATB expression were significantly higher in patients with hematogenous metastases. lncRNA-ATB may be involved in the progression of CRC and be a novel indicator of poor prognosis in patients with CRC. 25750289 2015 A Long Noncoding RNA, lncRNA-ATB, Is Involved in the Progression and Prognosis of Colorectal Cancer. lncRNA-ATB LOC109207222 109207222 NA NA NA esophageal squamous cell cancer NA NA qPCR, Western blot, Luciferase reporter assay, RIP etc. esophageal squamous cell carcinoma tissues, cell lines (KYSE150, KYSE140, KYSE410, KYSE520, KYSE510, Ec109, Ec9706 and KYSE30) up-regulated Upregulated lnc-ATB served as an independent prognosis predictor of ESCC patients. Moreover, loss-of-function assays in ESCC cells showed that knockdown of lnc-ATB inhibited cell proliferation and migration both in vitro and in vivo. Mechanistic investigation indicated that lnc-ATB exerted oncogenic activities via regulating Kindlin-2, as the anti-migration role of lnc-ATB silence was attenuated by ectopic expression of Kindlin-2. Further analysis showed that lnc-ATB functions as a molecular sponge for miR-200b and Kindlin-2. Dysregulated miR-200b/Kindlin-2 signaling mediated the oncogenic activity of lnc-ATB in ESCC. Our results suggest that lnc-ATB predicts poor prognosis and may serve as a potential therapeutic target for ESCC patients. The results showed that the median overall survival of patients with high lnc-ATB expression was 20 months, whereas the median overall survival for patients with low lnc-ATB expression was 51 months. 28640252 2017 Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis. lncRNA-ATB LOC109207222 109207222 NA NA NA osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay osteosarcoma tissues, cell lines (MG63, U2OS, SAOS2, and HOS) up-regulated LncRNA-ATB is also upregulated in osteosarcoma tissues and cell lines, and positively associated with Enneking stage, metastasis and recurrence. Increased lncRNA-ATB level indicates poor recurrence-free survival and overall survival. Mechanistically, we found that lncRNA-ATB inhibits miR-200s, and upregulates miR-200s target genes ZEB1 and ZEB2. 28469952 2017 Long noncoding RNA ATB promotes osteosarcoma cell proliferation, migration and invasion by suppressing miR-200s lncRNA-ATB LOC109207222 109207222 NA NA NA glioma NA M9380/3 qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. glioma tissues, cell lines (U251 and A172) up-regulated ATB is abnormally up-regulated both in glioma tissues and cell lines compared with normal brain tissues, and glioma patients with high ATB expression had shorter overall survival time. Knockdown of ATB significantly inhibits glioma malignancy, including cell proliferation, colony formation, migration, invasion in vitro, and the xenograft tumor formation in vivo. In addition, ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-B2. 27267902 2016 Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a. lncRNA-ATB LOC109207222 109207222 NA NA NA renal cell carcinoma C64.9 NA qPCR renal cell carcinoma tissues up-regulated The expression level of lncRNA-ATB was significantly upregulated in RCC tissues vs. corresponding non-tumor tissues (p<0.01) and the high expression of lncRNA-ATB was significantly associated with histological grade (p=0.008), lymph nodes metastasis (p=0.015), and distant metastasis (p=0.008). Also, Kaplan-Meier analysis indicated patients with high lncRNA-ATB expression that had a significantly shorter overall survival than those with low lncRNA-ATB expression (p<0.001). 28682434 2017 High expression of long non-coding RNA ATB is associated with poor prognosis in patients with renal cell carcinoma lncRNA-ATB LOC109207222 109207222 NA NA NA cervical cancer C53 NA qPCR cervical cacner tissues, cell lines (SiHa, HeLa, CaSki, MS750, and C33A) up-regulated LncRNA ATB was upregulated in cervical cancer cell lines and tissues (P < 0.05). Survival analysis indicated that patients with high ATB expression had a significantly shorter OS (P < 0.001) or PFS (P < 0.001) than those with low ATB expression 29237907 2017 Long noncoding RNA activated by transforming growth factor-B promotes cancer development and is a prognostic marker in cervical cancer lncRNA-ATB LOC109207222 109207222 NA NA NA non small cell lung cancer C34 M8046/3 qPCR, RNAi, Flow cytometry assay etc. NSCLC tissues, cell lines (A549 and NCI-H1299) up-regulated Real-time PCR results showed that lncRNA-ATB expression was up-regulated in both in NSCLC tissues and cell lines. High lncRNA-ATB expression in tumor tissue was associated with larger tumor size, lymph node metastasis, and distant metastasis in patients with NSCLC, respectively. In addition, the patients with high expression of lncRNA-ATB presented a lower survival probability. In vitro experiments showed that down-regulation of lncRNA-ATB promoted the cell apoptosis, whereas inhibited the cell viability, cell migration, and cell invasion. 27878433 2016 High expression of long non-coding RNA ATB indicates a poor prognosis and regulates cell proliferation and metastasis in non-small cell lung cancer. lncRNA-ATB LOC109207222 109207222 NA NA NA prostate cancer C61.9 NA qPCR, Western blot etc. primary prostate cancer tissues, cell lines (PC-3 and DU145) up-regulated We showed that lncRNA-ATB expression was significantly upregulated in tumor tissues in patients with prostate cancer in comparison with adjacent non-tumor tissues. Further analysis indicted that high lncRNA-ATB expression may be an independent prognostic factor for biochemical recurrence (BCR)-free survival in prostate cancer patients. Overexpression of lncRNA-ATB promoted, and knockdown of lncRNA-ATB inhibited the growth of prostate cancer cells via regulations of cell cycle regulatory protein expression levels. In addition, lncRNA-ATB stimulated epithelial-mesenchymal transition (EMT) associated with ZEB1 and ZNF217 expression levels via ERK and PI3K/AKT signaling pathways 27176634 2016 Long non-coding RNA ATB promotes growth and epithelial-mesenchymal transition and predicts poor prognosis in human prostate carcinoma lncRNA-ATB LOC109207222 109207222 NA NA NA pancreatic cancer C25 NA qPCR etc. pancreatic cancer tissues, cell lines (HPDE6c-7) down-regulated We found that lncRNA-ATB expression was decreased in pancreatic cancer tissues and pancreatic cancer cell lines. Low lncRNA-ATB expression levels were significantly correlated with lymph node metastases, neural invasion, and clinical stage. Moreover, patients with low lncRNA-ATB expression levels exhibited markedly worse overall survival prognoses. Multivariate analysis indicated that decreased lncRNA-ATB expression was an independent predictor of poor prognosis in pancreatic cancer patients. 26482611 2015 Downregulation of lncRNA-ATB correlates with clinical progression and unfavorable prognosis in pancreatic cancer lncRNA-ATB LOC109207222 109207222 NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR hepatocarcinoma tissues up-regulated Expression of lncRNA-ATB was significantly associated with portal vein thrombosis, intrahepatic or extrahepatic metastases, mUICC stage, and the BCLC stage. Large tumors (> 5 cm, HR = 3.851, 95% CI = 1.431–10.364, p = 0.008) and higher lncRNA-ATB expression (HR = 4.158, 95% CI = 1.226–14.107, p = 0.022) were the significant prognostic factors for overall survival. 29108251 2017 Clinical significance of lncRNA-ATB expression in human hepatocellular carcinoma. lncRNA-ATB LOC109207222 109207222 NA NA NA gastric cancer C16 NA qPCR, RNAi etc. cell line (HepG2，MCF7，UVECs), gastric cancer tissues down-regulated In gastric tissue samples,cancerous tissues had relatively lower lncRNA-ATB expression levels than noncancerous ones, although the difference was not statistically significant.lncRNA-ATB levels were inversely associated with depth of invasion (T). Trastuzumab resistance and invasion-metastasis cascade in breast cancer is mediated by sponging role of lncRNA-ATB for miR-200c and thus increasing ZEB1 and ZNF- 29657927 2018 Gene Expression Analysis of Two Epithelial-mesenchymal Transition-related Genes: Long Noncoding RNA-ATB and SETD8 in Gastric Cancer Tissues. lncRNA-ATB LOC109207222 109207222 NA NA NA gastric cancer C16 NA qPCR, Cell transfection, Western blot, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc. gastric cancer tissues, cell lines (BGC823 and SGC7901) up-regulated lnc-ATB was significantly upregulated in GC tissues compared to lnc-ATB expression in ANTs.These high lnc-ATB expression levels predicted poor prognosis in GC patients. Low levels of lnc-ATB inhibited GC cell proliferation and cell cycle arrest in vitro. Lnc-ATB was found to directly bind miR-141-3p. Moreover, TGF-B actives lnc-ATB and TGF-B2 directly binds mir-141-3p.Finally, we demonstrated that lnc-ATB fulfilled its oncogenic roles in a ceRNA-mediated manner. 28115163 2017 Lnc-ATB contributes to gastric cancer growth through a MiR-141-3p/TGFB2 feedback loop. lncRNA-ATB LOC109207222 109207222 NA NA NA gastric cancer C16 NA qPCR etc. gastric cancer tissues, cell lines (MKN1, MKN7, MKN28, MKN45, MKN74 etc.) differential expression The high lncRNA-ATB group experienced a lower overall survival rate compared with the low lncRNA-ATB group, and multivariate analysis indicated that lncRNA-ATB was an independent prognostic factor.LncRNA-ATB plays an important role in EMT to promote invasion and metastasis through the TGFb/miR-200s/ZEB axis, resulting in a poor prognosis in GC. LncRNA-ATB is a novel biomarker of lncRNA, indicative of a poor prognosis in GC patients. 25986864 2015 A Long Non-coding RNA Activated by Transforming Growth Factor-B is an Independent Prognostic Marker of Gastric Cancer. lncRNA-ATB LOC109207222 109207222 NA NA NA gastric cancer C16 NA qPCR, RNAi gastric cancer tissues, cell lines (MGC803, MKN45, BGC823, MKN28 and SGC7901,GES1) up-regulated higher expression of lncRNA-ATB was correlated with increased invasion depth, more distant metastasis and advanced tumor, node, metastasis stage. downregulated lncRNA-ATB expression suppressed cellular proliferation, invasion and migration of GC cells. Survival analysis also indicated the inverse relationship between lncRNA ATB expression and cancer prognosis. 29257203 2017 Long noncoding RNA-ATB promotes cell proliferation, migration and invasion in gastric cancer lncRNA-ATB LOC109207222 109207222 NA NA NA malignant melanoma NA M8720/3 qPCR, Western blot, Flow cytometry assay, Luciferase reporter assay, etc. MM cell lines, normal human epidermal melanocyte cell lines. MM tissues. up-regulated In conclusion, the present study revealed the expression and roles of lncRNA?ATB in MM, and indicated that lncRNA?ATB functions as a ceRNA to promote MM proliferation and invasion by sponging miR?590?5p. Despite the notable improvements in diagnosis and treatment made in recent years, the prognosis remains poor for patients diagnosed at the metastatic stage, with a median survival time of 6-9 months and a 5-year survival rate of only 10% (2-4). Finally, it was demonstrated that lncRNA?ATB functions as a competing endogenous RNA (ceRNA) to enhance Yes associated protein 1 expression by competitively sponging microRNA miR?590?5p in MM cells. 29956757 2018 lncRNA-ATB functions as a competing endogenous RNA to promote YAP1 by sponging miR-590-5p in malignant melanoma. lncRNA-BCHE NA NA NA NA NA breast cancer C50 NA qPCR, Microarray, etc. breast cancer tissues up-regulated lncRNA-BCHE is an oncogenic lncRNA enhancing the growth and metastatic potential of breast cancer cells. All breast cancer patients were subdivided into ITGB1low and ITGB1 high groups based on their ITGB1 transcript levels, and their distant metastasis-free survival (DMFS) and relapse-free survival (RFS) probability were plotted over time. In all patients, low ITGB1 gene expression was associated with a superior DMFS and RFS probability relative to the corresponding ITGB1 high group, 29948648 2018 Long non-coding RNA p10247, high expressed in breast cancer (lncRNA-BCHE), is correlated with metastasis. lncRNA-CLMAT3 CTB-113P19.1, CLMAT3 101927096 ENSG00000249035 NR_109873 GRCh38_5:151676945-151724782 colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues up-regulated The levels of lncRNA-CLMAT3 in the cancerous tissues were 2.26-fold higher than those in the normal colorectal tissues. In addition, lncRNA-CLMAT3 expression was significantly higher in the patients with liver metastasis than in those without liver metastasis and in the patients with lymph node metastasis than in those without lymph node metastasis. 26050227 2015 Aberrant expression of long noncoding RNAs in colorectal cancer with liver metastasis. lncRNA-HEIH HEIH, HCCAT2, LINC-HEIH, LINC00848, lncRNA-HEIH 100859930 ENSG00000278970 NR_045680 GRCh38_5:180829954-180831605 colorectal cancer C19.9 NA qPCR, Luciferase reporter assay, Western blot etc. cell line (NCM460, CRC, HT-29, SW480, HCT116) up-regulated In this study, we found that lncRNA-HEIH is significantly increased in CRC tissues and cell lines. lncRNA-HEIH expression is positively associated with tumor size, invasion depth, and poor prognosis of CRC patients. Enhanced expression of lncRNA-HEIH promotes CRC cell proliferation and decreases apoptosis in vitro, and promotes CRC tumor growth in vivo. Whereas knockdown of lncRNA-HEIH inhibits CRC cell proliferation and induces apoptosis in vitro, and suppresses CRC tumor growth in vivo. Mechanistically, lncRNA-HEIH physically binds to miR-939. The interaction between lncRNA-HEIH and miR-939 damages the binding between miR-939 and nuclear factor kB (NF-kB), increases the binding of NF-kB to Bcl-xL promoter, and promotes the transcription and expression of Bcl-xL. 29081216 2017 Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939-Mediated Transcriptional Repression of Bcl-xL lncRNA-HEIH HEIH, HCCAT2, LINC-HEIH, LINC00848, lncRNA-HEIH 100859930 ENSG00000278970 NR_045680 GRCh38_5:180829954-180831605 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. hepatocellular carcinoma tissues, cell lines (HEMa-LP, SK-MEL-28, A375, A2058, SK-MEL-2) up-regulated lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients. Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription. The expression of miR-200b is inversely associated with lncRNA-HEIH in melanoma tissues. In conclusion,we identified lncRNA-HEIH as a key oncogene in melanoma via transcriptional inhibition of miR-200b/a/429. Our data suggested that lncRNA-HEIH may serve as a promising prognostic biomarker and therapeutic target for melanoma. 28487474 2017 Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429. lncRNA-HEIH HEIH, HCCAT2, LINC-HEIH, LINC00848, lncRNA-HEIH 100859930 ENSG00000278970 NR_045680 GRCh38_5:180829954-180831605 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RIP, RNA pull-down assay etc. HCC tissues, cell lines (Huh7, HepG2) up-regulated The transcript levels of lncRNA-HEIH were higher in HCC tissues when compared with the corresponding non-tumor liver tissues from the same donor. And we found that patients with high lncRNA-HEIH expression in HCC had significantly worse prognosis than those with low lncRNA-HEIH expression. 21769904 2011 Long noncoding RNA high expression in hepatocellular carcinoma facilitates tumor growth through enhancer of zeste homolog 2 in humans. lncRNA-LET NPTN-IT1, lncRNA-LET 101241892 ENSG00000281183 NR_103844 GRCh38_15:73567012-73569294 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RIP, RNA pull-down assay etc. HCC tissues down-regulated AY129027, uc002pyc and DQ786243 were over-expressed in HCC, whereas the expression of AK055007 and AK123790 was decreased. 21769904 2011 Long noncoding RNA high expression in hepatocellular carcinoma facilitates tumor growth through enhancer of zeste homolog 2 in humans. lncRNA-LET NPTN-IT1, lncRNA-LET 101241892 ENSG00000281183 NR_103844 GRCh38_15:73567012-73569294 cervical cancer C53 NA qPCR etc. cervical cancer tissues down-regulated The results showed that lncRNA LET expression in cervical cancer tissues was significantly down-regulated compared with the adjacent non-tumor tissues. Decreased lncRNA LET expression was significantly correlated with FIGO stage, lymph node metastasis, and depth of cervical invasion, but not other clinical characteristics. 25755778 2015 Low expression of long non-coding RNA LET inhibits carcinogenesis of cervical cancer. lncRNA-LET NPTN-IT1, lncRNA-LET 101241892 ENSG00000281183 NR_103844 GRCh38_15:73567012-73569294 bladder cancer C67 NA qPCR, RIP, western blot etc. BC tissues, cell lines (T24, 5637, J82, SW780, BIU87, ScaBER and UMUC3) down-regulated LET was the only lncRNA that was downregulated more than 2 folds in GEM-treated xenografts derived from both T24 and 5637 cells. The array results were further validated in these cell lines treated with or without GEM. reduced lncRNA-LET increased the NF90 protein stability, which in turn repressed biogenesis of miR-145 and subsequently resulted in accumulation of CSCs evidenced by the elevated levels of stemness markers HMGA2 and KLF4. UBC patients which displayed lower expression levels of lncRNA-LET and miR-145 had a reduced survival rate, whereas TGFB1 expression level did not show significant difference in clinical outcome. 28839463 2017 TGFB1 Promotes Gemcitabine Resistance through Regulating the LncRNA-LET/NF90/miR-145 Signaling Axis in Bladder Cancer lncRNA-LET NPTN-IT1, lncRNA-LET 101241892 ENSG00000281183 NR_103844 GRCh38_15:73567012-73569294 gallbladder cancer C23.9 NA qPCR, Western blot, Flow cytometry assay etc. gallbladder cancer tissues, cell lines (GBC-SD, SGC-996, NOZ, EH-GB2) down-regulated In the present study, an obvious down-regulation of lncRNA-LET was observed in gallbladder cancer compared to their adjacent normal tissues. Meanwhile, patients with low expression of lncRNA-LET have significantly poorer prognosis than those with high expression. We confirmed that hypoxia decreased lncRNA-LET levels in gallbladder cancer cells. Moreover, lncRNA-LET overexpression was further validated to inhibit the invasion of gallbladder cancer cells under hypoxic or normoxic conditions in vitro. We demonstrated that lncRNA-LET overexpression conferred a proliferative advantage to tumor cells under hypoxic conditions. 25213660 2014 Long non-coding RNA-LET is a positive prognostic factor and exhibits tumor-suppressive activity in gallbladder cancer. lncRNA-LET NPTN-IT1, lncRNA-LET 101241892 ENSG00000281183 NR_103844 GRCh38_15:73567012-73569294 gastric cancer C16 NA qPCR etc. gastric cancer tissues down-regulated We found that lncRNA LET expression was markedly down-regulated in tumor tissues compared with adjacent non-tumor tissues, and associated with depth of invasion, lymph node metastasis, distant metastasis, and TNM stage. Univariate and multivariate analyses showed that low lncRNA LET expression was an independent poor prognostic factor for gastric cancer patients. 25674261 2015 Down-regulation of long non-coding RNA LET is associated with poor prognosis in gastric cancer. lncRNA-LET NPTN-IT1, lncRNA-LET 101241892 ENSG00000281183 NR_103844 GRCh38_15:73567012-73569294 esophageal squamous cell cancer NA NA qPCR, Luciferase reporter assay, Western blot esophageal squamous cell carcinoma tissues, cell lines (Het-1A,KYSE30,TE-1, KYSE150, KYSE410, and Eca-109) up-regulated Down-regulated lncRNA-LET also indicated poor overall survival of ESCC patients.lncRNA-LET inhibits the proliferation and migration of ESCC cells, and the effects of miR-548k on ESCC are dependent on the negative regulation of lncRNA-LET. 29126868 2017 Up-regulated miR-548k promotes esophageal squamous cell carcinoma progression via targeting long noncoding RNA-LET. lncRNA-LET NPTN-IT1, lncRNA-LET 101241892 ENSG00000281183 NR_103844 GRCh38_15:73567012-73569294 nasopharyngeal cancer C11 NA qPCR, RNAi, Western blot etc. NPC tissues, cell lines (CNE2, HNE2) down-regulated We found that lncRNA-LET was significantly downregulated in nasopharyngeal carcinoma (NPC) tissues compared with corresponding normal tissues. Decreased LET expression is significantly correlated with advanced clinical stage, larger tumor size, increased lymph node tumor burden, and poor survival of NPC patients. Knockdown of LET promoted NPC cells proliferation and inhibited cell apoptosis. Importantly, we found lncRNA-LET is transcriptional repressed by EZH2-mediated H3K27 histone methylation on the LET promoter. The expressions of EZH2 and lncRNA-LET are significantly inversely correlated in NPC tissues. 26243049 2015 Long noncoding RNA-LET, which is repressed by EZH2, inhibits cell proliferation and induces apoptosis of nasopharyngeal carcinoma cell. lncRNA-n336928 NA NA NA NA NA bladder cancer C67 NA microarray, qPCR etc. bladder cancer tissues up-regulated Results showed that the expression level of lncRNA-n336928 (noncode database ID: n336928) was significantly higher in bladder cancer tissues compared to that in adjacent noncancerous tissues. Collectively, our study shows that high expression of lncRNA-n336928 is associated with the progression of bladder cancer, and that lncRNA-n336928 might serve as a biomarker for prognosis of bladder cancer. 26551459 2015 Expression of long noncoding RNA lncRNA-n336928 is correlated with tumor stage and grade and overall survival in bladder cancer. lncRNA-NEF NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 RNA-seq, qPCR, Western blot liver cell lines (MiHA, SK-HEP-1, PLC/PRF/5, Hep3B and Huh7, HepG2, Bel7404) down-regulated the lncRNA-NEF was transcriptionally activated by EMT suppressor FOXA2 and frequently downregulated in HCC cell lines as well as clinical specimens. Although enhanced expression of lncRNA-NEF did not affect tumor cell growth, ectopic expression of lncRNA-NEF significantly suppressed EMT program and cell migration. Animal studies validated that lncRNA-NEF alleviated in vivo tumor metastasis and protected mice from tumor-induced mortality. Interestingly, we verified that lncRNA-NEF acted as a novel activator of its neighbor gene FOXA2, which formed a positive feedback loop. Subsequent studies revealed that lncRNA-NEF physically interacted with B-catenin to increase the binding of GSK3B with B-catenin and therefore promoted the inhibitory phosphorylation of B-catenin, leading to the suppression on Wnt/B-catenin signaling and activation of FOXA2 expression. 29311643 2018 LncRNA-NEF antagonized epithelial to mesenchymal transition and cancer metastasis via cis-regulating FOXA2 and inactivating Wnt/B-catenin signaling. lncRNA-NUTF2P3-001 NUTF2P3 NA ENSG00000228248 NA GRCh38_9:77580245-77580628 pancreatic cancer C25 NA microarray, qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc. pancreatic cancer tissues, cell lines (PANC-1 and BXPC-3) up-regulated lncRNA-NUTF2P3-001 is upregulated in pancreatic cancer cells under hypoxia and CoCl2 treatment, which is attributed to the binding of hypoxia-inducible factor-1a (HIF-1a) to hypoxia response elements (HREs) in the upstream of KRAS promoter. Data from pancreatic cancer patients show a positive correlation between lncRNA-NUTF2P3-001 and KRAS, which is associated with advanced tumor stage and worse prognosis. Hence, our data provide a new lncRNA-mediated regulatory mechanism for the tumor oncogene KRAS and implicate that lncRNA-NUTF2P3-001 and miR-3923 can be applied as novel predictors and therapeutic targets for pancreatic cancer. 26755660 2016 Hypoxia-induced lncRNA-NUTF2P3-001 contributes to tumorigenesis of pancreatic cancer by derepressing the miR-3923/KRAS pathway. LncRNA-RP11-317J10.2 NA NA NA NA GRCh38_8:85441851-85464915 colorectal cancer C19.9 NA qPCR colorectal cancer tissues, cell lines (NCM460, HT-29, HCT116, SW480, SW620 and LoVo) down-regulated LncRNA-RP11-317J10.2 is downregulated in CRC and decreased expression is significantly associated with advanced tumor stage, larger tumor size and poor prognosis. RNA interference-mediated knockdown of lncRNA-RP11-317J10.2 in CRC cells promotes G1-to-S cell cycle transition, enhances invasiveness and facilitates cell growth in vitro and in mouse tumor xenograft models. Cyclin D1 was upregulated by lncRNA-RP11-317J10.2 knockdown, and co-expression of cyclin D1-targeting siRNA abrogates the pro-tumorigenic effects of lncRNA-RP11-317J10.2 knockdown.over-expression of PIWIL3 and miR-367-3p together with OIP5-AS1 knockdown produced the smallest xenograft volume in contrast to their respective single application, contributing to the longest survival. 29073791 2017 Downregulation of LncRNA-RP11-317J10.2 promotes cell proliferation and invasion and predicts poor prognosis in colorectal cancer. lncRNA-TTN-AS1 NA 100506866 ENSG00000237298 NR_038272 GRCh38_2:178521183-178779963 esophageal squamous cell cancer NA NA Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RNAi, RIP ESCC tissue, ESCC cell lines (Eca-109, KYSE 30, KYSE 150, KYSE180, KYSE410, KYSE450, KYSE510, TE-10 and TE-13) up-regulated lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial-mesenchymal transition (EMT) cascade.Moreover,lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR,which further promotes ESCC invasion cascades. 29101304 2017 Functional Role of a Novel Long Noncoding RNA TTN-AS1 in Esophageal Squamous Cell Carcinoma Progression and Metastasis. lncRNA-UNMIBC NA NA NA NA NA bladder cancer C67 NA qPCR, Western blot, RIP, ChIP etc. bladder cancer tissues, cell lines (J82, UM-UC-3, HT-1376, T24, 5637, TCCSUP etc.) up-regulated The expression level of lncRNA-UNMIBC was up-regulated in the tissues of 45 cases of primary nonmuscle invasive bladder cancer compared with normal mucosa. We also found that lncRNA-UNMIBC had a key role in G0/G1 arrest. Furthermore, RNA and chromatin immunoprecipitation assays demonstrated that lncRNA-UNMIBC was physically associated with EZH2 and SUZ12, leading to an altered histone H3 lysine 27 methylation status of target genes. 27267320 2016 lncRNA Up-Regulated in Nonmuscle Invasive Bladder Cancer Facilitates Tumor Growth and Acts as a Negative Prognostic Factor of Recurrence. lncRNA-URHC NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, Western blot etc. HCC tissues, cell lines (DMEM, Gibco, Gaithersburg, MD, USA etc.) up-regulated We confirmed that URHC expression was up-regulated in 30 HCC cases (57.7%) and that its higher expression was correlated with poor overall survival. We further demonstrated that URHC inhibition reduced cell proliferation and promoted apoptosis. high URHC expression can promote cell proliferation and inhibit apoptosis by repressing ZAK expression through inactivation of the ERK/MAPK pathway. 25013376 2014 Long non-coding RNA URHC regulates cell proliferation and apoptosis via ZAK through the ERK/MAPK signaling pathway in hepatocellular carcinoma. lncTCF7 WSPAR, LncTCF7, TCONS_00009511, NR_033449 6932 ENSG00000081059 NA GRCh38_5:134114711-134151865 colorectal cancer C19.9 NA qPCR, Western blot colorectal cancer tissues, cell lines (DLD1 and LoVo) up-regulated LncTCF7 was upregulated in 52/58 CRC tissues, and its expression correlated with tumor size, lymph metastasis and tumor-node-metastasis stage in CRC. Knocking down lncTCF7 in colon cancer cell lines decreased cell proliferation, migration and invasion.lncTCF7 promoted cell proliferation in vivo. LncTCF7 activated the Wnt/B-catenin signaling pathway,which is essential for cancer development.patients with higher expression of lncTCF7 had significantly worse prognosis compared with patients with low expression. 29344178 2017 Long non-coding RNA lncTCF7 activates the Wnt/B-catenin pathway to promote metastasis and invasion in colorectal cancer. Lnc-THOR NA NA NA NA NA osteosarcoma NA M9180/3 qPCR, Western blot, in vitro knockdown etc. osteosarcoma tissues, cell lines (U2OS, MG-63 and SaOs-2) down-regulated In the current study, we show that Lnc-THOR is expressed in established and primary human OS cells. It is also detected in human OS tissues, but not in the surrounding normal bone tissues. siRNA-induced knockdown or CRSIPR/Cas9-mediated knockout Lnc-THOR significantly inhibited human OS cell survival and proliferation. Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) target mRNAs, including IGF2, GLI1 and CD44, were downregulated in Lnc-THOR-silenced OS cells as well. Conversely, forced over-expression of Lnc-THOR enhanced IGF2BP1 target mRNA expression, promoting OS cell survival and proliferation. In vivo, xenograft tumors of Lnc-THOR-knockout U2OS cells grew significantly slower than the control U2OS tumors. 29626476 2018 Long non-coding RNA THOR promotes human osteosarcoma cell growth in-vitro and in-vivo. Lnc-THOR NA NA NA NA NA renal cell carcinoma C64.9 NA qPCR, Western blot etc. renal cell carcinoma tissues, cell lines (HK-2, 786-O, A498 and ACH) up-regulated We show that THOR is expressed in human renal cell carcinoma (RCC) tissues and established/primary human RCC cells. It was not detected in normal renal tissues nor in HK-2 and primary human renal epithelial cells. THOR silencing (by targeted siRNAs) or CRISPR/Cas9 knockout inhibited RCC cell growth, viability and proliferation in vitro. Reversely, forced over-expression of THOR promoted RCC cell survival and proliferation. IGF2BP1-regulated genes, including IGF2, GLI1 and Myc, were downregulated by THOR silencing or knockout, but they were upregulated after THOR over-expression. 29752937 2018 LncRNA THOR promotes human renal cell carcinoma cell growth. LncTIC1 NA NA NA NA NA liver cancer C22.0 NA CRISPR, qPCR, western blot etc. liver cancer tissues up-regulated Here, we performed unbiased screening of lncRNAs in liver tumorigenesis and found lncTIC1 was highly expressed with liver tumorigenesis. Meanwhile, lncTIC1 expression levels were related to liver cancer relapse, metastasis and clinical prognosis. 29778568 2018 LncTIC1 interacts with β-catenin to drive liver TIC self-renewal and liver tumorigenesis lncUSMycN MYCNUT, MYCNUN, lncUSMycN 103752554 ENSG00000223850 NR_125783 GRCh38_2:15920399-15936017 neuroblastoma NA M9500/3 qPCR, RNAi etc. neuroblastoma tissues up-regulated The lncUSMycN gene was coamplified with MYCN in 88 of 341 human neuroblastoma tissues. lncUSMycN RNA bound to the RNA-binding protein NonO, leading to N-Myc RNA upregulation and neuroblastoma cell proliferation. High levels of lncUSMycN and NonO expression in human neuroblastoma tissues independently predicted poor patient prognoses. Treatment with antisense oligonucleotides targeting lncUSMycN in neuroblastoma-bearing mice statistically significantly hindered tumor progression. 24906397 2014 Effects of a novel long noncoding RNA, lncUSMycN, on N-Myc expression and neuroblastoma progression. lncWDR26 NA NA ENSG00000162923 NA GRCh38_1:224385143-224437033 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, in vitro knockdown etc. cell lines (SMMC-7721, PLC/PRF/5, Huh7, SK-Hep-1 and Hep3B, LO2), HCC tissue down-regulated lncWDR26 was significantly downregulated in HCC tissues and cells. Moreover, decreased lncWDR26 expression correlates with larger tumor size, higher clinical stage, and tumor metastasis, and also predicts poor prognosis in patients with HCC. In HCC cells, overexpression of lncWDR26 inhibited growth and metastasis, both in vitro and in vivo. Mechanistically, lncWDR26 suppressed HCC growth and metastasis by inhibiting WDR26 transcription. Notably, lncWDR26 was associated with SIX homeobox 3 (SIX3), and this association was required for the repression of WDR26 transcription. 29736313 2018 A novel long noncoding RNA lncWDR26 suppresses the growth and metastasis of hepatocellular carcinoma cells through interaction with SIX3. lnc-ZNF180-2 ZNF180, HHZ168 7733 ENSG00000167384 NA GRCh38_19:44474428-44500524 clear cell renal cell carcinoma C64.9 M8005/0 microarray, qPCR etc. ccRCC tissues down-regulated lnc-ZNF180-2 levels were similar in localized ccRCC and normal renal tissue, but we observed a significant increase of lnc-ZNF180-2 expression in advanced ccRCC tissue. Furthermore, lnc-ZNF180-2 expression levels were an independent predictor of progression-free survival, cancer-specific survival and overall survival in ccRCC patients. We also observed that lnc-CYP4A22-2/3 expression levels allowed discrimination of ccRCC and normal renal tissue. In conclusion, lncRNAs are involved in renal carcinogenesis, and quantification of lnc-ZNF180-2 may be useful for the prediction of ccRCC patients outcome following nephrectomy. 26609485 2015 The long non-coding RNA lnc-ZNF180-2 is a prognostic biomarker in patients with clear cell renal cell carcinoma. LOC100129148 LOC100129148 NA NA NA NA nasopharyngeal cancer C11 NA qPCR, RNAi, Western blot, Luciferase reporter assay, CCK-8 assay etc. NPC tissues, cell lines (SUNE-1, CNE-1, HNE-1, CNE-2, C666-1 and HONE-1) up-regulated LOC100129148 was up-regulated in NPC tissues and cell lines, and higher expression of LOC100129148 resulted in a markedly poorer survival time.Over-expressed LOC100129148 favored, but silenced LOC100129148 hampered cell proliferation in NPC cells. Additionally, LOC100129148 enhanced the KLF12 expression through functioning as a competitive 'sponge' for miR-539-5p. 28328537 2017 Long non-coding RNA LOC100129148 functions as an oncogene in human nasopharyngeal carcinoma by targeting miR-539-5p. LOC100130476 RP11-356I2.4, LOC100130476 NA NA NA NA gastric cardia adenocarcinoma C16.0 M8140/3 qPCR, RNAi, Cell proliferation assay etc. GCA tissues, cell lines (SGC-7901 and BGC-823) down-regulated Significant downregulation of LOC100130476 was detected in SGC-7901 and BGC-823 cell lines and primary GCA tissues. The findings of the association between LOC100130476 expression, methylation and TNM stage, pathological differentiation, and GCA patients' survival further identified the role of LOC100130476 as a tumor suppressor gene. Furthermore, the hypermethylation of LOC100130476 was also detected in peripheral white blood cells of GCA cases. Thus, LOC100130476 may be act as a tumor suppressor gene in GCA carcinogenesis and aberrant methylation at the CpG sites near the transcription start site within exon 1 may be critical for gene silencing. 27189370 2016 Methylation-mediated downregulation of long noncoding RNA LOC100130476 in gastric cardia adenocarcinoma. LOC146880 ARHGAP27P1 NA NA NA NA non small cell lung cancer C34 M8046/3 microarray, qPCR, Western blot, Luciferase reporter assay etc. NSCLC tissues, cell lines (A549, H1299, H1975 and PC9) up-regulated Two of the lncRNAs, LOC146880 and ENST00000439577, were positively correlated with expression of two cancer-related genes, KPNA2 and RCC2, respectively. High expression of LOC146880 and ENST00000439577 were also associated with poor survival. Analysis of lncRNA expression in relation to DNA methylation showed that LOC146880 expression was down-regulated by DNA methylation in its promoter. Lowering the expression of LOC146880 or ENST00000439577 in tumor cells could inhibit cell proliferation, invasion and migration. 27849024 2016 Analysis of Microarray Data on Gene Expression and Methylation to Identify Long Non-coding RNAs in Non-small Cell Lung Cancer. LOC285758 NA 285758 ENSG00000227502 NR_038863 GRCh38_6:113868013-113873351 acute myeloid leukemia NA M9861/3 Microarray, qPCR, Western blot Bone marrow of acutemyeloid leukemia, cell lines (KG-1a, THP-1) up-regulated Our results showed that the proliferation of those two cell lines were inhibited after knock-down of LOC285758. enhancer lncRNA LOC285758 showed thesignificant association with the poor overall survival based on 197AML samples from TCGA. 28203711 2017 Genome-wide characterization of lncRNAs in acutemyeloid leukemia LOC344887 NMRAL2P, NMRAL1P1 344887 ENSG00000171658 NA GRCh38_3:185959943-185980872 non small cell lung cancer C34 M8046/3 qPCR, microarray etc. gallbladder cancer tissues, cell lines up-regulated Our present work frstly reports the prognostic value of Loc344887 in NSCLC patients. Low expression of Loc344887 is a good prognosis indicator in patients with NSCLC. Further studies are needed to investigate the mechanism underlying the oncogenetic function of Loc344887 for this malignancy. 29875987 2017 Long non-coding RNA Loc344887 is a potential prognostic biomarker in non-small cell lung cancer LOC389641 RP11-1149O23.3, LOC389641 NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, RNAi, Western blot etc. PDAC tissues, cell lines (SW1990, AsPC-1, PANC-1, MIAPaCa-2, BxPC-3 and Capan-2) up-regulated Here, we found that a novel lncRNA, LOC389641, was upregulated in PDAC tissues and cell lines. Knockdown of LOC389641 impaired cell proliferation and invasion and induced cell apoptosis in vitro, whereas overexpression of LOC389641 had the opposite effetc. Further, a significant negative correlation was observed between E-cadherin levels and LOC389641 levels in vivo. Knockdown of LOC389641 upregulated E-cadherin expression, but knockdown of E-cadherin had a limited influence on LOC389641. Importantly, after E-cadherin was inhibited, the enhancement of LOC389641 on cell invasion was hindered. Moreover, the expression of LOC389641 was closely associated with its genomic neighboring gene TNFRSF10A. 26708505 2016 Long non-coding RNA LOC389641 promotes progression of pancreatic ductal adenocarcinoma and increases cell invasion by regulating E-cadherin in a TNFRSF10A-related manner. LOC400891 LRRC74B NA ENSG00000187905 NA GRCh38_22:21045960-21064168 prostate cancer C61.9 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. prostate cancer tissues, cell lines (PC-3, DU-145, 22RV1) up-regulated We found that the expression level of LOC400891 was higher in PCa tissues and cells compared to adjacent non-tumor tissues and normal prostate stromal immortalized cells WPMY-1. The patients with higher LOC400891 expression had an advanced clinical features and a shorter biochemical recurrence-free survival time than those with lower LOC400891 expression. We also found that knockdown of LOC400891 could inhibit cell proliferation, migration, and invasion in vitro study. 26797783 2016 Overexpression of long non-coding RNA LOC400891 promotes tumor progression and poor prognosis in prostate cancer. LOC440040 NA NA NA NA GRCh38_11:49558528-49810419 prostate cancer C61.9 NA qPCR, Western blot etc. cell lines (PC-3, DU-145, 22RV1) up-regulated LOC440040 expression was upregulated in PCa tissues and cell lines. Clinicopathological analysis showed that patients with high LOC440040 expression exhibited more advanced clinical features and shorter overall survival than those with low LOC440040 expression. Multivariate regression analysis revealed that LOC440040 expression was an independent prognostic factor in patients with PCa. Knockdown of LOC440040 inhibited PCa cell proliferation, migration and invasion. 29066914 2017 Upregulation of long noncoding rna lOc440040 promotes tumor progression and predicts poor prognosis in patients with prostate cancer LOC554202 MIR31HG, hsa-lnc-31, LncHIFCAR 554202 ENSG00000171889 NR_027054 GRCh38_9:21455642-21559669 oral cancer C06.9 NA qPCR, Western blot, Luciferase reporter assay, RIP etc. cell lines (HeLa and HEK293T) up-regulated Extensive analyses of clinical data indicate LncHIFCAR level is substantially upregulated in oral carcinoma, significantly associated with poor clinical outcomes and representing an independent prognostic predictor. Overexpression of LncHIFCAR induces pseudo-hypoxic gene signature, whereas knockdown of LncHIFCAR impairs the hypoxia-induced HIF-1a transactivation, sphere-forming ability, metabolic shift and metastatic potential in vitro and in vivo. Mechanistically, LncHIFCAR forms a complex with HIF-1a via direct binding and facilitates the recruitment of HIF-1a and p300 cofactor to the target promoters. Patients with high LncHIFCAR expression level had a significantly worse overall survivaland recurrence-free survival than those with low LncHIFCAR expression. 28639619 2017 Long noncoding RNA LncHIFCAR/MIR31HG is a HIF-1a co-activator driving oral cancer progression. LOC554202 MIR31HG, hsa-lnc-31, LncHIFCAR 554202 ENSG00000171889 NR_027054 GRCh38_9:21455642-21559669 cervical cancer C53 NA qPCR, Western blot etc. cervical tissues up-regulated Loc554202 is an independent poor prognostic factor through multivariate analysis. Subsequently, using cervical cancer cell lines, HeLa and ME-180, we decreased the expression levels of Loc554202 with siRNA. As results, the proliferation ability of cervical cancer cells was inhibited and apoptosis was induced after Loc554202 knockdown, as judged by viability assay, colony formation, and flow cytometry. Moreover, knockdown of Loc554202 expression downregulated Bcl-2 expression and conversely up-regulated Bax expression in cervical cancer cells using Western blotting analysis. In conclusion, elevated levels of Loc554202 are predictive of poor prognosis in cervical cancer. We suggest that Loc554202 may serve as a potential therapeutic target for cervical cancer. 29129878 2017 Elevated Expression Levels of Long Non-Coding RNA, Loc554202, Are Predictive of Poor Prognosis in Cervical Cancer LOC554202 MIR31HG, hsa-lnc-31, LncHIFCAR 554202 ENSG00000171889 NR_027054 GRCh38_9:21455642-21559669 colorectal cancer C19.9 NA qPCR etc. CRC tissues down-regulated Our findings showed that Loc554202 appeared to have lower expression in the CRC tissues, compared with the adjacent non-cancerous colorectal tissues. Down-regulated expression of Loc554202 was significantly associated with TNM stage, histologic grade, and lymph node metastasis. 27831651 2016 Long non-coding RNA Loc554202 expression as a prognostic factor in patients with colorectal cancer. LOC554202 MIR31HG, hsa-lnc-31, LncHIFCAR 554202 ENSG00000171889 NR_027054 GRCh38_9:21455642-21559669 esophageal cancer C15 NA qPCR etc. ESCC tissue down-regulated Down-regulated MIR31HG in ESCC patients was associated with malignant clinical characteristics. MIR31HG might be considered as a potential prognostic indicator and a potential target for therapeutic targets in ESCC. 28975978 2017 Down-regulation of lncRNA MIR31HG correlated with aggressive clinicopathological features and unfavorable prognosis in esophageal squamous cell carcinoma LOC554202 MIR31HG, hsa-lnc-31, LncHIFCAR 554202 ENSG00000171889 NR_027054 GRCh38_9:21455642-21559669 lung adenocarcinoma C34 M8140/3 qPCR, in vitro knockdown etc. cell lines (A549, H2228, H1975,H1299), lung adenocarcinoma tissue up-regulated MIR31HG was highly expressed in lung adenocarcinoma tissues and cell lines,and associated with clinical staging, N classification,M classification and differentiated degree.MIR31HG high-expression was an independent unfavorable prognostic factor for lung adenocarcinoma patients.Down-regulation of MIR31HG inhibited lung adenocarcinoma cells proliferation and blocked cell-cycle, but has no effect on cell.apoptosis.MIR31HG high-expression is an independent unfavorable prognostic factor for lung adenocarcinoma patients,and serves an oncogenic role to modulate lung adenocarcinoma cells proliferation and cell-cycle. 29367106 2018 LncRNA MIR31HG overexpression serves as poor prognostic biomarker and promotes cells proliferation in lung adenocarcinoma. LOC728290 NA 728290 ENSG00000243694 NR_132411 GRCh38_3:80993868-81095647 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. hepatocellular tissues down-regulated The results of the present study indicated that downregulation of LOC728290 in patients with HCC may be a powerful tumor biomarker, with potential clinical applications in prognosis as well as a therapeutic target. 29085452 2017 Decreased expression of long non-coding RNA LOC728290 in human hepatocellular carcinoma LOC90784 NA NA NA NA GRCh38_2:86020216-86023868 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot cell lines (HepG2, SMMC7721, Bel-7404, PLiver Cancer /PRF/5), liver cancer tissue up-regulated These results indicated that LOC90784 upregulation may be a critical oncogene and potential new biomarker in HCC. LOC90784 overexpression was associated with poor clinical features in the two cohorts and poor overall survival rates in HCC patients with clear resection margins (R0) in cohort 2. 28651931 2017 Upregulated long non-coding RNA LOC90784 promotes cell proliferation and invasion and is associated with poor clinical features in HCC. LOXL1-AS1 NA 100287616 ENSG00000261801 NR_040066 GRCh38_15:73908071-73928248 glioblastoma NA M9440/3 qPCR, Western blot etc. glioblastoma tissues, cell lines (U87MG) down-regulated We used transcriptomic data and experimental evidences to demonstrate that silencing LncRNA LOXL1-AS1 was a new regulator of NF-kB signaling pathway through repressing RELB directly, resulting in increased marker genes of PN subtype and decreased those of MES.GBM cell proliferation was functionally suppressed by LOXL1-AS1's knockdown expression,. Furthermore, RELB's rescue could reverse LOXL1-AS1's effects partially in GBM malignant behaviors. LOXL1-AS1 could clinically serve as a poor prognostic indicator for GBM patients. In conclusion, our results suggest that LOXL1-AS1 contributes to aggressive biological processes that are related with MES phenotype via NF-kB signaling, which expand our perceptions into the underlying mechanisms in LOXL1-AS1-based and subtype transition adapted medicine for GBM management. patients in the LOXL1-AS1 low-expressed group had significantly longer overall survival than those in the LOXL1-AS1 high-expressed group, which further highlight the suppressive character of LOXL1-AS1 for glioblastoma patients. 29678575 2018 Silencing LncRNA LOXL1-AS1 attenuates mesenchymal characteristics of glioblastoma via NF-kB pathway. LRB1 light-response BTB 1,T3F17.9 NA NA NA NA hepatocellular carcinoma C16 NA qRT-PCR ect. the tumor tissues, peripheral blood of the HCC patients, a second blood sample was obtained 10 days after surgery up-regulated the serum LRB1 levels in patients with HCC were significantly increased compared with healthy volunteers. The serum LRB1 levels were positively associated with a-fetoprotein (AFP) expression, large tumor sizes, tumor stage (tumor-node metastasis or Barcelona Clinic Liver Cancer stage) and venous invasion, and were negatively associated with overall survival. Additionally, the use of a combination of LRB1, AFP and des-r-carboxy prothrombin (DCP) markers for the diagnosis of HCC, the diagnostic accuracy was increased compared with using LRB1 alone. 30008842 2018 Serum long noncoding RNA LRB1 as a potential biomarker for predicting the diagnosis and prognosis of human hepatocellular carcinoma. LSINCT5 NA 101234261 NA NR_145480 GRCh38_5:2712591-2715237 colorectal cancer C19.9 NA qPCR etc. CRC tissues, cell lines (LoVo, Caco-2, DLD1,HCT-8, HCT-116) up-regulated The expression of LSINCT5 is significantly upregulated in gastrointestinal cancer tissues and cell lines relative to their normal counterparts. In addition, increased LSINCT5 expression was correlated with a larger tumor size, deeper tumor depth, and advanced clinical stage. 25526476 2014 Long Non-Coding RNA LSINCT5 Predicts Negative Prognosis and Exhibits Oncogenic Activity in Gastric Cancer. LSINCT5 NA 101234261 NA NR_145480 GRCh38_5:2712591-2715237 gastric cancer C16 NA qPCR etc. gastric cancer tissues, cell lines (AGS, MKN-45, MGC-803, BGC-823, HGC-27) up-regulated The expression of LSINCT5 is significantly upregulated in gastrointestinal cancer tissues and cell lines relative to their normal counterparts. In addition, increased LSINCT5 expression was correlated with a larger tumor size, deeper tumor depth, and advanced clinical stage. 25526476 2014 Long Non-Coding RNA LSINCT5 Predicts Negative Prognosis and Exhibits Oncogenic Activity in Gastric Cancer. LSINCT5 NA 101234261 NA NR_145480 GRCh38_5:2712591-2715237 bladder cancer C67 NA qPCR, western blot, RIP bladder cancer tissues, cell lines (UBC-40, T24, SW780, RT4 and J82) up-regulated Particularly, the lncRNA long stress-induced noncoding transcript 5 (LSINCT5) is significantly upregulated in human bladder cancer cell lines and tumor specimens. Meanwhile, high LSINCT5 expression correlates with poor prognosis, enhances tumor sphere formation and invasion in vitro. In vivo xenograft tumor growth is also elevated by LSINCT5 overexpression. 29772237 2018 LSINCT5 activates Wnt/b-catenin signaling by interacting with NCYM to promote bladder cancer progression LSINCT5 NA 101234261 NA NR_145480 GRCh38_5:2712591-2715237 non small cell lung cancer C34 M8046/3 qPCR, RIP, Microarray, Western blot, etc. All the lung cancer cell lines (WI-38, A549, H1299, 95D, 95C, H838) up-regulated In conclusion, our current work has revealed that lncRNA LSINCT5 serves as a novel oncogenic factor which is critically involved in NSCLC progression. LSINCT5 can enhance malignant phenotypes of lung cancer both in vitro and in vivo. LSINCT5 contributes to NSCLC tumorigenesis partially by physical interaction with and stabilizing HMGA2. Kaplan-Meier survival curves for patients with NSCLC. P < 0.01 by log-rank test. 29883241 2018 The long non-coding RNA LSINCT5 promotes malignancy in non-small cell lung cancerby stabilizing HMGA2. LUCAT1 LUCAT1, SCAL1 106182249 ENSG00000196634 NR_132442 GRCh38_6:147158925-147180992 colorectal cancer C19.9 NA qPCR etc. colorectal cancer tissues up-regulated LncRNA LUADT1 expression was up-regulated in colorectal cancer, and correlated with tumor size, metastasis, and TNM staging. Both univariate analysis and multivariate test indicated that lncRNALUADT1 high expression, TNM staging, and lymph node metastasis were closely related. Moreover, high expression of lncRNALUADT1 suggested the poor overall survival of patients 29762830 2018 LncRNALUADT1 is overexpressed in colorectal cancer and its expression level is related to clinicopathology LUCAT1 LUCAT1, SCAL1 100505994 ENSG00000248323 NR_103548 GRCh38_5:91303029-91314402 clear cell renal cell carcinoma C64.9 M8005/0 RNA-seq, RIP renal cancer cell lines, renal cancer tissues up-regulated We screened the lncRNAs’ profile in ccRCC from The Cancer Genome Atlas (TCGA) database, and selected Lucat1 for further study. MTS, colony formation assay and transwell assay were performed to examine the effect of Lucat1 on proliferation and metastasis of ccRCC. The Chip and Rip assay was performed to verify that Lucat1 can bind to polycomb PRC2 complex and suppress p57 expression.PRC2, a methyltransferase that is composed of enhancer of zeste homolog 2 (EZH2), suppressor of zeste 12 (SUZ12) and embryonic ectoderm development (EED), can catalyze the di- and trimethylation of lysine residue 27 of histone 3 (H3K27me3), thus modulating gene expression. Kaplan-Meier analysis indicated that high Lucat1 expression was related to a poorer overall survival and disease free survival. 29371934 2017 Long non-coding RNA Lucat1 is a poor prognostic factor and demonstrates malignant biological behavior in clear cell renal cell carcinoma. LUCAT1 LUCAT1, SCAL1 100505994 ENSG00000248323 NR_103548 GRCh38_5:91303029-91314402 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, RIP, ChIP, Flow cytometry assay, Cell proliferation assay etc. NSCLC tissues, cell lines (A549, SPC-A1 and H1703) up-regulated In this study, we found that the expression of LUCAT1 was significantly up-regulated in NSCLC tissues compared to non-tumor tissues, and its expression was associated with tumor size, tumor-node-metastasis (TNM) stage and overall survival (OS). Further experiments showed that LUCAT1 knockdown inhibited cell proliferation both in vitro and in vivo. Mechanistic investigations showed that LUCAT1 plays a key role in G0/G1 arrest. We further demonstrated that LUCAT1 was associated with polycomb repressor complexes (PRC2) and that this association was required for epigenetically repression of p21 and p57, thus contributing to the regulation of NSCLC cell cycle and proliferation. 28423699 2017 Long non-coding RNA LUCAT1 is associated with poor prognosis in human non-small lung cancer and regulates cell proliferation via epigenetically repressing p21 and p57 expression. LUCAT1 LUCAT1, SCAL1 100505994 ENSG00000248323 NR_103548 GRCh38_5:91303029-91314402 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, Western blot, Luciferase activity assay, etc. ccRCC tissues, cell lines (786-O, Caki-1, ACHN, HK-2) up-regulated Upregulated LUCAT1 was positively correlated with larger tumor size, advanced tumor-node-metastasis (TNM) stage, higher smoking frequency, nodal metastasis and shorter overall survival in patients with ccRCC. We then found that LUCAT1 directly bound and inhibited the expression of micoRNA-495-3p (miR-495-3p), which subsequently regulated the expression of special adenine-thymine (AT)-rich DNA-binding protein 1 (SATB1). 29932248 2018 Long noncoding RNA lung cancer associated transcript 1 promotes proliferation and invasion of clear cell renal cell carcinoma cells by negatively regulating miR-495-3p. LUNAR1 LUNAR1 104564224 NA NR_126487 GRCh38_15:99014704-99031050 diffuse large B-cell lymphoma NA M9680/3 qPCR, RNAi, Western blot, Flow cytometry assay, MTT assay etc. lymph node, cell lines (OCI-LY-3, OCI-LY-7, OCI-LY-10, SU-DHL-4, SU-DHL-6 and RCK-8) up-regulated LUNAR1 in tumor was significantly higher the normal. In cancerous tissues, LUNAR1 expression was at a level higher than that of normal specimens, with the median level of 0.756 compared with normal counterparts. The higher expression of LUNAR1 was significantly correlated with stage, rituximab and IPI. Further experiments revealed that LUNAR1 knockdown significantly repressed cell proliferation of DLBCL by regulating E2F1, cyclin D1 and p21. 26796267 2016 Long noncoding RNA LUNAR1 associates with cell proliferation and predicts a poor prognosis in diffuse large B-cell lymphoma. MACC1-AS1 NA 100874041 ENSG00000228598 NR_046756 GRCh38_7:20141916-20153531 gastric cancer C16 NA RNA-seq,qPCR, Western blot, Luciferase reporter assay cell lines (AGS, BGC803, BGC823, MKN45, SGC7901, GES-1), GC tissues up-regulated Elevated expression of MACC1-AS1 in gastric cancer tissues is linked to poor prognosis and promotes malignant phenotype upon cancer cells. MACC1-AS1 is elevated under metabolic stress and facilitates metabolic plasticity by promoting MACC1 expression through mRNA stabilization 29510730 2018 The lncRNA MACC1-AS1 promotes gastric cancer cell metabolic plasticity via AMPK/Lin28 mediated mRNA stability of MACC1. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 multiple myeloma C42.1 M9732/3 qPCR etc. bone marrow up-regulated MALAT1 was overexpressed in the newly diagnosed patients compared with post-treatment patients and healthy individuals. The expression of MALAT1 strongly correlated with disease status, and the magnitude of change in MALAT1 post-treatment had prognostic relevance. The patients with early progression had a significantly smaller change in MALAT1 after treatment. 25369863 2014 MALAT1 long non-coding RNA is overexpressed in multiple myeloma and may serve as a marker to predict disease progression. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 choriocarcinoma NA M9220/3 qPCR, Luciferase reporter assay, Western blot choriocarcinoma cell line (HT cells) up-regulated Being specifically upregulated in choriocarcinoma cell lines, the under-researched lncRNA-MALAT1 promoted choriocarcinoma cell growth by targeting miR-218. After MALAT1 knockdown,proliferation of human choriocarcinoma cell in vitro was dramatically hindered,and the tumor size in vivo was reduced。miR-218-mediated Fbxw8 regulation was required for MALAT1-induced choriocarcinoma cell proliferation.Taken together, MALAT1 might promote choriocarcinoma tumor growth through miR-218-mediated Fbxw8 regulation.MALAT1 might be an oncogenic lncRNA that promoted choriocarcinoma proliferation and could be therapeutically targeted in human choriocarcinoma.A higher expression of MALAT1 predicts a poorer prognosis, including a shorter overall survival, in patients with cervical cancer. 29096355 2017 The long non-coding RNA MALAT1 interacted with miR-218 modulates choriocarcinoma growth by targeting Fbxw8 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 extramedullary myeloma NA M9734/3 qPCR etc. cell lines (KMS11, KMS12PE, KMS12BM, KMS18) up-regulated MALAT1 expression level was positively correlated with expression of HSP90AA1, HSP90AB1 and HSP90B1 but not with TP53 expression. MALAT1 was significantly upregulated by bortezomib and doxorubicin. Considering the known functions of MALAT1, our results suggest that it acts as a stress response gene that is upregulated by chemotherapy, thereby linking chemotherapy to EMM formation. Elucidating the biological implication of long non-coding RNA contributes to deeper understanding concerning the pathogenesis and investigation of novel therapeutic targets for MM. 28770558 2017 Long non-coding RNA MALAT1 is an inducible stress response gene associated with extramedullary spread and poor prognosis of multiple myeloma MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 monocytic leukemia NA M9860/3 qPCR, Western blot leukemia cell lines (U-937 (catalog no. TCHu159), THP-1 (catalog no. TCHu 57)) up-regulated Taken together, these findings suggest that high MALAT-1 expression is closely associated with poor prognosis in M5 patients and may play a role in leukemia cell proliferation and apoptosis, and may serve as a promising theranostic marker. We found that MALAT-1 expression in patients with acute monocytic leukemia (M5) was significantly increased when compared with that of healthy controls, and the overall survival of M5 patients with high MALAT-1 expression was markedly reduced when compared with the overall survival of patients with low MALAT-1 expression. MALAT-1 knockdown was found to induce upregulated protein expression of cyclin E and cyclin-dependent kinase 2 (CDK2) by silencing tumor suppressor gene p53 and activating transcription factor E2F, as a consequence of G1/S phase transition to G2 phase (29). 28713913 2017 Upregulation of long non-coding RNA MALAT-1 confers poor prognosis and influences cell proliferation and apoptosis in acute monocytic leukemia. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 mantle cell lymphoma NA M9673/3 qPCR, RNAi, Western blot, RIP etc. blood, cell lines (Mino and Jeko-1) up-regulated We found that the expression of MALAT1 was elevated in human MCL tumors and cell lines as compared to normal controls, and the elevated levels of MALAT1 correlated with higher MCL international prognostic index (MIPI) and reduced overall survival. MCL with knockdown of MALAT1 showed impaired cell proliferation, facilitated apoptosis and produced fewer clonogenic foci. The increased expression of p21 and p27 upon MALAT1 knockdown was regulated by enhancer of zeste homolog 2 (EZH2). Moreover, decreased phosphorylation of EZH2 at T350 attenuated the binding to MALAT1. 27998273 2016 LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 bladder transitional cell carcinoma NA M8120/3 qPCR, Western blot etc. cell line (T24, BIU-87, HEK, 293T), bladder tissue up-regulated The effects of MALAT1 on BTCC cells were investigated by over-expression approaches in vitro and in vivo.Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were validated through bioinformatic analysis and luciferase assay. MALAT1 up-regulation positively correlated with advanced clinical pathological stage and shorter survival of BTCC patients. Furthermore, MALAT1 over-expression promoted proliferation,migration and invasion of BTCC cells in vitro and in vivo. Particularly, MALAT1 may function as a ceRNA to sponge miR-124,thus modulating the derepression of foxq1, miR-124 target gene,in post-transcriptional levels. 29736319 2018 LncRNA MALAT1 promotes tumor growth and metastasis by targeting miR-124/foxq1 in bladder transitional cell carcinoma (BTCC). MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 renal cell carcinoma C64.9 NA qPCR, Luciferase reporter assay etc. RCC tissues up-regulated We found that MALAT1 expression was higher in human RCC tissues where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. Reciprocal interaction between MALAT1 and miR-205 was also observed. 25600645 2015 Long noncoding RNA MALAT1 promotes aggressive renal cell carcinoma through Ezh2 and interacts with miR-205. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 esophageal cancer C15 NA qPCR, Cell proliferation assay etc. esophageal cancer tissues, cell lines (EC109, KYSE150, HEF-1A) up-regulated Expression levels of MALAT1 were significantly higher in EC tissues and cells than the controls. MALAT1 expression was tightly related to lymphatic invasion, distant metastasis and tumor differentiation, but shared no association with age, gender and tumor location. In addition, patients with high MALAT1 expression had a shorter overall survival than those with low MALAT1. 27470544 2016 Increased MALAT1 expression predicts poor prognosis in esophageal cancer patients. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, RNAi etc. ccRCC tissues, cell line (HK-2) up-regulated The expression level of MALAT1 was higher in ccRCC tissues and renal cancer cells compared to adjacent non-tumor tissues and normal human proximal tubule epithelial cells HK-2. The ccRCC patients with higher MALAT1 expression had an advanced clinical features and a shorter overall survival time than those with lower MALAT1 expression. Additionally, our data indicated that knockdown expression of MALAT1 decreased renal cancer cell proliferation, migration, and invasion. 25480417 2014 Upregulation of long non-coding RNA MALAT1 correlates with tumor progression and poor prognosis in clear cell renal cell carcinoma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 epithelial ovarian cancer C56.9 NA qPCR, western blot etc. cell lines (SKOV3, OVCAR3, HO8910, A2780, HO8910PM) up-regulated The present study discovered that MALAT1 was upregulated in tumor tissues and ovarian cancer cell lines. Further, the 5-year overall survival was higher in the lower expression of the MALAT1 group. 28770968 2017 LncRNA MALAT1 promotes proliferation and metastasis in epithelial ovarian cancer via the PI3K-AKT pathway MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 oral squamous cell carcinoma C06.9 M8070/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP etc. cell lines (Tca8113, SCC-25, CAL-27 and HN5 cells, Hs680), oral squamous cell carcinoma tissue up-regulated MALAT1 was upregulated in OSCC cell lines.Inhibition of MALAT1 can prevent OSCC proliferation while overexpressing MALAT1 promoted OSCC progression.In addition, miR-125b was a direct target of MALAT1,which indicated a negative correlation between MALAT1 and miR-125b.Downregulated MALAT1 greatly inhibited OSCC tumor growth and reversely upregualated MALAT1 promoted OSCC development via miR-125b/STAT3 axis, respectively.MALAT1 can function as a competing endogenous RNA (ceRNA) to modulate STAT3 expression by absorbing miR-125b in OSCC and could be used as a novel therapeutic target in OSCC diagnosis and treatment. 28926115 2018 Long non-coding RNA MALAT1 promotes oral squamous cell carcinoma development via microRNA-125b/STAT3 axis. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 renal cell carcinoma C64.9 NA qPCR, RNAi, Western blot, RIP, RNA pull-down assay etc. RCC tissues, cell lines (786-O and Caki-1) up-regulated LncRNA MALAT-1 and the Livin protein were highly expressed in RCC tissues, as well as in RCC 786-O and Caki-1 cell lines. MALAT-1 interference contributed to an increase in cell apoptosis and a reduction in the cell viability of 786-O and Caki-1 cells. The increase in apoptosis by si-MALAT-1 was reversed by overexpression of Livin. The RIP results showed that MALAT-1 promoted the expression of the Livin protein in 786-O and Caki-1 cells by enhancing the stability of the protein. 27655020 2016 Biological function and mechanism of MALAT-1 in renal cell carcinoma proliferation and apoptosis: role of the MALAT-1-Livin protein interaction. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 oral squamous cell carcinoma C06.9 M8070/3 qPCR, RNAi, Western blot etc. OSCC tissues, cell lines (Tscca, Tca8113P160, Tca8113, Hep-2) up-regulated We found that MALAT1 is overexpressed in OSCC tissues compared to normal oral mucosa by real-time PCR. MALAT1 served as a new prognostic factor in OSCC patients. When knockdown by small interfering RNA (siRNA) in OSCC cell lines TSCCA and Tca8113, MALAT1 was shown to be required for maintaining epithelial-mesenchymal transition (EMT) mediated cell migration and invasion. Western blot and immunofluorescence staining showed that MALAT1 knockdown significantly suppressed N-cadherin and Vimentin expression but induced E-cadherin expression in vitro. Meanwhile, both nucleus and cytoplasm levels of B-catenin and NF-B were attenuated, while elevated MALAT1 level triggered the expression of B-catenin and NF-B. More importantly, targeting MALAT1 inhibited TSCCA cell-induced xenograft tumor growth in vivo. 26522444 2015 Long Non Coding RNA MALAT1 Promotes Tumor Growth and Metastasis by inducing Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 colon cancer C18 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (HCT116 and RKO), CRC tissue down-regulated MALAT1 exerts a modulatory effect on pro-migratory markers such as epithelial cell adhesion molecule (EpCAM) and integrin B 4 (ITGB4),suggesting a potential mechanism for MALAT1-mediated regulation of tumorigenesis.In summary, we establish and characterize a PTEN-miRNA-MALAT1 axis that regulates migration and invasion. MALAT1 lncRNA possesses novel tumor suppressive properties in colon and breast cancers.MALAT1 is regulated by the PTEN-targeting microRNAs miR-17,20a and 106b. 29574704 2018 A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 esophageal squamous cell cancer NA NA qPCR etc. ESCC tissues up-regulated MALAT1 expression was increased in ESCC tissue than in adjacent normal tissue samples. MALAT1 level was positively related to pT stage. Kaplan-Meier analysis showed high expression levels of MALAT1 ware correlated with poor prognosis in ESCC patients. Patients with a high level of MALAT1 had a shorter DFS and OS than those with low MALAT1 expression. 26406400 2015 MALAT1 might be a predictive marker of poor prognosis in patients who underwent radical resection of middle thoracic esophageal squamous cell carcinoma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioma NA M9380/3 qPCR etc. glioma tissues up-regulated LncRNA MALAT1 expression was increased in glioma tissues compared with paired adjacent brain normal tissues. Furthermore, lncRNA MALAT1 was associated significantly with WHO grade and tumor size. Moreover, the level of lncRNA MALAT1 expression was markedly correlated with the glioma patients' overall survival. Multivariate analysis suggested that increased lncRNA MALAT1 expression was a poor independent prognostic predictor for glioma patients. 25613066 2015 Long noncoding RNA MALAT1 associates with the malignant status and poor prognosis in glioma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gallbladder cancer C23.9 NA qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. gallbladder carcinoma tissues, cell lines (GBC-SD, SGC-996 etc.) up-regulated In this study, we show that Malat1 is overexpressed in gallbladder cancer (GBC) tissue and cells. The high Malat1 levels correlated positively with tumor size and lymphatic metastasis, and correlated negatively with overall survival. We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206.Furthermore, in agreement with in vitro results, IHC data demonstrate that the levels of ANXA2 and KRAS are lower in the shRNA-Malat1 group than in the control group. 27191262 2016 Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gallbladder cancer C23.9 NA qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. GBC tissues, cell lines (SGC-996, NOZ) up-regulated n this study, we found that MALAT1 expression was up-regulated in GBC tissues. Luciferase reporter assays and RNA pull down assays showed that MALAT1 is a target of miR-363-3p. Real-time quantitative PCR and Western blot analysis indicated that MALAT1 regulated Myeloid cell leukaemia-1 (MCL-1) expression as a competing endogenous RNA (ceRNA) for miR-363-3p in GBC cells. Furthermore, MALAT1 silencing decreased GBC cell proliferation and the S phase cell population and induced apoptosis in vitro. 27420766 2016 The lncRNA MALAT1 functions as a competing endogenous RNA to regulate MCL-1 expression by sponging miR-363-3p in gallbladder cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, RIP, Luciferase reporter assay etc. lung adenocarcinoma tissues, cell lines (A549, H1299, H460, H446 etc.) up-regulated In this study, we found that MALAT1 upregulation was associated with larger tumor size and lymph-node metastasis, and also correlated with shorter overall survival of lung adenocarcinoma patients. Furthermore, MALAT1 promotes EMT and metastasis of lung adenocarcinoma cells in vitro and in vivo. In particular, MALAT1 upregulated the expression of miR-204 target gene SLUG through competitively 'spongeing' miR-204. In summary we unveil a branch of the MALAT1/miR-204/SLUG pathway that regulates the progression of lung adenocarcinoma. 27294002 2016 LncRNA MALAT1 exerts oncogenic functions in lung adenocarcinoma by targeting miR-204. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gallbladder cancer C23.9 NA qPCR, in vitro knockdown etc. cell lines, GBC tissues up-regulated MALAT1 acts as a biomarker in the recurrence, metastasis and prognosis of GBC.MALAT1 in GBC recurrence, metastasis, and prognosis. COX regression analysis was applied to analyze the independent influencing factors of GBC patients' survival status. ROC curve results showed that the MALAT1 expression could be a predictor of the GBC recurrence, metastasis, and prognosis. 29058818 2018 Prognostic significance of long non-coding RNA MALAT1 for predicting the recurrence and metastasis of gallbladder cancer and its effect on cell proliferation, migration, invasion, and apoptosis. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 lung cancer C34 NA RNAi, qPCR etc. cell line A549 up-regulated Our study reveals a novel mechanism by which Oct4 transcriptionally activates NEAT1 via promoter and MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis. 28615056 2017 Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gallbladder cancer C23.9 NA qPCR, Western blot etc. GBC tissues, cell lines (SGC-996, NOZ) up-regulated We found that MALAT1 was significantly upregulated in GBC tissues. Knockdown of MALAT1 could inhibit GBC cell proliferation and metastasis both in vitro and in vivo. Moreover, knockdown of MALAT1 led to the inactivation of the ERK-MAPK pathway. 24658096 2014 MALAT1 promotes the proliferation and metastasis of gallbladder cancer cells by activating the ERK/MAPK pathway. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR etc. PADC tissues, cell lines (Panc-1, Bxpc-3, HPDE6C-7 etc.) up-regulated The relative level of MALAT1 was significantly higher in PDAC compared to the adjacent normal pancreatic tissues. When comparing the MALAT1 level in the cultured cell lines, remarkably higher expression of MALAT1 was found in aspc-1 PDAC cells compared with the immortal pancreatic duct epithelial cell line HPDE6c-7. Furthermore, MALAT1 expression level showed significant correlation with tumor size, tumor stage and depth of invasion. Kaplan-Meier analysis revealed that patients with higher MALAT1 expression had a poorer disease free survival. 24815433 2014 Expression and prognostic significance of lncRNA MALAT1 in pancreatic cancer tissues. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Among them, AFAP1-AS1, BCAR4, H19, HOXA-AS2, MALAT1 and PVT1 were significantly up-regulated, and ADAMTS9-AS2 was significantly down-regulated in cancer tissue samples. 27596298 2016 Differentially expressed long non-coding RNAs and the prognostic potential in colorectal cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated The MALAT1 levels in cancerous tissues were 2.26 times higher than those measured in noncancerous tissues, and this difference was statistically significant. Based on their expression level of MALAT1, the patients were divided into a high MALAT1 expression group and a low expression group. Patients with tumours harbouring higher expression of MALAT1 showed a significantly worse prognosis with a HR of 2.863 for DFS and 3.968 for OS. Furthermore, patients with perineural invasion demonstrated significantly worse DFS and OS than those without perineural invasion. 25031737 2014 High expression of lncRNA MALAT1 suggests a biomarker of poor prognosis in colorectal cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 esophageal squamous cell cancer NA NA qPCR, RNAi, Western blot, Cell proliferation assay, Cell migration assay etc. ESCC tissues, cell lines (TE1, TE7, EC1, EC109, KYSE70 and KYSE450) up-regulated We found that the MALAT1 expression level was higher in human ESCC tissues, which was closely correlated with WHO grade, lymph node metastasis and prognosis. Silencing of MALAT1 expression inhibited cell proliferation, migration and tumor sphere formation, while increasing cell apoptosis of esophageal cancer in vitro. Down-regulation of MALAT1 decreased the expression of B-catenin, Lin28 and Ezh2 genes, while over-expressed Ezh2 combined with MALAT1 down-regulation completely reversed the si-MALAT1-mediated repression of B-catenin and Lin28 in esophageal cancer cells. Animal experiments showed that knockdown of MALAT1 decreased tumor formation and improved survival. 27015363 2016 Long noncoding RNA MALAT1 promotes malignant development of esophageal squamous cell carcinoma by targeting B-catenin via Ezh2. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 pancreatic cancer C25 NA qPCR, RNAi, Western blot, RIP, Flow cytometry assay, Cell proliferation assay etc. pancreatic cancer tissues, cell lines (CFPAC-1, SW1990, AsPC-1) up-regulated And knockdown of MALAT-1 upregulated E-cadherin mRNA expression in pancreatic cancer cell lines. Therefore, we hypothesized that EZH2 might be recruited by MALAT-1 to synergistically repress E-cadherin. To test this hypothesis, we first asked whether MALAT-1 bound to EZH2 using a RNA Immunoprecipitation (RIP) assay. There was an average of 14- and 18- fold enrichment for MALAT-1 in the AsPC-1 and CFPAC-1 cells over-expressing EZH2, respectively, as compared to the IgG group. These results suggest that MALAT-1 is physically associated with the EZH2, and silencing EZH2 could increase E-cadherin transcription. 26848980 2016 EZH2 promotes cell migration and invasion but not alters cell proliferation by suppressing E-cadherin, partly through association with MALAT-1 in pancreatic cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 esophageal squamous cell cancer NA NA qPCR, RNAi etc. ESCC tissues, cell lines (TE1, KYSE30, KYSE70, KYSE150, KYSE270, KYSE410, EC9706) up-regulated Human esophageal carcinoma cell lines EC9706 and KYSE150 were transfected with MALAT-1 small interference RNA. Cell proliferation, migration/invasion ability, cell cycle, and apoptosis were assessed. MALAT-1 expressed higher levels in esophageal cancer tissues when compared with paired adjacent normal tissues. This high expression was associated with a decreased survival rate. MALAT-1 knockdown induced a decrease in proliferation-enhanced apoptosis, inhibited migration/invasion, and reduced colony formation and led to cell cycle arrest at the G2/M phase 26493997 2015 Upregulation of MALAT-1 and its association with survival rate and the effect on cell cycle and migration in patients with esophageal squamous cell carcinoma MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 bladder cancer C67 NA qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. bladder cancer tissues, cell lines (T24, RT4 etc.) up-regulated TGFB1 induces malat1 expression and EMT in bladder cancer cells. malat1 overexpression is significantly correlated with poor survival in patients with bladder cancer. malat1 and E-cadherin expression is negatively correlated in vitro and in vivo. malat1 knockdown inhibits TGFB1 induced EMT. malat1 is associated with suz12, and this association results in decrease of E-cadherin expression and increase of N-cadherin and fibronectin expression. Targeted inhibition of malat1 or suz12 suppresses the migratory and invasive properties induced by TGFB1 We demonstrated that malat1 or suz12 knockdown inhibits tumor metastasis in animal models. 24449823 2014 TGFB1 induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 pancreatic cancer C25 NA qPCR, Western blot, Flow cytometry assay etc. pancreatic cancer tissues, cell lines (BxPC-3, CFPAC-1, CAPAN-1, SW1990 etc.) up-regulated In the present study, our results showed that MALAT-1 expression levels were upregulated in pancreatic cancer tissues compared with adjacent noncancerous controls. Further function analysis revealed that downregulation of MALAT-1 could inhibit tumor cell proliferation and decrease cell migration and invasion in vitro. 25269958 2014 Elevated expression level of long noncoding RNA MALAT-1 facilitates cell growth, migration and invasion in pancreatic cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR, RNAi cell lines (MNNG/HOS) differential expression MALAT1 plays an important role in OS progression by modulating the enhancers of zeste homolog 2 (EZH2).MALAT1 could inhibit the expression of E-cadherin and promote the expression of B-catenin, and tthis phenomenon might be the outcome of MALAT1-induced EZH2 activation. MALAT1 silencing using small interfering RNAs (siRNAs), the loss of E-cadherin of MNNG/HOS cells was rescued, and the abnormal expression and localization of B-catenin were corrected at the same time.The MALAT1/EZH2 axis participates in OS cell proliferation, migration, and cell survival in vitro. 29290771 2018 Targeting LncRNA-MALAT1 suppresses the progression of osteosarcoma by altering the expression and localization of B-catenin. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gastric cancer C16 NA qPCR, RNAi, RIP etc. cell lines (MKN45, AGS and GES-1) up-regulated We identified 8,256 transcripts, including both noncoding and coding transcripts, some of which were derived from cancer-related loci. In particular, we found that long noncoding RNA (lncRNA) MALAT1 binds EZH2, suppresses the tumor suppressor PCDH10, and promotes gastric cellular migration and invasion 26871474 2016 MALAT1 long ncRNA promotes gastric cancer metastasis by suppressing PCDH10 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 non small cell lung cancer C34 M8046/3 qPCR etc. cell lines (A549, plat-E, HTB-58 etc.) up-regulated MALAT-1 was highly expressed in several human NSCLC cell lines. MALAT-1 expression was regulated by an endogenous negative feedback loop. In A549 NSCLCs, RNAi-mediated suppression of MALAT-1 RNA suppressed migration and clonogenic growth. Forced expression of MALAT-1 in NIH 3T3 cells significantly increased migration. These data indicate that MALAT-1 expression levels are associated with patient survival and identify tumor-promoting functions of MALAT-1. 22088988 2011 The long noncoding MALAT-1 RNA indicates a poor prognosis in non-small cell lung cancer and induces migration and tumor growth. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated The novel MALAT-1 transcript is a noncoding RNA of more than 8000 nt expressed from chromosome 11q13. It is highly expressed in lung, pancreas and other healthy organs as well as in NSCLC. MALAT 1 expressed sequences are conserved across several species indicating its potentially important function.The identification of MALAT-1 emphasizes the potential role of noncoding RNAs in human cancer. 12970751 2003 MALAT-1, a novel noncoding RNA, and thymosin beta4 predict metastasis and survival in early-stage non-small cell lung cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioma NA M9380/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. glioma tissues, cell lines (U87 and SHG139) down-regulated The expression of MALAT1 was significantly decreased in glioma specimens than in noncancerous brain tissues. In addition, MALAT1 expression was significantly correlated with tumor size, WHO grade and Karnofsky Performance Status (KPS), and was an independent prognostic factor for survival of glioma patients. Further, MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7 mRNA was identified as a direct target of miR-155 in glioma. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for glioma progression mediated by MALAT1-miR-155 pathway. 27904771 2016 Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 prostate cancer C61.9 NA qPCR etc. prostate cancer tissues, cell lines (22RV1, LNCAP-AI etc.) up-regulated MALAT-1 was up-regulated in human prostate cancer tissues and cell lines. Higher MALAT-1 expression correlated with high Gleason score, prostate specific antigen, tumor stage and castration resistant prostate cancer. MALAT-1 down-regulation by siRNA inhibited prostate cancer cell growth, invasion and migration, and induced castration resistant prostate cancer cell cycle arrest in the G0/G1 phases. 23845456 2013 Long noncoding RNA MALAT-1 is a new potential therapeutic target for castration resistant prostate cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues up-regulated The increased expression of MALAT1 in HCC tissue may represent a good prognostic biomarker for curatively resected HCC. Terefore, in combination with other tumor prognostic factors, the determination of the expression levels of these lncRNAs may lead to a more accurate prediction of HCC prognosis.The increase in the expression levels of MALAT1 in HCC tissues was signifcantly correlated with better overall survival. 29170515 2017 Prognostic Value of Long NonCoding RNA HULC and MALAT1 Following the Curative Resection of Hepatocellular Carcinoma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown cell line (SKBR3) down-regulated MALAT1 exerts a modulatory effect on pro-migratory markers such as epithelial cell adhesion molecule (EpCAM) and integrin B4 (ITGB4),suggesting a potential mechanism for MALAT1-mediated regulation of tumorigenesis.In summary,we establish and characterize a PTEN-miRNA-MALAT1 axis that regulates migration and invasion. MALAT1 lncRNA possesses novel tumor suppressive properties in colon and breast cancers.MALAT1 is regulated by the PTEN-targeting microRNAs miR-17,20a and 106b. 29574704 2018 A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, Western blot, RIP, Luciferase reporter assay etc. breast cancer tissues up-regulated We reported that MALAT1 was upregulated in triple-negative breast cancer (TNBC) tissues. Knockdown of MALAT1 inhibited proliferation, motility, and increased apoptosis in vitro. In vivo study indicated that knockdown of MALAT1 inhibited tumor growth and metastasis. Patients with high MALAT1 expression had poorer overall survival time than those with low MALAT1 expression. In addition, our findings demonstrate a reciprocal negative control relationship between MALAT1 and miR-1: downregulation of MALAT1 increased expression of microRNA-1 (miR-1), while overexpression of miR-1 decreased MALAT1 expression. Slug was identified as a direct target of miR-1. 26676637 2015 Reciprocal regulation of Hsa-miR-1 and long noncoding RNA MALAT1 promotes triple-negative breast cancer development MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, Western blot, RIP, ChIP etc. cell lines (SKBR3, MDA-MB-468, MDA-MB-231, MCF7 ,H1299, HEK T293, OVCAR-3) differential expression oncogenic splicing factor SRSF1 bridges MALAT1 to mutant p53 and ID4 proteins in breast cancer cells. Mutant p53 and ID4 delocalize MALAT1 from nuclear speckles and favor its association with chromatin. This enables aberrant recruitment of MALAT1 on VEGFA pre-mRNA and modulation of VEGFA isoforms expression. VEGFA-dependent expression signatures associate with ID4 expression specifically in basal-like breast cancers carrying TP53 mutations. To evaluate the prognostic value of the signatures, we estimated the patients' survival probability using the Kaplan–Meier method. Serum-free media with or without recombinant VEGFA were used as controls. 28652379 2017 The mutant p53-ID4 complex controls VEGFA isoforms by recruiting lncRNA MALAT1. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN56), gastric adenocarcinomas tissues up-regulated MALAT1, H19, and TUG1 were among the top twenty overexpressed lncRNAs in gastric tumors 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay gastric cancer tissues, cell lines (MKN45, MKN28, BGC-823, and SGC-7901) up-regulated In this study, we demonstrated MALAT1 was up-regulation in GC tissues compared with adjacent normal tissues and higher MALAT1 expression was correlated with local invasion, lymph node metastasis and TNM stage. Patients with higher MALAT1 expression predicted a shorter survival and poor prognosis. Mechanistically, our results demonstrated that MALAT1 was negatively correlation with miR-1297 and functioned as a molecular sponging miR-1297, antagonizing its ability to suppress HMGB2 expression. 28396617 2017 Long non-coding RNA MALAT1 drives gastric cancer progression by regulating HMGB2 modulating the miR-1297 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR, Western blot etc. osteosarcoma tissues, cell lines (MG-63, U2OS, MNNG/HOS, hFOB 1.19) up-regulated MALAT1 was up-regulated and functioned as an oncogene in osteosarcoma via RhoA and its downstream ROCKs.we confirmed that MALAT1 could regulate ROCK1/ROCK2 and their mediated metastasis and proliferation by working as a ceRNA mechanism via miR-144-3p.an overexpression of MALAT1 inhibited ROCK1/ROCK2 expression and its mediated metastasis and proliferation by working as a competitive endogenous RNA (ceRNA) via miR-144-3p. 28938647 2017 Long non-coding RNA MALAT1 for promoting metastasis and proliferation by acting as a ceRNA of miR-144-3p in osteosarcoma cells. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay etc. OS tissues, cell lines (MG-63, SAOS-2, U2OS, SW1353, hFOB) up-regulated MALAT1 was significantly increased in osteosarcoma specimens and cell lines. serum lncRNA MALAT1 expression has considerable diagnostic and prognostic significance in discriminating osteosarcoma patients and non-tumor patients. MALAT1 may serve as a promising prognostic and therapeutic target for osteosarcoma patients. MALAT1 overexpression promoted cell metastasis and decreased E-cadherin level, however, this effect was partially reversed by EZH2 knockdown. MALAT1 is a potential diagnostic and prognostic factor in osteosarcoma and further demonstrates how MALAT1 confers an oncogenic function. 28388584 2017 MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Cell proliferation assay, Cell migration and invasion assay etc. NSCLC tissues, cell lines (SPC-A1, 16HBE, ACC-LC-319/bone2) up-regulated The present study found that MALAT1 was significantly highly expressed in NSCLC tissues with bone metastasis and in NSCLC cell lines with high bone metastatic ability. Downregulation of MALAT1 expression significantly inhibited proliferation and induced cell apoptosis in comparing with the negative controls. 27431200 2016 The role of lncRNA MALAT1 in bone metastasis in patients with non-small cell lung cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. NSCLC tissues, cell lines (H1915) up-regulated We observed that the level of MALAT1 was significantly higher in brain metastasis than that of non brain metastasis samples. The level of MALAT1 was associated with patients' survival. We found that MALAT1 is increased in highly invasive subline of brain metastasis lung cancer cells. Further functional studies indicate that silencing MALAT1 inhibits highly invasive subline of brain metastasis lung cancer cell migration and metastasis by inducing epithelial-mesenchymal transition (EMT). 25217850 2014 Long noncoding RNA MALAT1 promotes brain metastasis by inducing epithelial-mesenchymal transition in lung cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay etc. cancer tissues, osteosarcoma cell lines (MG-63, SAOS-2, U2OS, SW1353) up-regulated In conclusion, we revealed that enhanced MALAT1 expression predicted unfavourable outcome in osteosarcoma and promoted cell proliferation through suppressing miR-205 and activating SMAD4 function. Thus, lncRNA MALAT1 may serve as a promising prognostic and therapeutic target for osteosarcoma patients. Kaplan-Meier analysis indicated that patients with high expression of MALAT1 was associated with poor overall survival compared with the low expressing patients. Illustration of the putative predicted miR-205 binding site in the SMAD4 mRNA 3’UTR region, and the mutation within the binding site was generated. 29290978 2017 Long noncoding RNA MALAT1 promotes cell proliferation through suppressing miR-205 and promoting SMAD4 expression in osteosarcoma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 cervical cancer C53 NA qPCR, RNAi, Luciferase reporter assay, MTT assay etc. cervical cancer tissues, cell lines (HeLa, CaSki) up-regulated MALAT1 expression is significantly increased in cervical cancer than in normal tissues. Its expression in the cancerous tissues is also significantly higher than in adjacent normal tissues. MALAT1 expression is correlated with tumor size, FIGO stage, vascular invasion and lymph nodes metastasis and is an independent predictor for overall survival of cervical cancer. 26400521 2015 High MALAT1 expression predicts a poor prognosis of cervical cancer and promotes cancer cell growth and invasion. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay, Western blot hepatocellular carcinoma tissues, cell lines (Huh-6, HepG2, SMMC-7721, Bel-7402, LO2) up-regulated MALAT1 was upregulated in HCC tissues. ZEB1 was a target of miR-143-3p. miR-143-3p binds with MALAT1, and was regulated by MALAT1.The regulation of MALAT1 on ZEB1 was mediated by miR-143-3p. MALAT1 may regulate ZEB1 expression by sponging miR-143-3p and promotes hepatocellular carcinoma progression.the patients with higher MALAT1 expression had poor overall survival. 28543721 2017 Long Non-Coding RNA MALAT1 Regulates ZEB1 Expression by Sponging miR-143-3p and Promotes Hepatocellular Carcinoma Progression. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, Western blot, Luciferase reporter assay etc. breast cancer tissues, cell line (MCF-10A) up-regulated This study provided evidence that long non-coding RNA MALAT1 was up-regulated in breast cancer tissues and cell lines. MALAT1 promoted cancer cell invasion through inducing epithelial-mesenchymal transition. Interestingly, we revealed there was a reciprocal repression between MALAT1 and miR-204. ZEB2 was identified as a downstream target of miR-204 and MALAT1 exerted its function mainly through the miR-204/ZEB2 axis. Our findings suggested that MALAT1 may serve as a new diagnostic biomarker and therapy target for breast cancer. Patients with higher levels of MALAT1 expression had poorer overall survival than those with lower levels of MALAT1 expression. 28675122 2017 MiR-204/ZEB2 axis functions as key mediator for MALAT1-induced epithelial-mesenchymal transition in breast cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR breast cancer tissues, cell lines (MDA-MB-231 and MDA-MD-435) up-regulated The expression of MALAT1 in triple negative and Her-2 positive breast cancers was positively correlated to the number of metastatic lymph nodes in patients with breast cancer.MALAT1 promotes proliferation and invasion abilities of breast cancer cells through XBP1 (X-box binding protein 1)-HIF (hypoxia-inducible factor)-1a pathway in MDA-MB-231 and through Her-2 pathway in MDA-MD-435.MALAT1 could possibly be involved in regulation of MYC gene and CD47 (an immune checkpoint gene) in both cell lines.the expression levels of MALAT1 were negatively correlated to OS of patients with triple negative and Her-2 positive patients, but the correlations were not significant. 29416769 2017 Roles of MALAT1 in development and migration of triple negative and Her-2 positive breast cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, Luciferase reporter assays etc. TNBC tissues, cell lines (MDA-MB-231, MDA-MB-453, MCF-7, TB- 549, BT-474) up-regulated MALAT1 inhibition significantly induced cell cycle arrest in the G0/G1 phase. the roles of MALAT1 on TNBC cells progression was mediated by miR-129-5p. the “MALAT1-miR-129-5p” axis might play an important role in the progression of TNBC, thereby might provide a potential therapeutic strategy for the treatment of TNBC. patients with high MALAT1 expression had a poor overall survival compared to patients with low MALAT1 expression. 28915533 2017 Long non-coding RNA MALAT1 promotes proliferation and invasion via targeting miR-129-5p in triple-negative breast cancer MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR etc. breast cancer tissues, cell lines (ZR751, ZR7530, MCF7, SKBR3, BT474 and T47D) up-regulated MALAT1 expression was significantly up-regulated compared with adjacent normal tissues. Furthermore, of 204 breast cancer patients, high MALAT1 expression was associated with positive ER and progesterone receptor (PR) status. 27191888 2016 Long non-coding RNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) interacts with estrogen receptor and predicted poor survival in breast cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR etc. breast cancer tissues, cell lines (MDA-MB-231 and MDA-MB-453) down-regulated We found that MALAT1 was downregulated in breast tumor cell lines and cancer tissue, and showed that knockdown of MALAT1 in breast cancer cell lines induced an epithelial-to-mesenchymal transition (EMT) program via phosphatidylinositide-3 kinase-AKT pathways. Furthermore, lower expression of MALAT1 in breast cancer patients was associated with shorter relapse-free survival 26191181 2015 Downregulation of long noncoding RNA MALAT1 induces epithelial-to-mesenchymal transition via the PI3K-AKT pathway in breast cancer MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 esophageal squamous cell cancer NA NA qRT-PCR ect. The tumor tissues and para-carcinoma tissues up-regulated the up-regulation of UCA1 and MALAT1 lncRNAs in ESCC tissues can impact the degree of tumor progression and is predictive of postoperative survival. 30002691 2018 Expression of UCA1 and MALAT1 long-chain non-coding RNAs in esophageal squamous cell carcinoma tissues is predictive of patient prognosis. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 ovarian cancer C56.9 NA qPCR, Western blot, Flow cytometry, etc. ovarian cancer tissues, cell lines (SKOV3, OVCAR3, 3AO, HO8910) up-regulated MALAT1 was overexpressed in ovarian cancer and associated to the poor prognosis. The down-regulation of MALAT1 inhibited cell proliferation, invasion and migration, arrested cell cycle progression in S phase and induced cell apoptosis by restraining the activation of Wnt/B-catenin signaling pathway in ovarian cancer cells. Three-year survival rate in high expression of MALAT1 was lower than that in low expression of MALAT1. 29949143 2018 Long non-coding RNA MALAT1 regulates ovarian cancer cell proliferation, migration and apoptosis through Wnt/β-catenin signaling pathway. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR breast cancer tissues, cell lines (HEK-293T, MDA-MB-231) up-regulated Malat1 confers an inhibitory effect on cell growth and migration which is lost following Malat1 KO, but in a Nisch-dependent context. Specifically, Malat1 KO in the background of low Nischarin expression had a limited effect on cell functions, while Malat1 KO in cells with high levels of Nischarin led to significant increases in cell proliferation and migration. Nischarin (Fig 4F) were found to positively correlate with enhanced patient recurrence-free survival. 29912916 2018 Expression of long noncoding RNA MALAT1 correlates with increased levels of Nischarin and inhibits oncogenic cell functions in breast cancer. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 ovarian cancer C56.9 NA qPCR, Luciferase reporter assay etc. ovarian cancer tissues, cell line (SKOV3) up-regulated Our results indicate that the long noncoding RNA MALAT1 could sponge miR-211 as a competing endogenous RNA and potentially up-regulate PHF19 expression, thus facilitating the OC progression. These findings suggest that the MALAT1/miR-211/PHF19 axis may act as a key mediator in OC and provide new insight into the prevention of this disease. MALAT1 expression was up-regulated in OC tissues compared with normal ovarian tissues. A significant positive correlation was noted between MALAT1 and PHF19 . Meanwhile, TCGA cohort analysis showed that higher expression of MALAT1 was correlated with shorter survival times for patients with OC. To confirm the role of MALAT1 in OC, we further knocked down the expression of MALAT1 in SKOV3 cells . The results show that silence of MALAT1 significantly inhibited cell proliferation and colony formation ability in SKOV3 cells. Moreover, an increasing number of apoptotic cells were observed in MALAT1- silenced SKOV3 cells . In addition, silence of MALAT1 also dramatically suppressed the migration of SKOV3 cells. In vivo, the xenograft experiment showed that infection with MALAT1 shRNA lentivirus in SKOV3 cells significantly reduced the tumor growth rate. These data suggest that MALAT1 may be an oncogenic lncRNA in OC. 29874124 2018 miR-211 sponges lncRNA MALAT1 to suppress tumor growth and progression through inhibiting PHF19 in ovarian carcinoma. MALAT2 NA NA NA NA NA gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissues up-regulated MALAT2 was frequently over-expressed in cancer tissues and this over-expression was found to significantly correlate with lymph node metastasis and tumor stage.The expression of MALAT2 is upregulated in GC tissues, and a higher expression level of MALAT2 might serve as a negative prognostic marker in stage II/III GC patients which implies the potential application of MALAT2 in the therapeutic treatment of GC. 25721209 2015 MALAT2-activated long noncoding RNA indicates a biomarker of poor prognosis in gastric cancer. MAP3K20 MLK7, MLTK, MLTKalpha, MLTKbeta, MRK, ZAK 51776 ENSG00000091436 NA GRCh38_2:173075435-173268010 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP etc. cell line (HGC27, SGC7901, MGC803, AGS and MKN-45, GES-1), gastric cancer tissues up-regulated MLK7-AS1 interacted with Dnmt1 and recruited it to miR-375 promotor, hyper-methylating miR-375 promotor and repressing miR-375 expression. Our findings demonstrate that knockdown of MLK7-AS1 by siRNA inhibits gastric cancer growth by epigenetically regulating miR-375. Knockdown of MLK7-AS1 by siRNA increased the expression of miR-375. MiR-375 wasfound to be an important tumor suppressor in gastric cancer bytargeting Janus kinase 2 (JAK2). 29428732 2018 Knockdown of long non-coding RNA MAP3K20 antisense RNA 1 inhibits gastric cancer growth through epigenetically regulating miR-375. MBNL3 NA NA ENSG00000076770 NA GRCh38_X:132369317-132489968 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. HCC tissues, cell lines (QSG-7701, SMMC-7721, HCCLM3, MHCC97H, Huh7, HepG2 and Hep3B) up-regulated MBNL3 knckdoown almost completely abolishes hepatocellular carcinoma tumorigenesis.Mbnl3 was upregulated in mouse fetal livers compared with adult livers. high MBNL3 protein level in HCC tissues correlated with reduced recurrence-free survival and overall survival.In our previous microarray result of mouse liver development, Mbnl3 was upregulated in mouse fetal livers compared with adult livers.Bioinformatic analysis by Miranda and TargetScan predicted one miR-24 binding site in the 30UTR of PXN mRNA complementary to PXN-AS1-L.Kaplan–Meier analyses of the correlations between MBNL3 mRNA level and recurrence-free survival or overall survival of n=68 HCC patients. 28553938 2017 The MBNL3 splicing factor promotes hepatocellular carcinoma by increasing PXN expression through the alternative splicing of lncRNA-PXN-AS1. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 acute myeloid leukemia NA M9861/3 MSP-PCR etc. bone marrow down-regulated MEG3 hypermethylation occurred in 15 MDS patients (34.9%), and in 20 AML patients (47.6%). SNRPN hypermethylation was observed in 15 MDS patients (34.9%), and in 21 AML patients (50%). There were no significant correlations between WHO subtype, WPSS score, karyotype, haemoglobin levels, white blood cell count, platelet count and CpG methylation of any gene. MEG3 hypermethylation was associated with significantly reduced overall survival in individuals with AML, while SNRPN CpG methylation was not associated with survival. 19595458 2010 CpG methylation analysis of the MEG3 and SNRPN imprinted genes in acute myeloid leukemia and myelodysplastic syndromes. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 esophageal squamous cell cancer NA NA qPCR, Cell transfection, Western blot, Flow cytometry assay etc. ESCC tissues, cell lines (KYSE-410, HEEC, ECA-109, TE-1, and TE-13) down-regulated We found MEG3 was significantly downregulated in ESCC tissues compared with normal tissues by qRT-PCR. Low expression of MEG3 was correlated with lymph node metastasis and advanced TNM stages of ESCC patients and indicated shorter survival. Ectopic expression of MEG3 in ESCC cells inhibited cell proliferation, promoted apoptosis, and suppressed metastasis. Further investigation showed enforced expression of MEG3 activated p53 and its target genes by downregulation of mouse double minute 2 homolog (MDM2). 27778235 2016 The long non-coding RNA maternally expressed gene 3 activates p53 and is downregulated in esophageal squamous cell cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 pancreatic cancer C25 NA qPCR, Western blot, in vitro knockdown PC cell lines (SW 1990, COLO357,MIA PaCa-2, T3M4, AsPC-1, BxPC-3, CAPAN-1 and PANC-1) down-regulated Loss of MEG3 expression was observed in both the cancerous tissues and cancer cell lines. Although the absence of expression of MEG3 was not statistically correlated to either histological grade or TNM stage in the 25 cases, the prognosis was significantly worse. MEG3 knockdown enhanced cell proliferation, promoted cell migration and invasion, induced epithelial mesenchymal transition (EMT), increased the sphere-forming ability and cancer stem cell (CSC) properties, and decreased the chemosensitivity to gemcitabine in-vitro. In contrast, forced expression of MEG3 resulted in a reverse effect. 29328401 2018 Long non-coding RNA MEG3 functions as a tumour suppressor and has prognostic predictive value in human pancreatic cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 osteosarcoma NA M9180/3 qPCR etc. osteosarcoma tissues down-regulated Our findings showed that expression of lncRNA MEG3 was clearly lower in osteosarcoma tissues compared with adjacent non-tumor tissues. The expression of lncRNA MEG3 was associated with clinical stage and distant metastasis. Furthermore, multivariate analysis revealed that decreased expression of lncRNA MEG3, advanced clinical stage and distant metastasis were all independent predictors to overall survival of osteosarcoma patients 26823857 2016 Decreased expression of long non-coding RNA MEG3 acts as a potential predictor biomarker in progression and poor prognosis of osteosarcoma MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 esophageal cancer C15 NA qPCR, Western blot, Luciferase report assay etc. ESCC tissues, cell lines (TE1, TE13, Eca109, YES2, T.Tn, HEEpiC) down-regulated Significant downregulation of MEG3 was detected in esophageal cancer cells and ESCC tissues and the expression level of MEG3 was significantly increased in cancer cells after treated with the DNA methyltransferase inhibitor 5-Aza-dC. Upregulation of MEG3 led to the inhibition of proliferation and invasiveness of the cancer cells. The aberrant promoter hypermethylation of MEG3 indicates silencing of its expression. Furthermore, MEG3 acts as a ceRNA to regulate the expression of E-cadherin and FOXO1 by binding hsa-miR-9. downregulation and hypermethylation of MEG3 was associated with ESCC patients' survival. 28539329 2017 Aberrant Methylation-Mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 colorectal cancer C19.9 NA qPCR Human colorectal cancer cell lines (HT29, SW480) down-regulated In conclusion, our integrated approach demonstrated that decreased expression of lncRNA MEG3 in CRC confers potent poor therapeutic efficacy, and that MEG3 promotes chemosensitivity by enhancing oxaliplatin-induced cell apoptosis. Thus, overexpression of MEG3 may be a future direction by which to develop a novel therapeutic strategy to overcome oxaliplatin resistance of CRC patients. 28731151 2017 MEG3 is a prognostic factor for CRC and promotes chemosensitivity by enhancing oxaliplatin-induced cell apoptosis. Overall survival (OS) was updated on February 1, 2012 and was defined as the time from inclusion to death for any reason. Recurrence-free survival (RFS) was defined as the time from inclusion to recurrence or metastatic progression. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 breast cancer C50 NA qPCR etc. breast cancer tissues down-regulated Our findings revealed that the MEG3 expression was significantly decreased in clinical BC tissues compared to adjacent normal tissues. MEG3 level was significantly associated with differentiation grade, TNM stage and lymph nodes metastasis. 28051255 2016 Down-regulation of long non-coding RNA MEG3 serves as an unfavorable risk factor for survival of patients with breast cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 colorectal cancer C19.9 NA qPCR etc. CRC and liver tissues down-regulated The expression levels of four lncRNAs (GAS5, H19, MEG3 and Yiya) were significantly different between liver metastases and primary tumors of stage IV CRC patients. Furthermore, the high expression levels of GAS5 and Yiya were significantly associated with future occurrence of liver metastases in early stage CRC patients. 27391432 2016 Long non-coding RNAs: novel prognostic biomarkers for liver metastases in patients with early stage colorectal cancer MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 colorectal cancer C19.9 NA qPCR, Western blot, Flow cytometry assay etc. CRC tissues down-regulated The lower expression of MEG3 was remarkably correlated with low histological grade, deep tumor invasion, and advanced tumor node metastasis (TNM) stage. Multivariate analyses revealed that MEG3 expression served as an independent predictor for overall survival. Further experiments revealed that overexpressed MEG3 significantly inhibited CRC cell proliferation both in vitro and in vivo. MEG3 is involved in the development and progression of colorectal cancer by regulating cell proliferation and shows that MEG3 may be a potential diagnostic and prognostic target in patients with colorectal cancer. 25636452 2015 Decreased expression of long noncoding RNA MEG3 affects cell proliferation and predicts a poor prognosis in patients with colorectal cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 prostate cancer C61.9 NA qPCR, RNAi, Western blot, Flow cytometry assay etc. prostate cancer tissues, cell lines (PC3, Du145) down-regulated MEG3 decreased significantly in prostate cancer tissues relative to adjacent normal tissues. MEG3 inhibited intrinsic cell survival pathway in vitro and in vivo by reducing the protein expression of Bcl-2, enhancing Bax and activating caspase 3. We further demonstrated that MEG3 inhibited the expression of cell cycle regulatory protein Cyclin D1 and induced cell cycle arrest in G0/G1 phase. 26610246 2015 Long Non-Coding RNA MEG3 Inhibits Cell Proliferation and Induces Apoptosis in Prostate Cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 bladder cancer C67 NA qPCR, Western blot etc. bladder cancer tissues, cell line (T24) down-regulated A significant negative correlation was observed between MEG3 levels and LC3-II (autophagy marker) levels in vivo. We further demonstrated that MEG3 markedly suppressed autophagy activation, whereas MEG3 knockdown activated autophagy in human bladder cancer cell lines. Downregulated expression of MEG3 inhibited cell apoptosis, whereas autophagy inhibition increased MEG3-knockdown cell apoptosis. MEG3 knockdown also increased cell proliferation. 23295831 2013 Downregulated MEG3 activates autophagy and increases cell proliferation in bladder cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) down-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 glioma NA M9380/3 qPCR glioma tissues down-regulated Expression of lncRNAs MEG3, JPX, RNCR3, and ZFAS1 significantly differed between low and high malignancy grade. MEG3, JPX, RNCR3, and ZFAS1 showed significant decrease with tumour malignant progression. Expression of certain lncRNAs seems to be associated with patient's age at the time of diagnosis as correlation analysis showed moderate negative association for MEG3 (rs = 0.336, p = 0.009, R2 = 0.113), ZFAS1 (rs = 0.368, p = 0.004, R2 = 0.164), and RNCR3 (rs = 0.431, p = 0.001, R2 = 0.186). 29138748 2017 Identifying Novel Glioma-Associated Noncoding RNAs by Their Expression Profiles MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 colorectal cancer C19.9 NA Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (RKO, SW1116, HT29, HCT116,LoVo, SW620, SW480, 293 T), CRC tissue down-regulated MEG3 was down-regulated in CRC tissues and CRC patients with lower MEG3 showed poorer overall survival and disease-free survival than those with higher MEG3 level.MEG3 over-expression represses CRC cells proliferation and migration in vivo and in vitro,while MEG3 knockdown leads to the enhanced proliferation and metastasis of CRC cells.In CRC cells, MEG3 over-expression is related to decreased Clusterin mRNA and the corresponding protein levels,and it also directly binds to Clusterin protein through its 732-1174 region.In further, Clusterin over-expression rescues the compromised abilities of proliferation and metastasis induced by MEG3 over-expression,suggesting that MEG3 inhibits the CRC progression through regulating the Clusterin activities.Additionally,we found that 1a,25-(OH)2D and vitamin D receptor (VDR) stimulate MEG3 expression in CRC cells through directly binding to its promoter. 29628342 2018 MEG3 Activated by Vitamin D Inhibits Colorectal Cancer Cells Proliferation and Migration via Regulating Clusterin. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissue, cell lines (SGC7901, BGC823, MKN45, HGC27, GES) up-regulated lncRNA MEG3 was highly expressed in the adjacent tissue, compared to the one in gastric cancer tissue. What’s more, we also found that overexpression of lncRNA MEG3 could decrease the proliferation and metastasis of gastric cancer cells. Finally, overexpression of lncRNA MEG3 could also increase the expression of p53. 28975980 2017 lncRNA MEG3 inhibit proliferation and metastasis of gastric cancer via p53 signaling pathway MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 cervical cancer C53 NA qPCR, RNAi, MSP-PCR, Western blot etc. cervical cancer tissues, cell lines (HeLa and CaSki) down-regulated The results of qRT-PCR analysis showed that MEG3 expression was significantly lower in cervical cancer tissues compared to corresponding normal tissues. In addition, our follow-up data showed that low MEG3 expression was correlated with recurrence and short overall survival. Moreover, hypermethylation of the MEG3 promoter was observed in most cervical cancer tissue samples, and demethylation of the MEG3 promoter led to re-expression of MEG3 and inhibited proliferation of HeLa and CaSki cells. 28057015 2017 Downregulation of long noncoding RNA MEG3 is associated with poor prognosis and promoter hypermethylation in cervical cancer. MEG9 MEG9, LINC00584 100507257 ENSG00000223403 NR_047664 GRCh38_14:101064151-101072937 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated Eight (lincRNA-VLDLR, MEG9, H19 antisense, ncR-uPAR, NEAT1 (family), LUST, UM9-5, and HOTAIR) were significantly down-regulated in HCC tumor compared to non-tumor tissues at a significance level of. 26378581 2015 Exploration of Deregulated Long Non-Coding RNAs in Association with Hepatocarcinogenesis and Survival. MFI2-AS1 NA NA NA NA NA clear cell renal cell carcinoma C64.9 M8005/0 qPCR osteosarcoma cell lines up-regulated Overall, MFI2-AS1 status improves patient stratification in localized ccRCC, which supports further integration of lncRNAs in molecular cancer classifications.Kaplan-Meier estimates for disease-free survival (DFS) in the validation set. 28819235 2017 Expression of long non-coding RNA MFI2-AS1 is a strong predictor of recurrence in sporadic localized clear-cell renal cell carcinoma. MGC27382 MGC27382 NA NA NA GRCh38_1:78229599-78369464 lung adenocarcinoma C34 M8140/3 RNA-seq, qPCR etc. LUAD tissues down-regulated The results showed that CHIAP2, LINC00472, LINC00961 and MGC27382 were downregulated in LUAD tumor tissues when compared with adjacent non-tumor lung tissues, while AFAP1-AS1, CHIAP2 and FER1L4 were upregulated in LUAD tumor tissues. 27826625 2016 Integrated analysis of long non-coding RNA-associated ceRNA network reveals potential lncRNA biomarkers in human lung adenocarcinoma. MHENCR NA 100505771 ENSG00000232442 NR_132417 GRCh38_20:63627227-63628824 melanoma NA M8720/3 qPCR, Western blot, RIP malignant melanoma tissues, cell lines (A375 and SK-MEL-2) up-regulated In this study, we identified a novel lncRNA MHENCR which was upregulated in melanoma tissues and further upregulated in metastatic melanoma. Increased expression of MHENCR indicted poor survival of melanoma patients. 28123636 2017 Long noncoding RNA MHENCR promotes melanoma progression via regulating miR-425/489-mediated PI3K-Akt pathway MINCR MINCR, LINC01604 100507316 ENSG00000253716 NR_120682 GRCh38_8:143280161-143281690 gallbladder cancer C23.9 NA qPCR, RIP, Dual-luciferase reporter assay etc. gallbladder carcinoma tissues up-regulated High MINCR expression levels in GBC were positively associated with tumor volume and lymph node metastasis and were negatively correlated with overall survival (OS). Upregulation of MINCR and enhancer of zeste homolog 2 (EZH2) in GBC coincided with the downregulation of miR-26a-5p in GBC. Mechanistically, MINCR/miR-26a-5p/EZH2 axis was found to be involved in cell proliferation, cell invasive and apoptosis in GBC cells. Moreover, knockdown of MINCR suppressed cell proliferation, decreased S-phase cell numbers, increased cell apoptosis, and inhibited cell invasion by inhibiting the epithelial-mesenchymal transition (EMT) phenomenon in GBC cells. 27345740 2016 Long non-coding RNA MINCR promotes gallbladder cancer progression through stimulating EZH2 expression. MIR100HG MIR100HG, AGD1, linc-NeD125, lncRNA-N2 399959 ENSG00000255248 NR_024430 GRCh38_11:122028327-122556721 pancreatic ductal adenocarcinoma C25.3 M8500/3 RNA-seq, qPCR, Western blot etc. cell lines (BxPC-3, PANC-1 and COLO357) up-regulated although the pro-tumourigenic miR-100 and miR-125b accordingly increase,the amount of anti-tumourigenic let-7a is unchanged, as TGF-B also induces LIN28B inhibiting its maturation.Notably, we demonstrate that inactivation of miR-125b or miR-100 affects the TGF-B-mediated response indicating that these miRNAs are important TGF-B effectors.We integrate AGO2-RIP-seq with RNA-seq to identify the global regulation exerted by these miRNAs in PDAC cells.Transcripts targeted by miR-125b and miR-100 significantly overlap and mainly inhibit p53 and cell-cell junctions'pathways.Together, we uncover that TGF-B induces an lncRNA, whose encoded miRNAs, miR-100, let-7a and miR-125b play opposing roles in controlling PDAC tumourigenesis. 29748571 2018 TGF-B induces miR-100 and miR-125b but blocks let-7a through LIN28B controlling PDAC progression. MIR100HG MIR100HG, AGD1, linc-NeD125, lncRNA-N2 399959 ENSG00000255248 NR_024430 GRCh38_11:122028327-122556721 cervical cancer C53 NA microarray, qPCR etc. cervical cancer tissues differential expression To validate the results of data mining and determine the clinical relevance of lncRNA dysregulation, we detected the expression levels of the above four lncRNAs in 35 clinical tissues with and without pelvic lymph node metastasis (PLNM) by qRT-PCR. The qRT-PCR result was consistent with our analysis, in that expression of all 4 lncRNAs had statistical difference with the same trend. 27035672 2016 Characterization of long non-coding RNA expression profiles in lymph node metastasis of early-stage cervical cancer. MIR100HG MIR100HG, AGD1, linc-NeD125, lncRNA-N2 399959 ENSG00000255248 NR_024430 GRCh38_11:122028327-122556721 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. hepatocellular carcinoma tissues, cell lines (MHCC97L, SMCC-7721, Huh-7, MHCC97H and LO2) up-regulated We totally identified a set of four lncRNAs(MIR100HG, SERHL, CTD-2574D22.4 and SNHG20) that were significantly correlated with patient's survival. We then measured the expression levels of these four lncRNAs using TCGA data, and found that it was significantly up-regulated in HCC tumors compared with normal tissues. Further analysis indicated that three lncRNAs showed a positive coefficient in univariate analysis(SERHL, CTD-2574D22 and SNHG20), suggesting that a higher level of expression was associated with shorter survival. The negative coefficient for the remaining one lncRNAs(MIR100HG)suggested that their higher expression levels were associated with longer survival. 29684484 2018 Characterization of long non-coding RNAs to reveal potential prognostic biomarkers in hepatocellular carcinoma. MIR100HG MIR100HG, AGD1, linc-NeD125, lncRNA-N2 399959 ENSG00000255248 NR_024430 GRCh38_11:122028327-122556721 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Cell proliferation assay, Cell migration assay etc. cell lines (HepG2, SMMC-7721 and HCCLM9) differential expression Knockdown of seven of the ten candidate lncRNAs significantly affected cell migration in at least one cell line; knockdown of three lncRNAs produced accordant alterations in cell migration in at least two cell lines by suppressing or promoting cell migration 28194035 2017 Recurrently deregulated lncRNAs in hepatocellular carcinoma. MIR155HG MIR155HG, BIC, MIRHG2, NCRNA00172 114614 ENSG00000234883 NR_001458 GRCh38_21:25561909-25575168 glioma NA M9380/3 microarray, qPCR etc. glioma tissues up-regulated The expression of four lncRNAs in different grades showed that AGAP2-AS1, LINC01198 and MIR155HG were increased with tumor grade, while TPT1-AS1 was decreased. Knockdown of AGAP2-AS1 can inhibit the cell proliferation, migration and invasion, while increase the apoptosis cell rates in vitro. 27764782 2016 LncRNA profile study reveals four-lncRNA signature associated with the prognosis of patients with anaplastic gliomas. MIR210HG uc009yby.1 100506211 ENSG00000247095 NR_038262 GRCh38_11:565660-568457 osteosarcoma NA M9180/3 qPCR, Luciferase reporter assay, Western blot osteosarcoma tissues, cell lines (U2OS, Saos-2, HOS,MG-63, and 143B, NHOst, FOB) up-regulated miR210HG expression level was significantly upregulated in 55 cases of osteosarcoma tissue samples compared to adjacent normal tissue.the aberrantly enhanced miR210HG expression predicted poor prognosis and lower survival rate.miR210HG knockdown suppressed the osteosarcoma cell proliferation, invasion, and epithelial-mesenchymal transition-related marker(N-cadherin and vimentin) expression.miR210HG silencing decreased the tumor growth. miR-503 was verified to be the target miRNA of miR210HG.miR-503 could reverse the role of miR210HG on osteosarcoma cells.miR210HG sponges miR-503 to facilitate osteosarcoma cell invasion and metastasis,revealing the oncogenic role of miR210HG on osteosarcoma cells. 28972855 2017 Long Noncoding RNA miR210HG Sponges miR-503 to Facilitate Osteosarcoma Cell Invasion and Metastasis. MIR210HG uc009yby.1 100506211 ENSG00000247095 NR_038262 GRCh38_11:565660-568457 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, RNAi, Cell proliferation assay etc. ccRCC tissues, cell lines (786-O, ACHN, HK-2) up-regulated The results showed that the expressions of uc009yby.1 was markedly increased in ccRCC compared with the matched normal tissues. Furthermore, knockdown of uc009yby.1 suppressed renal cell proliferation. 27602119 2016 lncRNA uc009yby.1 promotes renal cell proliferation and is associated with poor survival in patients with clear cell renal cell carcinomas. MIR22HG MIR22HG, C17orf91 84981 ENSG00000186594 NR_028502 GRCh38_17:1711493-1717174 ovarian cancer C56.9 NA qPCR, RNAi, Western blot, Cell migration and invasion assay etc. cell lines (Hey, 293T) up-regulated Elevated expression of C17orf91 was observed in omental metastases when compared with matched primary ovarian tumors. Loss-of-function studies further demonstrated that C17orf91 repression impaired migration, invasion and viability of ovarian cancer cells, and downregulated the pro-metastatic gene, MYC, at both mRNA and protein level. 27535740 2016 Long noncoding RNA C17orf91 is a potential prognostic marker and functions as an oncogene in ovarian cancer. MIR22HG MIR22HG, C17orf91 84981 ENSG00000186594 NR_028502 GRCh38_17:1711493-1717174 lung cancer C34 NA qPCR etc. lung cancer tissues, cell lines (PC-9, H1975, H1299, H838 and H2228) down-regulated MIR22HG was significantly downregulated in lung cancer;this decreased expression was associated with poor patient survival. MIR22HG bound and stabilized the YBX1 protein.Silencing of MIR22HG triggered both cell survival and cell death signaling through dysregulation of the oncogenes YBX1,MET,and p21. In this MIR22HG network,p21 played an oncogenic role by promoting cell proliferation and anti-apoptosis in lung cancers.MIR22HG played a tumor suppressor role as indicated by inhibition of multiple cell cycle-related genes in human primary lung tumors. 29669758 2018 Silencing of long non-coding RNA MIR22HG triggers cell survival/death signaling via oncogenes YBX1, MET, and p21 in lung cancer. MIR4697HG MIR4697HG, LINC00947 283174 ENSG00000280237 NR_024344 GRCh38_11:133896438-133901601 ovarian cancer C56.9 NA qPCR, RNAi, Western blot, Cell migration and invasion assay etc. ovarian cancer tissues, cell lines (CoC1, CaoV-3, OVCAR3, and SKOV3) up-regulated The transcriptional level of MIR4697HG was increased in cancerous tissues and ovarian cancer cell lines.MIR4697HG knockdown by specific shRNA significantly inhibited cell proliferation and colony formation in both OVCAR3 and SKOC3 cells. Furthermore, MIR4697HG knockdown inhibited cell migration and invasion capacities. MIR4697HG knockdown also caused a decrease in matrix metalloprotease-9, phosphorylated ERK, and phosphorylated AKT. 28168162 2017 Long Noncoding RNA MIR4697HG Promotes Cell Growth and Metastasis in Human Ovarian Cancer. MIR503HG MIR503HG, H19X, MIR503HG2 84848 ENSG00000223749 NA GRCh38_X:134543337-134546632 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. MIR503HG MIR503HG, H19X, MIR503HG2 84848 ENSG00000223749 NR_024607 GRCh38_X:134543337-134546632 hepatocellular carcinoma C22.0 M8170/3 microarray, RIP etc. hepatocellular carcinoma tissues, celllines (SMMC-7721 and Huh7) up-regulated Expression level of miR503HG is significantly associated with the time to recurrence and overall survival and is an independent risk factor for recurrence and survival. Enhanced expression of miR503HG could noticeably inhibit HCC invasion and metastasis in vitro and in vivo. 29774077 2018 Long noncoding RNA miR503HG, a prognostic indicator, inhibits tumor metastasis by regulating the HNRNPA2B1/NF-kB pathway in hepatocellular carcinoma MLLT4-AS1 MLLT4 antisense RNA 1 NA NA NA GRCh38_6:167823876-167826709 gastric cancer C16 NA microarray, qPCR gastric cancer tissues down-regulated the downregulation of MLL4-AS1 was significantly associated with advanced Tumor-Node-Metastasis stage (P=0.007) and lymph node metastasis (P=0.008). decreased expression of MLLT4-AS1 is a potential biomarker and a predictor of a poor prognosis for gastric cancer. 28927028 2017 Decreased expression of the long non-coding RNA MLLT4 antisense RNA 1 is a potential biomarker and an indicator of a poor prognosis for gastric cancer MNX1-AS1 MNX1-AS1, CCAT5 645249 ENSG00000243479 NR_038835 GRCh38_7:157010805-157016426 colorectal cancer C19.9 NA microarray, qPCR, Luciferase reporter assay etc. CRC tissues, cell lines (HCT116, RKO, HT29, SW620 etc.) up-regulated Of the seletced lncRNAs, four lncRNAs named CCAT3, CCAT4, CCAT5, and CCAT6 (also named MYCLo-2) are upregulated in CRC cell lines, and two lncRNAs named CCAT7 and CCAT8 are downregulated in CRC cell lines. MYC-regulated lncRNAs, named MYCLos. The MYC-regulated MYCLos may function in cell proliferation and cell cycle by regulating MYC target genes such as CDKN1A (p21) and CDKN2B (p15), suggesting new regulatory mechanisms of MYC-repressed target genes through lncRNAs. 25663692 2015 Role of MYC-regulated long noncoding RNAs in cell cycle regulation and tumorigenesis. MNX1-AS1 MNX1-AS1, CCAT5 645249 ENSG00000243479 NR_038835 GRCh38_7:157010805-157016426 ovarian cancer C56.9 NA qPCR epithelial ovarian cancer tissues up-regulated the levels of MNX1-AS1 were higher in EOC tissue than in matched normal tissues.MNX1-AS1 expression level was significantly positively correlated with FIGO stage, grade and distant metastasis.poorer progression-free survival and overall survival than those with low-MNX1-AS1 expression.FIGO stage,distant metastasis, and MNX1-AS1 expression were independent prognostic factors of both overall survival and progression-free survival for patients with EOC. 29271994 2017 Overexpression of lncRNA MNX1-AS1 is associated with poor clinical outcome in epithelial ovarian cancer. MRCCAT1 NA 22936 ENSG00000118985 NA GRCh38_5:95885098-95962071 clear cell renal cell carcinoma C64.9 M8005/0 Microarray, qPCR, Western blot etc. clear cell renal cell carcinoma tissues, cell lines(786-O and Caki-1) up-regulated The microarray analysis identified a novel lncRNA termed metastatic renal cell carcinoma-associated transcript 1 (MRCCAT1), which is highly expressed in metastatic ccRCC tissues and associated with the metastatic properties of ccRCC. Multivariate Cox regression analysis revealed that MRCCAT1 is an independent prognostic factor for ccRCC patients. Overexpression of MRCCAT1 promotes ccRCC cells proliferation, migration, and invasion. Mechanistically, MRCCAT1 represses NPR3 transcription by recruiting PRC2 to NPR3 promoter, and subsequently activates p38-MAPK signaling pathway. Cumulative recurrence free survival and overall survival rates were significantly better in patients with lower MRCCAT1 expression than in those with higher MRCCAT1 expression. Multivariate analysis identified high expression level of MRCCAT1 as an independent prognostic factor for ccRCC patients. 28659173 2017 Long noncoding RNA MRCCAT1 promotes metastasis of clear cell renal cell carcinoma via inhibiting NPR3 and activating p38-MAPK signaling. MT1DP MT1JP, MT1, MT1J, MT1NP, MTB NA ENSG00000205361 NA GRCh38_16:56643705-56644786 gastric cancer C16 NA qPCR, Western blot etc. gastric mucosa tissues, cell lines (AGS, BGC823, HGC27, MGC803, SGC7901, MKN28, MKN45) down-regulated MTM expression was significantly lower in GC cell lines and tissues, and closely correlated with lymphatic metastasis, invasive depth, tumor staging and overall survival. Overexpression of MTM significantly inhibited GC cell migration and invasion, suppressed cell proliferation and induced cell apoptosis. In addition, we found a positive correlation between the expression level of MTM and MT1F both in cell and tissue samples. MT1F overexpression decreased GC cell migration and invasion, while knockdown of MT1F restored cell migration and invasion in MTM-overexpressing GC cells, suggesting MT1F as a key target of MTM. 29228617 2017 Decreased long non-coding RNA MTM contributes to gastric cancer cell migration and invasion via modulating MT1F MT1JP MT1JP, MT1, MT1J, MT1NP, MTB NA ENSG00000255986 NA GRCh38_16:56635739-56637086 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay etc. gastric cancer tissues down-regulated LncRNA MT1JP was significantly lower in GC tissues than adjacent normal tissues,and higher MT1JP was remarkably related to lymph node metastasis and advance stage. Functional analysis showed that lncRNA MT1JP regulated FBXW7 expression by competitively binding to miR-92a-3p. MiR-92a-3p and down-regulated FBXW7 reversed cell phenotypes caused by lncRNA MT1JP by rescue analysis.MT1JP, a down-regulated lncRNA in GC,was associated with malignant tumor phenotypes and survival of GC.MT1JP regulated the progression of GC by functioning as a competing endogenous RNA (ceRNA) to competitively bind to miR-92a-3p and regulate FBXW7 expression. Our study provided new insight into the post-transcriptional regulation mechanism of lncRNA MT1JP,and suggested that MT1JP may act as a potential therapeutic target and prognosis biomarker for GC. 29720189 2018 LncRNA MT1JP functions as a ceRNA in regulating FBXW7 through competitively binding to miR-92a-3p in gastric cancer. MT1JP MT1JP, MT1, MT1J, MT1NP, MTB NA ENSG00000255986 NA GRCh38_16:56635739-56637086 gastric cancer C16 NA qPCR, Western blot, RNAi etc. gastric cancer tissues, cell lines (SGC-7901, MGC-803, HGC-27 and AGS) down-regulated MT1JP was found downregulated in GC tissues and cells. Low expression of MT1JP was significantly correlated with advanced TNM stage and lymphatic metastasis. Gain- and loss-of-function of MT1JP revealed that MT1JP functioned as a ceRNA for miR-214-3p to facilitate RUNX3 expression and then upregulated p21 and Bim levels suppressing GC cell proliferation, invasion and migration, and promoting apoptosis. Furthermore, MT1JP overexpression suppressed tumor growth and inhibited the expression of miR-214-3p and proliferation antigen Ki-67, but increased the expression of RUNX3, p21 and Bim in vivo. Our results suggest a potential ceRNA regulatory network involving MT1JP regulates RUNX3 expression by competitively binding endogenous miR-214-3p in tumorigenesis and progression of GC. 29742512 2018 LncRNA MT1JP Suppresses Gastric Cancer Cell Proliferation and Migration Through MT1JP/MiR-214-3p/RUNX3 Axis. MUC5B-AS1 NA NA NA NA NA lung cancer C34 NA qPCR, Western blot etc. lung cancer tissues, cell lines (HBE, A549, H1299, SPCA1, H1975, and H460) up-regulated We identified one novel lncRNA, MUC5B-AS1 (Ensembl: ENST00000532061.2). MUC5B-AS1 was upregulated in lung adenocarcinoma tissues compared with normal lung tissues. Moreover, MUC5B-AS1 promoted lung cancer cell migration and invasion in vitro and promoted lung cancer cell metastasis in vivo. The high expression of MUC5B was significantly associated with poor outcomes in lung adenocarcinoma. Our findings highlight MUC5B-AS1 functions as an oncogenic lncRNA in tumor metastasis and implicate MUC5B-AS1 as an attractive candidate target for lung adenocarcinoma treatment. 29670111 2018 Long non-coding RNA MUC5B-AS1 promotes metastasis through mutually regulating MUC5B expression in lung adenocarcinoma. MVIH AK094613 NA NA NA NA glioma NA M9380/3 qPCR glioma tissues, cell lines (U251, U87, U118, LN18) up-regulated We found that MVIH was significantly upregulated in glioma cell lines and tissues. Patients with MVIH high expression tumors had a worse overall survival compared to patients with MVIH high expression tumors. 27981545 2017 Long non-coding RNA MVIH acts as a prognostic marker in glioma and its role in cell migration and invasion MVIH AK094613 NA NA NA NA breast cancer C50 NA qPCR, RNAi, Flow cytometry assay etc. breast cancer tissues, cell lines (MDA-MB-231, MCF-7, T47D, BT-549, UACC-812) up-regulated Our research revealed that the expression levels of MVIH in breast cancer tissues were higher than in adjacent noncancerous tissues, and high MVIH expression was correlated with Ki67 expression. Moreover, breast cancer patients with high MVIH expression levels showed poor overall survival and disease-free survival. Multivariate analysis results indicated that MVIH was an independent prognostic factor in breast cancer. In addition, upregulated MVIH expression levels promoted cell proliferation and cell cycle, and inhibited cell apoptosis, while reduced MVIH expression showed the converse. 26555546 2015 Long non-coding RNA MVIH is associated with poor prognosis and malignant biological behavior in breast cancer. MVIH AK094613 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated In this study, we found that lncRNA MVIH was generally overexpressed in HCC. In a cohort of 215 HCC patients, the overexpression of MVIH was associated with frequent microvascular invasion and a higher tumor node metastasis stage as well as decreased recurrence-free survival (RFS) and overall survival. We also found that MVIH could promote tumor growth and intrahepatic metastasis by activating angiogenesis in mouse models. Subsequent investigations indicated that MVIH could activate tumor-inducing angiogenesis by inhibiting the secretion of phosphoglycerate kinase 1(PGK1). 22706893 2012 Long noncoding RNA associated with microvascular invasion in hepatocellular carcinoma promotes angiogenesis and serves as a predictor for hepatocellular carcinoma patients' poor recurrence-free survival after hepatectomy. Myd88 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blotting etc. cell lines (HepG2, SNU423, SMMC-7721, Hep3B, 97H, 97 L, Huh7) up-regulated Myd88 aberrant upregulated in HCC located upstream of Myd88 and verified a positive regulation relationship between them indicating that LncMyd88 might participate in the enhanced expression of Myd88 in HCC. The gain- and loss-of-function analysis revealed that LncMyd88 could promote the proliferation and metastasis of HCC both in vitro and in vivo. In addition, ChIP assays demonstrated that Lnc-Myd88 might increase Myd88 expression through enhancing H3K27Ac in the promoter of Myd88 gene, thus resulting in the activation of both NF-kB and PI3K/AKT signal pathways. In conclusion, we proposed that Lnc-Myd88 might serve as a novel diagnosis and therapeutic target for HCC. 29022910 2017 Long non-coding RNA Myd88 promotes growth and metastasis in hepatocellular carcinoma via regulating Myd88 expression through H3K27 modification MYLK-AS1 MYLK-AS1 100506826 ENSG00000239523 NR_038266 GRCh38_3:123585542-123644568 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. n340790 NA NA NA NA NA thyroid cancer C73.9 NA qPCR, Western blot etc. thyroid cancer tissues, cell line (SW579) up-regulated Here, we found that the lncRNA n340790 was highly expressed in human thyroid cancer tissues and was strongly correlated with the clinical characteristics of patients. There was a good prognostic value of n340790 for thyroid cancer. Furthermore, we discovered that n340790 could act as an endogenous sponge by directly binding to miR-1254 and downregulating miR-1254 expression. 28559970 2017 The lncRNA n340790 accelerates carcinogenesis of thyroid cancer by regulating miR-1254 NAG7 LINC00312, ERR-10, ERR10, LMCD1DN, LOH3CR2A, NAG-7, NAG7, NCRNA00312 29931 NA NR_024065 NA non small cell lung cancer C34 M8046/3 qPCR, RNAi, ChIP, Cell proliferation assay etc. blood, NSCLC tissues, cell lines (A549, SPC-A1, H1299, H1975, PC9 etc.) down-regulated Here, we found linc00312 was down-regulated in paired NSCLC tissues and correlated with poor clinical outcome; decreased linc00312 expression in NSCLC was associated with larger and later stage tumours. linc00312 could inhibit cell proliferation and promote apoptosis in vitro and in vivo. Furthermore, we found that HOXA5 could bind in the promoter of linc00312 and up-regulated the expression of it. Moreover, linc00312 was down-regulated in the plasma of NSCLC patients. 28338293 2017 Long non-coding RNA 00312 regulated by HOXA5 inhibits tumour proliferation and promotes apoptosis in Non-small cell lung cancer. NAG7 LINC00312, ERR-10, ERR10, LMCD1DN, LOH3CR2A, NAG-7, NAG7, NCRNA00312 29931 NA NR_024065 NA nasopharyngeal cancer C11 NA microarray, ISH etc. NPC, TMA tissues down-regulated We found that LINC00312 was significantly down-regulated in NPC tissues compared with non-cancerous nasopharyngeal epithelium tissues. Positive expression of LINC00312 was negatively correlated with tumor size but positively correlated with lymph node metastasis. A receiver operating characteristic (ROC) analysis revealed that LINC00312 expression could distinguish non-cancerous patients from NPC patients. These observations indicated that LINC00312 could represent a potential biomarker for metastasis, progression and prognosis in NPC. 23529758 2013 Expression of LINC00312, a long intergenic non-coding RNA, is negatively correlated with tumor size but positively correlated with lymph node metastasis in nasopharyngeal carcinoma. NBAT1 NBAT1, CASC14, NBAT-1 729177 ENSG00000260455 NR_034143 GRCh38_6:22134957-22147193 breast cancer C50 NA microarray, qPCR, Western blot, RIP, ChIP etc. cell lines (MCF-7, T47D, ZR75-1, BT-474, MDA-MB-453, BT-549, SK-BR-3 etc.) down-regulated Here, we report that NBAT1 is down-regulated in various types of cancer. Particularly, reduced NBAT1 in breast cancer is associated with tumor metastasis and poor patient prognosis. In vitro, ectopic NBAT1 inhibits migration and invasion of breast cancer cells. Mechanistic study shows that NBAT1 is associated with PRC2 member EZH2 and regulates global gene expression profile. Among them, DKK1 (dickkopf WNT signaling pathway inhibitor 1) is found to be regulated by NBAT1 in a PRC2 dependent manner, and is responsible for NBAT1's effects in inhibiting migration and invasion of breast cancer cells. 26378045 2015 NBAT1 suppresses breast cancer metastasis by regulating DKK1 via PRC2. NBAT1 NBAT1, CASC14, NBAT-1 729177 ENSG00000260455 NR_034143 GRCh38_6:22134957-22147193 osteosarcoma NA M9180/3 qPCR, Luciferase reporter assay etc. OS tissues, cell lines (MG63, U2OS, 143b, LM7, KHOS, Nhost) down-regulated NBAT1 functions as a tumor suppressor in some cancers. However, the expression pattern,the biological function and the mechanisms of NBAT1 in OS progress have not been elucidated. In this study, for the frst time, we found that NBAT1 expression is downregulated in OS tissues and cell lines and is associated with clinical stage, distant metastasis and poor prognosis. Loss- and gain-of-function assays showed that NBAT1 played a negative regulatory role in OS growth and metastasis in vitro and in vivo. Further investigation demonstrated that NBAT1 physically interacted with miR-21 and then suppressed its expression. NBAT1 also regulated downstream genes targeted by miR-21, including PTEN, PDCD4, TPM1 and RECK. 29119050 2017 Long noncoding RNA NBAT1 negatively modulates growth and metastasis of osteosarcoma cells through suppression of miR-21 NBAT1 NBAT1, CASC14, NBAT-1 729177 ENSG00000260455 NR_034143 GRCh38_6:22134957-22147193 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN51), gastric adenocarcinomas tissues down-regulated Downregulation of LINCROR, POU3F3, HOTAIR, FALEC, NBAT1, and ZEB2-AS2 lncRNAs in TCGA gastric tumor datasets 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. NBAT1 NBAT1, CASC14, NBAT-1 729177 ENSG00000260455 NR_034143 GRCh38_6:22134957-22147193 glioblastoma NA M9440/3 qPCR, western blot glioblastoma tissue, cell lines ( SVGP12, U251, U87, U373, T98, and LZ229) up-regulated Upregulated NBAT1 inhibits proliferation of T98 and U87 cells via regulating Akt, indicating that NBAT1 may be related to the malignancy and prognosis of gliomas 29771423 2018 Effect of downregulated lncRNA NBAT1 on the biological behavior of glioblastoma cells NBAT1 NBAT1, CASC14, NBAT-1 729177 ENSG00000260455 NR_034143 GRCh38_6:22134957-22147193 ovarian cancer C56.9 NA qPCR, Western blot etc. ovarian cancer tissues, cell lines (A2780, TOV112D, HO-8910, OVCAR-3, and SKOV3) down-regulated We found that lncRNA NBAT-1 was obviously downregulated in OC tissue compared to normal ovarian tissue (P<0.001) which was free of OC, and the detected levels of NBAT-1 were associated with the International Federation of Gynecology and Obstetrics stage and tumor size guidelines. Moreover, it has been shown that lower levels of NBAT-1 predict poor outcomes of OC. 28435289 2017 Long noncoding RNA NBAT-1 suppresses tumorigenesis and predicts favorable prognosis in ovarian cancer NBAT1 NBAT1, CASC14, NBAT-1 729177 ENSG00000260455 NR_034143 GRCh38_6:22134957-22147193 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, RNAi etc. ccRCC tissues, cell lines (786-O, ACHN, Caki-1 etc.) down-regulated NBAT-1 expression is significantly decreased in ccRCC tissues and renal cancer cells compared with adjacent normal tissues and normal human proximal tubule epithelial cell line HK-2, and its low level is associated with advanced features and poor prognosis. NBAT-1 is a novel molecular correlated with ccRCC progression and it may represent a prognostic biomarker and therapeutic target in renal cancer diagnosis and treatment. 26097558 2015 Decreased expression of long non-coding RNA NBAT-1 is associated with poor prognosis in patients with clear cell renal cell carcinoma. nc886 VTRNA2-1, CBL-3, CBL3, MIR886, MIRN886, VTRNA2, hsa-mir-886, hvg-5, nc886, svtRNA2-1a 100126299 ENSG00000270123 NR_030583 GRCh38_5:136080470-136080597 gastric cancer C16 NA RNA-seq, qPCR etc. gastric cancer tissues, gastric cell lines down-regulated Our real-time RT-PCR data (Fig 1A) indicated that the expression level of nc886 was lower in a subpopulation of tumor tissues than in normal tissues. nc886 inhibits cell proliferation when ectopically expressed in gastric cancer cells. 25003254 2014 nc886, a non-coding RNA of anti-proliferative role, is suppressed by CpG DNA methylation in human gastric cancer. ncC11orf49 C11orf49 NA ENSG00000149179 NA GRCh38_11:46936689-47164385 renal cell carcinoma C64.9 NA microarray, qPCR, Western blot etc. RCC tissues up-regulated Four lncRNAs mapping to intronic regions, namely ncC11orf49, ncHDAC5, ncRAB31 and ncSRPK1, showed a significant differential expression between tumor and nontumor paired samples as measured by qPCR. 24238219 2013 Expression analysis and in silico characterization of intronic long noncoding RNAs in renal cell carcinoma: emerging functional associations. ncHDAC5 HDAC5, HD5, NY-CO-9 NA NA NA NA renal cell carcinoma C64.9 NA microarray, qPCR, Western blot etc. RCC tissues up-regulated Four lncRNAs mapping to intronic regions, namely ncC11orf49, ncHDAC5, ncRAB31 and ncSRPK1, showed a significant differential expression between tumor and nontumor paired samples as measured by qPCR. 24238219 2013 Expression analysis and in silico characterization of intronic long noncoding RNAs in renal cell carcinoma: emerging functional associations. NCK1-AS1 NA NA ENSG00000239213 NA GRCh38_3:136841726-136862054 cervical cancer C53 NA Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown cervical squamous cell carcinoma tissues, cervical cancer cell lines (HeLa, C33A and SiHa and CaSki) up-regulated Functionally,we screened the CC-associated lncRNA NCK1-AS1 as a new candidate lncRNA and regulator which promotes development and progression in CC. qRT-PCR and RNA in situ hybridization (RISH) results showed that NCK1-AS1 was significantly up-regulated in 77.4% of the CC tissue group compared with the normal group.Interestingly,we demonstrated that transcription factor SP1 directly binds to the promoter to activate NCK1-AS1 expression in SiHa cells.In vitro and in vivo assays of silencing NCK1-AS1 significantly inhibited cell proliferation and invasion, with induction of cell arrest in S phase of the cell cycle. NCK1-AS1 functioned as a molecular sponge for miR-6857, antagonizing its ability to repress CDK1/6 protein translation. 29416014 2018 LncRNA NCK1-AS1 promotes proliferation and induces cell cycle progression by crosstalk NCK1-AS1/miR-6857/CDK1 pathway. ncRAB31 RAB31, Rab22B NA NA NA NA renal cell carcinoma C64.9 NA microarray, qPCR, Western blot etc. RCC tissues up-regulated Four lncRNAs mapping to intronic regions, namely ncC11orf49, ncHDAC5, ncRAB31 and ncSRPK1, showed a significant differential expression between tumor and nontumor paired samples as measured by qPCR. 24238219 2013 Expression analysis and in silico characterization of intronic long noncoding RNAs in renal cell carcinoma: emerging functional associations. ncRuPAR NCRUPAR, NCRNA00193, ncR-uPAR 100302746 NA NR_028375 NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated Eight (lincRNA-VLDLR, MEG9, H19 antisense, ncR-uPAR, NEAT1 (family), LUST, UM9-5, and HOTAIR) were significantly down-regulated in HCC tumor compared to non-tumor tissues at a significance level. 26378581 2015 Exploration of Deregulated Long Non-Coding RNAs in Association with Hepatocarcinogenesis and Survival. ncSRPK1 SRPK1, SFRSK1 NA NA NA NA renal cell carcinoma C64.9 NA microarray, qPCR, Western blot etc. RCC tissues up-regulated Four lncRNAs mapping to intronic regions, namely ncC11orf49, ncHDAC5, ncRAB31 and ncSRPK1, showed a significant differential expression between tumor and nontumor paired samples as measured by qPCR. 24238219 2013 Expression analysis and in silico characterization of intronic long noncoding RNAs in renal cell carcinoma: emerging functional associations. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422798-65426526 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 thyroid cancer C73.9 NA qPCR, RNAi, Western blot, RNA pull-down assay, Cell migration and invasion assay etc. cell lines (CBMs, TAMs, BMDMs, RAW 264.7) up-regulated NEAT1 was highly expressed in patients with thyroid cancer. NEAT1 knockout inhibited thyroid cancer cell survival, migration and invasion, along with reduced B-catenin (a direct target of miRNA-214) protein expression. Furthermore, NEAT1 significantly accelerated thyroid cancer cell growth and metastasis in vitro and increased tumor size in vivo. Upregulation of NEAT1 decreased the expression of miRNA-214, presenting a reciprocal repression correlation. 28000845 2016 Long non-coding RNA NEAT1 promotes malignant progression of thyroid carcinoma by regulating miRNA-214. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 glioblastoma NA M9440/3 qPCR etc. GNS cell lines up-regulated In addition, we detected 26 differentially expressed long non-coding RNAs 23046790 2012 Digital transcriptome profiling of normal and glioblastoma-derived neural stem cells identifies genes associated with patient survival NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 renal cell carcinoma C64.9 NA qPCR, Western blot, in vitro knockdown renal cell carcinoma tissues, cell lines (ACHN, 786-O, A498, and Caki-1) up-regulated NEAT1 is up-regulated in RCC tissue compared to corresponding non-tumor tissue.High NEAT1 expression was associated with tumor progression and poor survival in RCC patients.Mechanistic analysis revealed that NEAT1 acts as a competitive sponge for miR-34a, which prevents inhibition of c-Met. Thus, NEAT1 promotes RCC progression through the miR-34a/c-Met axis. 28968960 2017 The long non-coding RNA NEAT1 enhances epithelial-to-mesenchymal transition and chemoresistance via the miR-34a/c-Met axis in renal cell carcinoma NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 pancreatic cancer C25 NA qPCR, RNAi, Dual-luciferase reporter assay, Cell proliferation assay etc. primary PC tissues, cell lines (AsPC-1, BxPC-3, SW1990 and PANC-1) up-regulated Here, we found that the expression level of NEAT1 was higher in PC tissues compared to the corresponding non-tumor tissues. Besides, our findings indicate that high NEAT1 expression level is closely correlated with tumor progression and poor survival in PC patients. Furthermore, we also found that knockdown of NEAT1 remarkably suppressed cell proliferation by inducing cell cycle arrest and apoptosis promotion in PC cells. Moreover, bioinformatics analysis and luciferase reporter assay revealed that NEAT1 directly bound to the miR-506-3p, which has been reported to act as a tumor suppressor in diverse cancers. 27888106 2016 Long non-coding RNA NEAT1 facilitates pancreatic cancer progression through negative modulation of miR-506-3p. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 cholangiocarcinoma NA M810/3 qPCR, Western blot, RNAi, RIP, ChIP CCA tissues, cell lines (QBC939, RBE, Hu CCT1, TFK-1, HIBEpic) up-regulated NEAT1 expression was higher in CCA tumors than matched adjacent non-tumor tissue.therapeutic procedures that have been accomplished for CCA in recent years, overall survival rates of CCA patients is quite poor due to recurrence and metastasis 28810932 2039 LncRNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, RNAi, Western blot, Flow cytometry assay, CCK-8 assay etc. ccRCC tissues, cell lines (Caki-1, Caki-2, 786-O and ACHN) up-regulated The expression levels of NEAT1 was up-regulated in ccRCC tissues. NEAT1 knock-down suppressed cell proliferation and induced cell apoptosis in ccRCC cell lines. In addition, NEAT1 knock-down suppressed cell invasion and migration and inhibited the mRNA and protein expression levels of epithelial-mesenchymal transition-related markers in ccRCC cell lines. 28269753 2017 LncRNA, NEAT1 is a prognosis biomarker and regulates cancer progression via epithelial-mesenchymal transition in clear cell renal cell carcinoma. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 osteosarcoma NA M9180/3 RNA-seq, qPCR, RNAi, Luciferase reporter assay, Cell growth assay etc. cell lines (SaOS2, U2OS, MCF7, A549, H1299) up-regulated In this study, analysis of next-generation chromatin immunoprecipitation-sequencing (ChIP-seq) data for p53 revealed that the lncRNA NEAT1 is a direct transcriptional target of p53. The suppression of NEAT1 induction by p53 attenuates the inhibitory effect of p53 on cancer cell growth and also modulates gene transactivation, including that of many lncRNAs. Furthermore, low expression of NEAT1 is related to poor prognosis in several cancers. 28295289 2017 Long non-coding RNA NEAT1 is a transcriptional target of p53 and modulates p53-induced transactivation and tumor-suppressor function. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 ovarian cancer C56.9 NA qPCR etc. ovarian cancer tissues up-regulated NEAT1 is upregulated in ovarian cancer tissues compared with the corresponding adjacent non-neoplastic tissues. The expression level of NEAT1 was positively correlated with FIGO stage, tumor grade and distant metastasis. 27608895 2016 Clinical significance of up-regulated lncRNA NEAT1 in prognosis of ovarian cancer. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 oral squamous cell carcinoma C06.9 M8070/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (SCC-9,SCC-25, HN4, Tca-8113,Cal-27), OSCC tissues up-regulated Functionally,knockdown of NEAT1 significantly inhibited cell proliferation and invasion and induced cell cycle arrest at the G0/G1 phase and apoptosis, whereas inhibition of miR-365 abolished the suppressive effect of NEAT1 knockdown on cellular processes. RGS20, a direct target of miR-365, could reverse the tumor suppressive role of miR-365 mimic by enhancing cell viability and motility. Moreover, the protein levels of RGS20, cyclin D1, E-cadherin, N-cadherin and vimentin could be regulated by the NEAT1/miR-365 axis.NEAT1 silencing also inhibited tumor growth in vivo. NEAT1/miR-365/RGS20 axis may be a novel mechanism or therapeutic strategy for OSCC treatment. 29484420 2018 lncRNA NEAT1 promotes cell proliferation and invasion by regulating miR-365/RGS20 in oral squamous cell carcinoma. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 cervical cancer C53 NA qPCR, Luciferase reporter assay, Western blot, RIP cervical cancer tissues, cell lines (HeLa and SiHa) up-regulated the overexpression of NEAT1 accelerated proliferation,The effect of NEAT1 on cell proliferation was dependent on the dose of ionizing radiation. And the silence of NEAT1 also caused cell cycle arrest in G0/G1 phase, and triggered more apoptosis.NEAT1 could function as a ceRNA to regulate cyclin D1 through sponging miR-193b-3p in cervical cancer.miR-193b-3p and cyclin D1 could inhibit NEAT1-mediated suppressive effect on proliferation, and its stimulative effect on cell cycle arrest and apoptosis. And the overexpression of NEAT1 improved the survival rate in an ionizing radiation-dependent manner, while the silence of NEAT1 decreased the survival rate in the ionizing radiation-mediated way. 29416780 2017 LncRNA NEAT1 enhances the radio-resistance of cervical cancer via miR-193b-3p/CCND1 axis. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 osteosarcoma NA M9180/3 qPCR, RNAi etc. osteosarcoma tissues, cell lines (hFOB1.19, MG63, 143B, HOS and Saos2) up-regulated NEAT1 was overexpressed in OS tissues, which positively correlated with tumor size, Enneking stage and distant metastasis of OS patients. The elevated level of NEAT1 was confirmed in OS cell lines including MG63 and HOS in vitro Knockdown of NEAT1 by two siRNAs induced impaired cell vitalities,promotes the apoptosis and G0/G1 arrest in two cell lines,which was associated with inhibited anti-apoptosis signals BCL-2 pathway and cell cycle-related cyclin D1 (CCND1) signals.Moreover, the tumor suppressor microRNA-34c (miR-34c) was negatively regulated and inhibited by NEAT1 in OS. Suppression of miR-34c could up-regulate the expressions of its target genes BCL-2 and CCND1 to antagonize the effects of NEAT1 knockdown. Furthermore, overexpressed NEAT1 reduced the sensitivity of cisplatin (DDP) and inhibited DDP-induced apoptosis and cell cycle arrest via miR-34c. 29654165 2018 Knockdown of the oncogene LncRNA NEAT1 restores the availability of miR-34c and improves the sensitivity to cisplatin in osteosarcoma. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 cervical cancer C53 NA qPCR, Luciferase reporter assay, in vitro knockdown cervical cancer specimens tissues, Cervical cancer cell lines (SiHa, Caski, HeLa) up-regulated the expression of NEAT1 was higher in cervical cancer cells/tissues compared with that in normal human keratinocytes/tissues.downregulation of NEAT1 inhibited colony formation, cell migration and invasion. Further investigation using the luciferase reporter assay revealed that the expression of mircoRNA-101 (miR-101) target gene Fos was positively associated with NEAT1 expression due to NEAT1-competitive molecular sequestering of miR-101 via base pairing. Furthermore, reduction of miR-101 expression by inhibitor transfection reversed the effect of NEAT1 siRNA on cervical cancer cells. 29207151 2017 Long non-coding nuclear paraspeckle assembly transcript 1 acts as prognosis biomarker and increases cell growth and invasion in cervical cancer by sequestering microRNA-101. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 nasopharyngeal cancer C11 NA qPCR, Western blot, Luciferase reporter assay etc. cell lines (CNE-2, HONE-1, 5-8F, SUNE-1 etc.) up-regulated We found that lncRNA NEAT1 was significantly upregulated in NPC cell lines and tissues. Knockdown of NEAT1 could sensitize NPC cells to radiation in vitro. Further investigation found that NEAT1 regulated radioresistance by modulating EMT phenotype. Furthermore, we found that there was reciprocal repression between NEAT1 and miR-204. ZEB1 was identified as a downstream target of miR-204 and NEAT1 upregulated ZEB1 expression by negatively regulating miR-204 expression. 27020592 2016 The long non-coding RNA NEAT1 regulates epithelial to mesenchymal transition and radioresistance in through miR-204/ZEB1 axis in nasopharyngeal carcinoma NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 lung cancer C34 NA RNA-seq, qPCR, RNAi, Luciferase reporter assay, Cell growth assay etc. cell lines (SaOS2, U2OS, MCF7, A549, H1299) up-regulated In this study, analysis of next-generation chromatin immunoprecipitation-sequencing (ChIP-seq) data for p53 revealed that the lncRNA NEAT1 is a direct transcriptional target of p53. The suppression of NEAT1 induction by p53 attenuates the inhibitory effect of p53 on cancer cell growth and also modulates gene transactivation, including that of many lncRNAs. Furthermore, low expression of NEAT1 is related to poor prognosis in several cancers. 28295289 2017 Long non-coding RNA NEAT1 is a transcriptional target of p53 and modulates p53-induced transactivation and tumor-suppressor function. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 lung cancer C34 NA RNAi, qPCR etc. cell line A549 up-regulated Our study reveals a novel mechanism by which Oct4 transcriptionally activates NEAT1 via promoter and MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis. 28615056 2017 Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Results showed that NEAT1 expression in colorectal cancer was up-regulated in 72.0% (172/239) cases compared with corresponding normal counterparts, and related to tumor differentiation, invasion, metastasis and TNM stage. NEAT1 was associated with both disease-free survival and overall survival of patients with colorectal cancer that patients with high NEAT1 expression tend to have unfavorable outcome. These results provided the first evidence that the expression of NEAT1 in colorectal cancer may play an oncogenic role in colorectal cancer differentiation, invasion and metastasis. 26314847 2015 NEAT expression is associated with tumor recurrence and unfavorable prognosis in colorectal cancer. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 esophageal squamous cell cancer NA NA qPCR, RNAi etc. ESCC tissues, cell lines (SHEE, SHEEC) up-regulated We found that the expression of NEAT1 was higher in ESCC tissues and cells compared with the normal counterparts. Pearson analysis showed that elevated NEAT1 levels were extraordinarily correlated with the tumor size, lymph node metastasis and clinical stage. 26609486 2015 Up regulation of the long non-coding RNA NEAT1 promotes esophageal squamous cell carcinoma cell progression and correlates with poor prognosis. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 gastric cancer C16 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. gastric cancer tissues, cell lines (NCI-N87, SGC-7901, MKN-45, AGS) up-regulated LncRNA NEAT1 was overexpressed in gastric cancer tissues and cell lines and corrected with clinical stage, histological type, lymph node metastasis, and distant metastasis. Furthermore, patients with high levels of LncRNA NEAT1 had poorer survival than those with lower levels of LncRNA NEAT1. Moreover, knocking down LncRNA NEAT1 expression significantly suppressed the gastric cancer cell migration and invasion in vitro and regulated EMT-associated proteins expression. 27095450 2016 Long noncoding RNA NEAT1 is an unfavorable prognostic factor and regulates migration and invasion in gastric cancer. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay, Western blot, RIP cell lines (Huh7, Hep3B, HepG2, Bel-7404, SK-Hep1, LO2 and HEK-293T) up-regulated miR-485 was significantly downregulated in HCC cells.miR-485 was increased by sh-NEAT1 and miR-485 can modulate NEAT1 expression negatively. miR-485 was confirmed as a interacting target of NEAT1.STAT3 was recognized as a direct target of miR-485 and miR-485 mimics can inhibit STAT3 expression.NEAT1 can act as a competing endogenous lncRNA (ceRNA) to regulated STAT3 by sponging miR-485 in HCC. Taken these together, NEAT1 can be used as an important biomarker in HCC diagnosis and treatment.STAT3 can regulate various genes which can control proliferation, survival, and invasion process. 29219178 2017 The long noncoding RNA NEAT1 contributes to hepatocellular carcinoma development by sponging miR-485 and enhancing the expression of the STAT3. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated Our results revealed that NEAT1 appeared to have higher expression in the HCC tissues, compared with the adjacent non-cancerous liver tissues. High levels of NEAT1 promoted the clinical features of HCC, including the number of tumor nodes, metastasis, clinical TNM stage, the status of portal vein tumor embolus, vaso-invasion and the infiltration of tumor cells. Additionally, high NEAT1 expression levels were significantly associated with the expression level of MDTH, NM23 and MALAT1 26191242 2015 Clinical implication of long non-coding RNA NEAT1 expression in hepatocellular carcinoma patients NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated Eight (lincRNA-VLDLR, MEG9, H19 antisense, ncR-uPAR, NEAT1 (family), LUST, UM9-5, and HOTAIR) were significantly down-regulated in HCC tumor compared to non-tumor tissues at a significance level of. 26378581 2015 Exploration of Deregulated Long Non-Coding RNAs in Association with Hepatocarcinogenesis and Survival. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, ISH etc. cell lines (MCF-7, MDA-MB-231, MDAMB-468) up-regulated Induction of NEAT1 in hypoxia also leads to accelerated cellular proliferation, improved clonogenic survival and reduced apoptosis, all of which are hallmarks of increased tumorigenesis. Furthermore, in patients with breast cancer, high tumor NEAT1 expression correlates with poor survival, all of which are hallmarks of increased tumorigenesis. 25417700 2014 Tumor hypoxia induces nuclear paraspeckle formation through HIF-2a dependent transcriptional activation of NEAT1 leading to cancer cell survival. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, RNA pull-down assay etc. Lung cancer tissues, cell lines (A549, SPC-A1, H1299, 95D, SK-MES-1, NCI-H520 etc.) up-regulated We identified NEAT1 was highly expressed in patients with NSCLC and was a novel regulator of NSCLC progression. Patients whose tumors had high NEAT1 expression had a shorter overall survival than patients whose tumors had low NEAT1 expression. Further, NEAT1 significantly accelerates NSCLC cell growth and metastasis in vitro and tumor growth in vivo. Additionally, we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression. 27351135 2016 Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown cell lines (A549, H1299, H446, H460, NCI-H1650), NSCLC tissues up-regulated NEAT1 was detected to be significantly upregulated in NSCLC tissues and closely associated with advanced TNM stages,lymph node metastasis, distant metastasis, and poor prognosis.Further experiments revealed that lncRNA NEAT1 silencing inhibited cell proliferation and invasion in vitro. In addition, mechanistic analysis showed that lncRNA NEAT1 upregulated the miR-181a-5p-targeted gene HMGB2 through acting as a competitive sponge of miR-181a-5p. 28762332 2017 Long Noncoding RNA NEAT1 Promotes Proliferation and Invasion via Targeting miR-181a-5p in Non-Small Cell Lung Cancer. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Cell migration and invasion assay, CCK-8 assay etc. NSCLC tissues, cell lines (A549, H1299, SPCA1 and H358) up-regulated We observed that the expression of NEAT1 in NSCLC tissues and cell lines were much higher than that in normal control, respectively. High NEAT1 expression was statistically associated with poor differentiation, Lymph node metastasis and advanced TMN stage. Moreover, the downregulation of NEAT1 expression significantly inhibited the NSCLC cells proliferation, migration, and invasiveness. Finally, we found that decreased expression of NEAT1 inhibited the Wnt/B-catenin signaling pathway activity. 28239820 2017 Long non-coding RNA NEAT1 acts as oncogene in NSCLC by regulating the Wnt signaling pathway. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. hepatocellular carcinoma tissues, cell line (L02) up-regulated the lipolytic enzyme,ATGL is highly expressed in human HCC tissues and predicts poor prognosis.high levels of DAG and FFA are present in HCC tissues.Furthermore,the lncRNA-NEAT1 was found to modulate ATGL expression and disrupt lipolysis in HCC cells via ATGL. Notably, ATGL and its products, DAG and FFA, were shown to be responsible for NEAT1-mediated HCC cell growth. NEAT1 regulated ATGL expression by binding miR-124-3p.Additionally, NEAT1 knockdown attenuated HCC cell growth through miR-124-3p/ATGL/DAG+FFA/PPARa signaling. NEAT1 was demonstrated to function as a competing endogenous RNA (ceRNA) by competitively binding common micro-RNAs. 29764424 2018 Long non-coding RNA NEAT1-modulated abnormal lipolysis via ATGL drives hepatocellular carcinoma proliferation. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, luciferase assay etc. Two human breast cancer cell lines (MCF-7 , SK-BR-3), breast cancer tissues down-regulated NEAT1 expression was significantly up-regulated in breast cancer tissues compared to adjacent normal tissues, and higher NEAT1 was positively associated with lymph node metastasis and TNM stage. Patients with higher NEAT1 had a poor prognosis. In addition, NEAT1 promoted cell invasion and proliferation by negatively regulating miR-218 in breast cancer.MiR-218 is a direct target of NEAT1. Kaplan-Meier analysis and the log-rank test were used to establish the relationship between NEAT1 and overall survival. Recent studies have shown that lncRNAs play a crucial effect in multiple processes in cells by acting as competing endogenous (ceRNAs) to regulate miRNAs. 28946559 2017 NEAT1 negatively regulates miR-218 expression and promotes breast cancer progression. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. HCC tissues, cell lines (HepG2, L02, Huh7) down-regulated the expression of NEAT1 was significantly increased in the HCC tissues and cell lines.Meanwhile, after downregulating NEAT1 expression in HepG2/Huh7 cell lines, the cell viability was significantly lowered, whereas the corresponding rate of apoptosis was significantly increased. Additionally, it was found that the NEAT1 and miR-129-5p expression showed a negative correlation in HCC tissues. In the present study, it was concluded that the expression of NEAT1 was significantly increased in the HCC tissues and cell lines. Meanwhile, after downregulating NEAT1 expression in HepG2/Huh7 cell lines, the cell viability was significantly lowered, whereas the corresponding rate of apoptosis was significantly increased.Additionally,it was found that the NEAT1 and miR-129-5p expression showed a negative correlation in HCC tissues. 28526689 2017 Long non-coding RNA NEAT1 promotes hepatocellular carcinoma cell proliferation through the regulation of miR-129-5p-VCP-IkB. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, RNAi, Western blot, MTT assay etc. breast cancer tissues, cell lines (MDA-MB-231, MDAMB-468, MCF-7, T47D and BT-547) up-regulated lncRNA NEAT1 was highly expressed in BC tissue, and the expression was also closely related to the tumor size and lymph node metastasis. MTT and Wound Healing assays showed that suppression of lncRNA NEAT1 could lead to decreased proliferation and metastasis in BC cell lines. Western blot also showed that B-catenin and N-cad were decreased while E-cad was increased after lncRNA NEAT1 being suppressed. 28338194 2017 lncRNA NEAT1 is closely related with progression of breast cancer via promoting proliferation and EMT. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi etc. hepatocarcinoma tissues, cell lines (SMMC-7721, Huh-7, Hep3B, MMC-7721, Huh-7 and Hep3B) up-regulated over-expression of lncRNA NEAT1 was closely related to liver cirrhosis (P = 0.026), microvascular invasion (MVI) (P = 0.023), and TNM stage.Overexpression of lnc RNA NEAT1 was associated with a decreasing 1-, 3-, 5-years OS rates 28732670 2017 Long non-coding RNA NEAT1 overexpression is associated with unfavorable prognosis in patients with hepatocellular carcinoma after hepatectomy: A Chinese population-based study. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 cholangiocarcinoma NA M810/3 qPCR, Western Blot, RIP, ChIP, etc. The human cholangiocacinoma cell lines (QBC939, RBE, HuCCT1, TFK-1). normal biliary epithelium cell line HIBEpic. CCA tumors, adjacent non-tumor tissue up-regulated These findings indicate that NEAT1 exerts oncogenic effects in CCA. We postulate that NEAT1 is a potentially useful diagnostic and therapeutic target for CCA. CCA is aggressive cancer with a median survival of fewer than 24 months after diagnosis. 29970216 2018 Long Noncoding RNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells. NKILA AK056098 105416157 ENSG00000278709 NR_131157 GRCh38_20:57710183-57712780 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell line (QSG-7701, SMMC-7721, Hep3B, HCCLM3, HepG2), HCC tissues down-regulated NKILA is down-regulated in HCC and reduced expression of NKILA indicts poor survival of HCC patients. Overexpression of NKILA enhances the roles of baicalein on HCC cell proliferation inhibition, apoptosis induction, and migration inhibition in vitro and tumor growth suppression in vivo. Conversely, knockdown of NKILA suppresses the effects of baicalein. Mechanistically, we found that NKILA inhibits IkBa phosphorylation, NF-kB nuclear translocation, and NF-kB activity. NKILA also enhances the inhibitory effects of baicalein on NF-kB signaling. Furthermore, the effects of NKILA on baicalein-induced NF-kB activity inhibition, cell growth inhibition, apoptosis induction, and migration inhibition are reversed by NF-kB nuclear translocation inhibitor JSH-23. 29481769 2018 Long noncoding RNA NKILA enhances the anti-cancer effects of baicalein in hepatocellular carcinoma via the regulation of NF-kB signaling. NKILA AK056098 105416157 ENSG00000278709 NR_131157 GRCh38_20:57710183-57712780 breast cancer C50 NA qPCR, Western blot etc. cell lines (MCF-7 and BT474) up-regulated In this study, we found that TGF-B activates the NF-kB pathway. Inhibition of NF-kB signaling markedly abrogates TGF-B-induced EMT. By studying the regulatory mechanism of TGF-B-induced NF-kB signaling, we found that lncRNA NKILA was upregulated by TGF-B and was essential for the negative feedback regulation of the NF-kB pathway. Accordingly, overexpression of NKILA significantly reduced TGF-B-induced tumor metastasis in vivo. Consistent with the results from mice, the expression of NKILA was negatively correlated with EMT phenotypes in clinical breast cancer samples. Collectively, our study findings indicated that the NKILA-mediated negative feedback affects TGF-B-induced NF-kB activation and that NKILA may be a therapeutic molecule in breast cancer metastasis via inhibition of EMT. 29761481 2018 LncRNA NKILA Suppresses TGF-B-induced Epithelial-Mesenchymal Transition by Blocking NF-kB Signaling in Breast Cancer. NKILA AK056098 105416157 ENSG00000278709 NR_131157 GRCh38_20:57710183-57712780 laryngeal cancer C32 NA qPCR, Western blot, Luciferase reporter assay, RIP etc. laryngeal cancer tissues, cell lines (HEp-2 and TU212) down-regulated We demonstrated a low NKILA expression in laryngeal cancer and its correlation with shorter overall survival in patients with laryngeal cancer. NKILA serves as a tumor suppressor in laryngeal cancer by suppressing laryngeal cancer cell viability and migration, whereas promoting cell apoptosis; NKILA knockdown reverses the cytotoxicity of X-ray radiation on laryngeal cancer cells through combining with NF-kB: IkB complex to inhibit IkB phosphorylation, inhibit p65 nuclear translocation, and finally inhibit NF-kB activation. NF-kB binds to the promoter region of NKILA to activate its transcriptional activity, upregulated NKILA then inhibits IkB phosphorylation and NF-kB activation, thus forming a negative feedback loop to sensitize laryngeal cancer cell to X-ray radiation. 29573243 2018 lncRNA-NKILA/NF-kB feedback loop modulates laryngeal cancer cell proliferation, invasion, and radioresistance. NKILA AK056098 105416157 ENSG00000278709 NR_131157 GRCh38_20:57710183-57712780 tongue squamous cell carcinoma C02 M8070/3 qPCR, Western blot, ISH etc. TSCC tissues, cell lines (CAL27, Tca8113) down-regulated NKILA is down-regulated in TSCC cancer tissues than that in matched adjacent noncancerous tissues. And low NKILA expression in TSCC is significantly correlated with tumor metastasis and poor patient prognosis. In vitro, overexpression of NKILA decreases TSCC cells migration and invasion. Mechanistic study shows that NKILA inhibits the phosphorylation of IkBa and NF-kB activation as well as the induction of the epithelial-mesenchymal transition (EMT) process. 27613832 2016 Long non-coding RNA NKILA inhibits migration and invasion of tongue squamous cell carcinoma cells via suppressing epithelial-mesenchymal transition. NKILA AK056098 105416157 ENSG00000278709 NR_131157 GRCh38_20:57710183-57712780 breast cancer C50 NA qPCR, RNAi, RIP etc. breast cancer tissues down-regulated Importantly, NKILA is essential to prevent over-activation of NF-B pathway in inflammation-stimulated breast epithelial cells. Furthermore, low NKILA expression is associated with breast cancer metastasis and poor patient prognosis. Therefore, lncRNAs can directly interact with functional domains of signaling proteins, serving as a class of NF-B modulators to suppress cancer metastasis. 25759022 2015 A Cytoplasmic NF-B Interacting Long Noncoding RNA Blocks IB Phosphorylation and Suppresses Breast Cancer Metastasis. NKILA AK056098 105416157 ENSG00000278709 NR_131157 GRCh38_20:57710183-57712780 esophageal squamous cell cancer NA NA qPCR, Western blot, in vitro knockdown ESCC cancer tissues, esophageal cancer cell lines (Eca109, Eca9706, KYSE30, KYSE510, KYSE520, KYSE140 and KYSE150) down-regulated NKILA was downregulated in ESCC tissues and cancer cells compared with their normal counterparts.NKILA inhibited proliferation and migration of ESCC cells in vitro, suppressed tumor growth and lung metastasis in vivo. Mechanistically, NKILA could inhibit phosphorylation of IkBa, suppress p65 nuclear translocation and downregulate the expression of NF-kB target genes in ESCC cells. 29348395 2018 NKILA inhibits NF-kB signaling and suppresses tumor metastasis. NNT-AS1 NA 100652772 ENSG00000248092 NR_073113 GRCh38_5:43571594-43603230 breast cancer C50 NA qPCR, Western blot etc. breast cancer tissues, cell lines (MD-MB-231, MD-MB-468, MCF-7 and MCF-10A) up-regulated Loss of function assay was carried out to detect the effects of silenced NNT-AS1 on proliferation, metastasis and EMT process of BC cells. Subcellular fractionation assay demonstrated that NNT-AS1 was located in the cytoplasm of BC cells. we found the combination between NNT-AS1 and miR-142-3p through conducting bioinformatics analysis, RIP and luciferase reporter assays. Similarly, the combination between miR-142-3p and ZEB1 was verified. Finally, the recue assays were carried out to demonstrate the effects of NNT-AS1/miR-142-3p/ZEB1 axis on the biological behaviors of BC cells.All the above findings revealed a fact that NNT-AS1 affects breast cancer progression through modulating miR-142-3p/ZEB1 axis. 29710510 2018 Long non-coding RNA NNT-AS1 affects progression of breast cancer through miR-142-3p/ZEB1 axis. NNT-AS1 NA 100652772 ENSG00000248092 NR_073113 GRCh38_5:43571594-43603230 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay, RIP etc. hepatocarcinoma tissues, Human hepatocarcinoma cell lines up-regulated In present study, our team identified the up-regulated expression of NNT-AS1 in HCC tissue and cell lines compared with adjacent noncancerous tissue and normal cells. Moreover, HCC patients with high NNT-AS1 levels had poor prognosis than that with low NNT-AS1 level.In vitro, gain- and loss-of-function experiments revealed that enhanced NNT-AS1 expression promoted the proliferation ability and alleviated the cycle arrest and apoptosis, while NNT-AS1 knockdown suppressed the proliferation and induced G0/G1 phase arrest and apoptosis.In vivo, NNT-AS1 knockdown inhibited the HCC neoplastic tumor volume and weight. Bioinformatics analysis and luciferase reporter assay validated that miR-363 targeted NNT-AS1 and CDK6 3'-UTR. MiR-363 was down-regulated in HCC tissue and cells. NNT-AS1 competed with CDK6 for miR-363 binding and could increase CDK6 expression. 29179477 2017 Long noncoding RNA NNT-AS1 promotes hepatocellular carcinoma progression and metastasis through miR-363/CDK6 axis NNT-AS1 NA 100652772 ENSG00000248092 NR_073113 GRCh38_5:43571594-43603230 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Cell proliferation assay, Cell migration and invasion assay etc. CRC tissues, cell lines (SW480 and SW620) up-regulated NNT-AS1 was expressed higher in tumor tissues than that in adjacent noncancer tissues, and higher expression of NNT-AS1 was significantly correlated with lymph node metastasis, TNM stage, vessel invasion and differentiation. Knockdown of NNT-AS1 significantly impaired CRC cell proliferation, migration and invasion in vitro and silencing NNT-AS1 also suppressed tumor growth and metastasis in nude mice. The western blot experiments revealed that silencing NNT-AS1 inhibited epithelial-mesenchymal transition (EMT) and inactivated MAPK/Erk signaling pathway in CRC cell lines. 27966450 2017 Upregulated NNT-AS1, a long noncoding RNA, contributes to proliferation and migration of colorectal cancer cells in vitro and in vivo. NNT-AS1 NA 100652772 ENSG00000248092 NR_073113 GRCh38_5:43571594-43603230 gastric cancer C50 NA RT-PCR, Western blot analysis, Luciferase reporter assay, RIP, RNA pull-down assay GC cell lines (SGC-7901, BGC-823, MGC-803 and MKN-45) Normal gastric mucosa cell line GES-1, the tumour tissue and adjacent normal tissues up-regulated NNT-AS1 expression level was significantly up-regulated in GC tissue and cell lines compared with adjacent normal tissue and normal cell lines.NNT-AS1 knockdown suppressed the proliferation and invasion ability and induced the GC cell cycle progression arrest at G0/G1 phase. miR-424 targeted the 3'-UTR of NNT-AS1.the molecular binding within NNT-AS1 and miR-424, therefore jointly forming the RNA-induced silencing complex (RISC). Moreover, E2F1 was verified to act as the target gene of NNT-AS1/miR-424, indicating the NNT-AS1/miR-424/E2F1 axis. 30006956 2018 Long non-coding RNA NNT-AS1 sponges miR-424/E2F1 to promote the tumorigenesis and cell cycle progression of gastric cancer. NONHSAG010125 NA NA NA NA NA clear cell renal cell carcinoma C64.9 M8005/0 microarray, qPCR etc. primary RCCC tissues up-regulated For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data. 26765468 2016 Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma. NONHSAG011264 NA NA NA NA NA head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. HNSC tissues down-regulated We selected top 10 differentially expressed lncRNAs (NONHSAT083749, NONHSAT095654, NONHSAG048989, NONHS AT018263, NONHSAT0-40523, NONHSAT006502, TCONS_l2_00008966, FR302050, NONHSAG-011264, NONHSAT008740) between HPV-positive and HPV-negative group to detect their expression levels by qRT-PCR. The data demonstrated the same trends of up-and down-regulation and the fold changes of qRT-PCR as the microarray data. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. NONHSAG019720 NA NA NA NA NA clear cell renal cell carcinoma C64.9 M8005/0 microarray, qPCR etc. primary RCCC tissues up-regulated For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data. 26765468 2016 Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma. NONHSAG048989 NA NA NA NA NA head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. HNSC tissues up-regulated We selected top 10 differentially expressed lncRNAs (NONHSAT083749, NONHSAT095654, NONHSAG048989, NONHS AT018263, NONHSAT0-40523, NONHSAT006502, TCONS_l2_00008966, FR302050, NONHSAG-011264, NONHSAT008740) between HPV-positive and HPV-negative group to detect their expression levels by qRT-PCR. The data demonstrated the same trends of up-and down-regulation and the fold changes of qRT-PCR as the microarray data. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. NONHSAT006502 NA NA NA NA NA head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. HNSC tissues down-regulated We selected top 10 differentially expressed lncRNAs (NONHSAT083749, NONHSAT095654, NONHSAG048989, NONHS AT018263, NONHSAT0-40523, NONHSAT006502, TCONS_l2_00008966, FR302050, NONHSAG-011264, NONHSAT008740) between HPV-positive and HPV-negative group to detect their expression levels by qRT-PCR. The data demonstrated the same trends of up-and down-regulation and the fold changes of qRT-PCR as the microarray data. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. NONHSAT008740 NA NA NA NA NA head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. HNSC tissues down-regulated We selected top 10 differentially expressed lncRNAs (NONHSAT083749, NONHSAT095654, NONHSAG048989, NONHS AT018263, NONHSAT0-40523, NONHSAT006502, TCONS_l2_00008966, FR302050, NONHSAG-011264, NONHSAT008740) between HPV-positive and HPV-negative group to detect their expression levels by qRT-PCR. The data demonstrated the same trends of up-and down-regulation and the fold changes of qRT-PCR as the microarray data. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. NONHSAT018263 NA NA NA NA NA head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. HNSC tissues up-regulated We selected top 10 differentially expressed lncRNAs (NONHSAT083749, NONHSAT095654, NONHSAG048989, NONHS AT018263, NONHSAT0-40523, NONHSAT006502, TCONS_l2_00008966, FR302050, NONHSAG-011264, NONHSAT008740) between HPV-positive and HPV-negative group to detect their expression levels by qRT-PCR. The data demonstrated the same trends of up-and down-regulation and the fold changes of qRT-PCR as the microarray data. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. NONHSAT024642 NA NA NA NA NA clear cell renal cell carcinoma C64.9 M8005/0 microarray, qPCR etc. primary RCCC tissues up-regulated For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data. 26765468 2016 Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma. NONHSAT040523 NA NA NA NA NA head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. HNSC tissues up-regulated We selected top 10 differentially expressed lncRNAs (NONHSAT083749, NONHSAT095654, NONHSAG048989, NONHS AT018263, NONHSAT0-40523, NONHSAT006502, TCONS_l2_00008966, FR302050, NONHSAG-011264, NONHSAT008740) between HPV-positive and HPV-negative group to detect their expression levels by qRT-PCR. The data demonstrated the same trends of up-and down-regulation and the fold changes of qRT-PCR as the microarray data. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. NONHSAT062994 NA NA NA NA NA colorectal cancer C19.9 NA qPCR, Western blot etc. CRC tissues, cell lines (SW620, LS174T, SW480, DLD-1, RKO, HCT116, and LoVo) down-regulated We here reported that NONHSAT062994 was significantly downregulated in human CRC tissues and cell lines. Moreover, its expression was inversely correlated with tumor size and overall survival (OS) time in CRC patients. In CRC cells, the overexpression and knockdown of NONHSAT062994 inhibited and enhanced CRC cell growth, respectively, in vitro and in vivo. Mechanistically, NONHSAT062994 functioned as a tumor suppressor to inhibit CRC cell growth by inactivating Akt signaling. Notably, the NONHSAT062994 expression status was negatively correlated with the Akt downstream targets c-Myc and Cyclin D1 in clinical CRC samples. 28978149 2017 The long non-coding RNA NONHSAT062994 inhibits colorectal cancer by inactivating Akt signaling. NONHSAT066293 NA NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues up-regulated Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. NONHSAT083749 NA NA NA NA NA head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. HNSC tissues up-regulated We selected top 10 differentially expressed lncRNAs (NONHSAT083749, NONHSAT095654, NONHSAG048989, NONHS AT018263, NONHSAT0-40523, NONHSAT006502, TCONS_l2_00008966, FR302050, NONHSAG-011264, NONHSAT008740) between HPV-positive and HPV-negative group to detect their expression levels by qRT-PCR. The data demonstrated the same trends of up-and down-regulation and the fold changes of qRT-PCR as the microarray data. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. NONHSAT095654 NA NA NA NA NA head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. HNSC tissues up-regulated We selected top 10 differentially expressed lncRNAs (NONHSAT083749, NONHSAT095654, NONHSAG048989, NONHS AT018263, NONHSAT0-40523, NONHSAT006502, TCONS_l2_00008966, FR302050, NONHSAG-011264, NONHSAT008740) between HPV-positive and HPV-negative group to detect their expression levels by qRT-PCR. The data demonstrated the same trends of up-and down-regulation and the fold changes of qRT-PCR as the microarray data. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. NONHSAT104436 NA NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues up-regulated Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. NONHSAT112918 NA NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues up-regulated To better understand the roles of lncRNAs in ESCC, we first checked the expression levels of the 4 lncRNAs (ENST00000480669, NONHSAT104436, NONHSAT126998 and NONHSAT112918). The expression of lncRNAs were quantified via RT-PCR in ESCC tissues and matched noncancerous tissues. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. NONHSAT123350 NA NA NA NA NA clear cell renal cell carcinoma C64.9 M8005/0 microarray, qPCR etc. primary RCCC tissues down-regulated For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data. 26765468 2016 Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma. NONHSAT126998 NA NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues up-regulated To better understand the roles of lncRNAs in ESCC, we first checked the expression levels of the 4 lncRNAs (ENST00000480669, NONHSAT104436, NONHSAT126998 and NONHSAT112918). The expression of lncRNAs were quantified via RT-PCR in ESCC tissues and matched noncancerous tissues. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. NONHSAT142035 NA NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues down-regulated Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. NONHSAT147911 NA NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues up-regulated Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. NORAD NORAD, LINC00657, ASHGA5P032173 647979 ENSG00000260032 NR_027451 GRCh38_20:36045618-36050960 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. cell lines (HepG2, Huh7, Hep3B, Bel-7402, SMMC-7721, HCCM3) down-regulated The expression level of LINC00657 was downregulated in HCC tissues and HCC cell lines.Moreover,we illustrated the role of LINC00657 in suppressing the growth, invasion, migration of HCC in vitro.In addition, we found that LINC00657 can act as a ceRNA for PTEN mRNA through miR-106a-5p.Finally, we confirmed the role of LINC00657 in vivo.These results deepen our understanding of the role of LINC00657 in HCC. 28919047 2017 Long non-coding RNA 657 suppresses hepatocellular carcinoma cell growth by acting as a molecular sponge of miR-106a-5p to regulate PTEN expression NORAD NORAD, LINC00657, ASHGA5P032173 647979 ENSG00000260032 NR_027451 GRCh38_20:36045618-36050960 breast cancer C50 NA qPCR, in vitro knockdown, MTT assay etc. cell lines (MCF-7, MDA-MB-231, HMLE) up-regulated We found that LINC00657 was upregulated in breast cancer cell lines MCF-7 and MDA-MB-231 cells as compared to non-malignant HMLE cells. LINC00657 knockout significantly suppresses tumor cell growth and proliferation, suggesting that it plays an oncogenic role. 26942882 2016 Long non-coding RNAs as prognostic markers in human breast cancer. NORAD NORAD, LINC00657, ASHGA5P032173 647979 ENSG00000260032 NR_027451 GRCh38_20:36045622-36050960 colorectal cancer C19.9 NA qPCR, Western blot, Luciferase reporter assay etc. colorectal cancer tissues, cell lines(HT29, SW620 and HCT116) down-regulated the down-regulation of Linc00675 in both CRC cells and clinical CRC tissues.Expression of Linc00675 was also relatively low in metastatic tumors and advanced tumors.Further studies also showed that overexpression of Linc00675 inhibited the proliferation,invasion and migration of CRC cells.In addition,our data also revealed the negative regulation of miR-942 by Linc00675 and the relatively higher expression of miR-942 in clinical CRC tissues.More importantly, the inhibitory effect of Linc00675 on proliferation, invasion and migration of HCT116 cells was also significantly attenuated in the presence of miR-942 mimic, suggesting that down-regulation of miR-942 represented one of the mechanisms by which Linc00675 inhibited the proliferation and metastasis of CRC. 29524886 2018 Long non-coding RNA Linc00675 suppresses cell proliferation and metastasis in colorectal cancer via acting on miR-942 and Wnt/B-catenin signaling. NORAD NORAD, LINC00657, ASHGA5P032173 647979 ENSG00000260032 NR_027451 GRCh38_20:36045622-36050960 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR, RNAi, Western blot etc. PDAC tissues, cell lines (cell lines PANC1, Capan2, BXPC-3, Mia PaCa2, SW1990) up-regulated The expression of Linc00675 in PDAC tissue samples was shown to be 672 times that in chronic pancreatitis tissue samples by microarray screening. This finding was confirmed in tumor tissues from 90 patients with PDAC compared with adjacent normal tissue samples by quantitative RT-PCR. We found that linc00675 overexpression positively correlated with lymph node metastasis, perineural invasion, and poor survival. 26309360 2015 Linc00675 is a novel marker of short survival and recurrence in patients with pancreatic ductal adenocarcinoma. NORAD NORAD, LINC00657, ASHGA5P032173 647979 ENSG00000260032 NR_027451 GRCh38_20:36045622-36050960 colorectal cancer C19.9 NA qRT-PCR, Western blot, in vitro knockdown, Luciferase reporter assay Human CRC cancer cell lines (SW480 and HCT116) up-regulated NORAD served as a competing endogenous RNA for miR-202-5p.We found that there was an inversely relationship between the expression of NORAD and miR-202-5p in CRC tissues.Moreover, overexpression of miR-202-5p in SW480 and HCT116 cells significantly inhibited cellular proliferation,migration and invasion.Taken together,our study demonstrated NORAD/miR-202-5p axis plays a pivot function on CRC progression. 29471886 2018 LncRNA NORAD contributes to colorectal cancer progression by inhibition of miR-202-5p. NORAD NORAD, LINC00657, ASHGA5P032173 647979 ENSG00000260032 NR_027451 GRCh38_20:36045622-36050960 pancreatic cancer C25 NA qPCR, Western blot etc. cell lines (SW1990, Capan-1, PANC-1, AsPC-1, CFPAC-1, MIAPaCa-2, BxPC-3) up-regulated NORAD is highly expressed in pancreatic cancer tissues and upregulated in hypoxic conditions. NORAD upregulation is correlated with shorter overall survival in pancreatic cancer patients. Furthermore, NORAD overexpression promoted the migration and invasion of pancreatic carcinoma cells, while NORAD depletion inhibited EMT and metastasis in vitro and in vivo. In particular, NORAD may function as a ceRNA to regulate the expression of the small GTP binding protein RhoA through competition for hsa-miR-125a-3p, thereby promoting EMT. 29121972 2017 Long noncoding RNA NORAD, a novel competing endogenous RNA, enhances the hypoxia-induced epithelial-mesenchymal transition to promote metastasis in pancreatic cancer NORAD NORAD, LINC00657, ASHGA5P032173 647979 ENSG00000260032 NR_027451 GRCh38_20:36045622-36050960 esophageal squamous cell cancer NA NA qPCR esophageal squamous cell carcinoma tissues up-regulated The relative expression levels of NORAD were significantly upregulated in tumor tissues (p < 0.001) compared to adjacent normal tissues. In addition, high expression of NORAD was correlated with larger tumor size (p =0.021) and T stage (p = 0.045). Kaplan-Meier analysis indicated that patients with high NORAD expression had poor overall and disease-free survival (p < 0.001). 28482344 2017 NORAD Expression Is Associated with Adverse Prognosis in Esophageal Squamous Cell Carcinoma NR_003573 ANXA2P2, ANX2L2, ANX2P2, LPC2B NA NA NA NA gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues up-regulated The expression levels of AK001091 and AK024171 in gastric cancerous tissues were lower than those in non-cancerous gastric tissues, while the expression levels of AK093735, BC003519 and NR_003573 in gastric cancerous tissues were higher than those in non-cancerous gastric tissues. These results were consistent with those shown in the expression microarray data sets. 27460075 2016 Identification of a five-lncRNA signature for the diagnosis and prognosis of gastric cancer. NR_026817 LOC148696 NA NA NA NA colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues down-regulated The expression of all 18 candidate lncRNAs was evaluated by RT-qPCR, using 80 pairs of CRC and control tissue samples. Among these, eight lncRNAs (MALAT-1, NR_029373, NR_046321, NR_034119, GAS5, BANCR, NR_026817 and PCAT-1) were found significantly dysregulated in CRC tumor tissues compared with controls. 27591862 2016 Identification of long noncoding RNAs as potential novel diagnosis and prognosis biomarkers in colorectal cancer. NR_029373 LEF1-AS1, LEF1NAT 641518 ENSG00000232021 NR_029373 GRCh38_4:108176288-108256836 acute myeloid leukemia NA M9861/3 microarray, qPCR etc. bone marrow down-regulated To confirm the microarray data, we selected 97 dysregulated lncRNAs from the microarray analysis of 22 pediatric AML samples and 20 control samples using qRT-PCR. Our data revealed that the lncRNA expression profile in pediatric AML was significantly different from normal controls. A total of 24 lncRNAs were confirmed to be dysregulated in pediatric AML 26573779 2016 Microarray profiling of bone marrow long non-coding RNA expression in Chinese pediatric acute myeloid leukemia patients. NR_029373 LEF1-AS1, LEF1NAT 641518 ENSG00000232021 NR_029373 GRCh38_4:108167525-108256836 colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues down-regulated The expression of all 18 candidate lncRNAs was evaluated by RT-qPCR, using 80 pairs of CRC and control tissue samples. Among these, eight lncRNAs (MALAT-1, NR_029373, NR_046321, NR_034119, GAS5, BANCR, NR_026817 and PCAT-1) were found significantly dysregulated in CRC tumor tissues compared with controls. 27591862 2016 Identification of long noncoding RNAs as potential novel diagnosis and prognosis biomarkers in colorectal cancer. NR_036468.1 CIDEA, CIDE-A NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues down-regulated Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. NR_046028 ACOT2, CTE-IA, CTE1A, MTE1, PTE2, PTE2A, ZAP128 NA NA NA NA clear cell renal cell carcinoma C64.9 M8005/0 microarray, qPCR etc. primary RCCC tissues down-regulated For the lncRNAs, the results demonstrated that TCONS_12_00012336, NR_046028.1, and NONHSAT123350 were downregulated, and that NONHSAT024642, NONHSAG019720, and NONHSAG010125 were upregulated in RCCC tissues relative to their matched counterparts, and these results were consistent with the microarray data. 26765468 2016 Screening for the Key lncRNA Targets Associated With Metastasis of Renal Clear Cell Carcinoma. NR_046321 GPX2, GI-GPx, GPRP, GPRP-2, GPx-2, GPx-GI, GSHPX-GI, GSHPx-2 NA NA NA NA colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues down-regulated The expression of all 18 candidate lncRNAs was evaluated by RT-qPCR, using 80 pairs of CRC and control tissue samples. Among these, eight lncRNAs (MALAT-1, NR_029373, NR_046321, NR_034119, GAS5, BANCR, NR_026817 and PCAT-1) were found significantly dysregulated in CRC tumor tissues compared with controls. 27591862 2016 Identification of long noncoding RNAs as potential novel diagnosis and prognosis biomarkers in colorectal cancer. NR_073085 PRSS21, ESP-1, ESP1, TEST1, TESTISIN NA ENSG00000007038 NA GRCh38_16:2817180-2826304 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues up-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. OIP5-AS1 OIP5-AS1, cyrano, linc-OIP5 729082 ENSG00000247556 NR_026757 GRCh38_15:41283990-41309737 hepatoblastoma C22.0 M8970/3 qPCR, Western blot, RIP etc. hepatoblastoma tissues, cell lines (HepG2, HuH-6, SMMC-7721, QSG-7701 and L-02) up-regulated OIP5-AS1 was oncogenic in hepatoblastoma for the high expression of it in hepatoblastoma tissues and cells. OIP5-AS1 knockdown was carried out in cancer cells.Unsurprisingly,this action was verified to be able to inhibit cell proliferation, metastasis and EMT progress in hepatoblastoma.We discovered OIP5-AS1 is located in nucleus of cancerous cells.It could target to miR-186a-5p and up-regulate the target gene of miR-186a-5p (ZEB1).Based on all above findings,we came into a conclusion that OIP5-AS1 is a ceRNA in Hepatoblastoma cells through modulating miR-186a-5p/ZEB1. 29475118 2018 Kockdown of OIP5-AS1 expression inhibits proliferation, metastasis and EMT progress in hepatoblastoma cells through up-regulating miR-186a-5p and down-regulating ZEB1. OIP5-AS1 OIP5-AS1, cyrano, linc-OIP5 729082 ENSG00000247556 NR_026757 GRCh38_15:41283990-41309737 lung adenocarcinoma C34 M8140/3 qRT-PCR, Western blot, Luciferase reporter assay, RIP lung adenocarcinoma tissues, human lung adenocarcinoma cell lines (H1975 and HCC827) up-regulated the expression of OIP5-AS1 was definitely high in lung adenocarcinoma tissues and cells, while miR-448 was sluggishly expressed in lung adenocarcinoma. OIP5-AS1 and miR-448 was negatively related to each other, the result was obtained from Pearson correlation analysis. We discovered a fact that OIP5-AS1 could directly sponge miR-448 through using dual luciferase reporter assay, RIP assay and RNA pull-down assay. Cell proliferation, migration and invasion were restrained after we disrupted the expression of OIP5-AS1 in lung adenocarcinoma. We also certified that OIP5-AS1 could sponge and regulate miR-448 to affect cell function in lung adenocarcinoma. MiR-448 could target Bcl-2 and affect the expression of Bcl-2. 29247949 2017 Long non-coding RNA OIP5-AS1 functions as an oncogene in lung adenocarcinoma through targeting miR-448/Bcl-2. OIP5-AS1 OIP5-AS1, cyrano, linc-OIP5 729082 ENSG00000247556 NR_026757 GRCh38_15:41283990-41309737 glioma NA M9380/3 qPCR, Luciferase reporter assay, Western blot, RIP glioma tissues, cell lines (HEK-293T, U87 and U251) up-regulated Over-expression of PIWIL3, piR-30188 and miR-367-3p or knockdown of OIP5-AS1 resulted in inhibition of glioma cells progression.OIP5-AS1 knockdown or miR-367-3p over-expression contributed to a decrease in CEBPA (CCAAT/enhancer binding protein alpha) protein. Furthermore, CEBPA was detected as a target of miR-367-3p and played an oncogenic role in glioma. knockdown of OIP5-AS1 combined with over-expression of PIWIL3 and miR-367-3p resulted in tumor regression and extended survival in vivo. 29464001 2018 PIWIL3/OIP5-AS1/miR-367-3p/CEBPA feedback loop regulates the biological behavior of glioma cells. OIP5-AS1 OIP5-AS1, cyrano, linc-OIP5 729082 ENSG00000247556 NR_026757 GRCh38_15:41283990-41309737 lung cancer C34 NA qPCR, Western blot, RIP, Luciferase reporter assay, etc. lung cancer tissues, cell lines (A54, H520) up-regulated OIP5-AS1 overexpression increased lung cancer cell proliferation in vitro. Further investigation revealed that OIP5-AS1 functions as a competing endogenous RNA of miR-378a-3p. MiR-378a-3p overexpression inhibited cell proliferation and caused proliferation-associated proteins CDK4 and CDK6 to decrease in A549 cells. Patients in the OIP5-AS1low group achieved higher total survival than in the OIP5-AS1high. 29897167 2018 Long non-coding RNA OIP5-AS1 promotes proliferation of lung cancer cells and leads to poor prognosis by targeting miR-378a-3p. OIP5-AS1 OIP5-AS1, cyrano, linc-OIP5 729082 ENSG00000247556 NR_026757 GRCh38_15:41283990-41309737 colorectal cancer C19.9 NA Microarray, qPCR, Western blot etc. colorectal cancer tissues, cell line (LoVo, SW480 and HEK293T) down-regulated LncRNA OIP5-AS1 and DYRK1A were down-regulated in radio-resistant CRC cell lines. OIP5-AS1 suppressed the expression of miR-369-3p, thus up-regulating DYRK1A, the downstream gene of miR-369-3p. OIP5-AS1 and DYRK1A impaired cell clonogenic survival and promoted cell apoptosis after irradiation, improving radiosensitivity of CRC cells. Low expression of OIP5-AS1 and DYRK1A was correlated with a poor survival. 29773344 2018 LncRNA OIP5-AS1 regulates radioresistance by targeting DYRK1A through miR-369-3p in colorectal cancer cells. OR3A4 OR3A4P, OLFRA05, OLFRA06, OR17-13, OR17-16, OR17-24, OR17-25, OR24, OR25, OR3A4, OR3A5P NA NA NA NA breast cancer C50 NA qPCR, Western blot breast cancer tissues, cell lines (MDA-MB-231, MDAMB-468, MCF-7, MCF-10A) up-regulated OR3A4 was over-expressed in human breast cancer tissues and cell lines and associated with clinicopathological characteristics.the silence of OR3A4 suppressed the proliferation of breast cancer cells by influencing cell cycle and apoptosis, and repressed the cell metastasis via EMT.all the functions of OR3A4 in breast cancer were realized in the transcriptional level.OR3A4 played a significant role in BC and might be regarded as a specific biomarker for poor prognosis. 29031201 2017 Long non-coding RNA OR3A4 promotes proliferation and migration in breast cancer. OR3A4 OR3A4P, OLFRA05, OLFRA06, OR17-13, OR17-16, OR17-24, OR17-25, OR24, OR25, OR3A4, OR3A5P NA NA NA NA gastric cancer C16 NA microarray, qPCR, Western blot, RIP, Flow cytometry assay etc. gastric cancer tissues, cell lines (MKN-45, SGC-7901, NCI-N87, SNU-1, SNU-16, AGS, and KATO-III) up-regulated Significant overexpression of OR3A4 was observed in the cancer group compared with healthy controls. The expression levels of lncRNA OR3A4 were significantly associated with lymphatic metastasis, the depth of cancer invasion, and distal metastasis in 130 paired gastric cancer tissues. The effects of OR3A4 were assessed by overexpressing and silencing OR3A4 in gastric cancer cells. OR3A4 promoted cancer cell growth, angiogenesis, metastasis, and tumorigenesis in vitro and in vivo. 26863570 2016 Long noncoding RNA OR3A4 promotes metastasis and tumorigenicity in gastric cancer. OTUB1-isoform2 OTUB1, HSPC263, OTB1, OTU1 NA NA NA NA gastric cancer C16 NA qPCR, Western blot, Cell proliferation assay, Cell invasion assay etc. gastric cancer tissues, cell lines (AGS, MGC-803, MKN45, NCI-N87 and HGC-27) up-regulated The OTUB1-isoform 2 expression levels were higher in the gastric cancer samples than in the paratumorous gland samples. OTUB1-isoform 2 expression levels tightly correlated with tumor size, lymph node metastasis and TNM staging. Higher OTUB1-isoform 2 expression levels led to significantly poorer OS and DFS rates, and a multivariate analysis revealed that OTUB1-isoform 2 was an independent risk factor for DFS. Ectopic overexpression of OTUB1-isoform 2 in gastric cancer cells stimulated proliferation by inducing G1-S transition, suppression of cell apoptosis and promotion of tumor cell invasion and migration. 27019636 2016 Upregulation of the Non-Coding RNA OTUB1-isoform 2 Contributes to Gastric Cancer Cell Proliferation and Invasion and Predicts Poor Gastric Cancer Prognosis. P15INK4B CDKN2B, CDK4I, INK4B, MTS2, P15, TP15, p15INK4b NA NA NA NA ovarian cancer C56.9 NA qPCR, Western blot etc. cell lines (SKOV3, OVCAR3, A2780, Hey, OVCA429, and OVCA433) down-regulated we evaluated ANRIL expression in epithelial ovarian cancer (EOC) and defined its clinical implications and biological functions. ANRIL was overexpressed in EOC tissues relative to normal controls. Overexpression correlated with advanced International Federation of Gynecologists and Obstetricians stage and high histological grade. Multivariate analysis indicated that ANRIL is an independent prognostic factor for overall survival in EOC. Gain- and loss-of-function experiments demonstrated that ANRIL promotes EOC cell proliferation both in vitro and in vivo. The proliferative effect was linked to the promotion of cell cycle progression and inhibition of apoptosis and senescence. Down-regulation of P15INK4B and up-regulation of Bcl-2 by ANRIL may partially explain ANRIL-induced EOC cell proliferation 27095571 2016 The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer PAGBC NA NA NA NA NA gallbladder cancer C23.9 NA qPCR, microarray, Western blot, Luciferase reporter assay, RIP etc. cell lines (GBC-SD, SGC-996, NOZ, EH-GB) down-regulated In this study, we identify a group of differentially expressed lncRNAs in human GBC tissues, including prognosisassociated gallbladder cancer lncRNA (lncRNA-PAGBC), which we find to be an independent prognostic marker in GBC. Functional analysis indicates that lncRNA-PAGBC promotes tumour growth and metastasis of GBC cells. More importantly, as a competitive endogenous RNA (ceRNA), lncRNA-PAGBC competitively binds to the tumour suppressive microRNAs miR-133b and miR-511. This competitive role of lncRNA-PAGBC is required for its ability to promote tumour growth and metastasis and to activate the AKT/mTOR pathway. 28887321 2017 LncRNA-PAGBC acts as a microRNA sponge and promotes gallbladder tumorigenesis pancEts-1 NA NA NA NA NA neuroblastoma NA M9500/3 RNA-seq,qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP etc. cell lines (NB-1643, SK-N-BE(2), NB-1691, IMR32, BE(2)-CSK-N-AS, SH-SY5Y, and SK-N-SH), NB tissues up-regulated LncRNA pancEts-1 promoted the growth, invasion, and metastasis of neuroblastoma cells in vitro and in vivo Mechanistically, pancEts-1 bound to hnRNPK to facilitate its physical interaction with B-catenin, whereas hnRNPK stabilized the B-catenin by inhibiting proteasome-mediated degradation, resulting in transcriptional alteration of target genes associated with neuroblastoma progression. Both pancEts-1 and hnRNPK were upregulated in clinical neuroblastoma tissues, and were associated with unfavorable outcome of patients. 29311158 2018 Long Noncoding RNA pancEts-1 Promotes Neuroblastoma Progression through hnRNPK-Mediated B-Catenin Stabilization. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN57), gastric adenocarcinomas tissues up-regulated PANDA had a significant correlation with gastric cancer-associated genes . 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues down-regulated The lncRNAs HOTAIR, H19 and MALAT1 were up-regulated, while PANDAR and TUG1 were down-regulated in NSCLC cancer tissues compared with the corresponding adjacent normal tissue. 28121347 2017 The use of lncRNA analysis for stratification management of prognostic risk in patients with NSCLC. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 cervical cancer C53 NA qPCR etc. cervical squamous tissues, cell lines (HeLa, C33-A) up-regulated The results of qRT-PCR showed that the expression level of PANDAR was signifcantly up-regulated in cervical cancer tissues compared with that in cancer-adjacent tissues. Statistical analysis showed that PANDAR expression was correlated with International Federation of Gynecology and Obstetrics (FIGO) staging, tumor size and tumor invasion degree. Kaplan-Meier survival analysis showed that the survival time of patients with highly expressed PANDAR was shorter than that of patients with lowly expressed PANDAR. Cox multivariate regression analysis showed that PANDAR could be used as an independent prognostic factor for patients with cervical cancer. CCK-8 results showed that interference in PANDAR signifcantly inhibited tumor cell proliferation. 29131264 2017 Upregulation of LncRNA PANDAR predicts poor prognosis and promotes cell proliferation in cervical cancer PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 gastric cancer C16 NA qPCR etc. gastric cancer tissues up-regulated Our results showed that the expression of PANDAR was significantly increased in gastric cancer tissues compared with paired adjacent normal tissues. Furthermore, high expression of PANDAR was correlated with depth of invasion, TNM stage and lymphatic metastasis. Importantly, high expression of PANDAR could serve as an independent unfavorable prognostic role in gastric cancer. 26898439 2016 Increased expression of LncRNA PANDAR predicts a poor prognosis in gastric cancer. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi etc. HCC tissues, cell lines (HCCLM3, Hep3B, HepG2) up-regulated PANDAR was overexpressed in HCC tissues and cell lines. Moreover, its expression level was significantly correlated with liver cirrhosis, HBsAg, AFP, tumor nodule, vascular invasion and TNM stage. PANDAR overexpression was associated with poorer survival and shorter recurrence and served as an independent prognostic marker of patients with HCC. 26054684 2015 Long non-coding RNA PANDAR correlates with poor prognosis and promotes tumorigenesis in hepatocellular carcinoma. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, Western blot etc. clear cell renal cell carcinoma tissues, cell lines (7860 and Caki-1) up-regulated PANDAR expression was significantly upregulated in tumor tissues and cell lines compared with normal counterparts. Moreover, PANDAR served as an independent predictor of overall survival, and increased PANDAR expression was positively correlated with an advanced TNM stage. 28545465 2017 An increase in long non-coding RNA PANDAR is associated with poor prognosis in clear cell renal cell carcinoma PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 non small cell lung cancer C34 M8046/3 qPCR, Western blot, RIP etc. lung cancer tissues, cell lines (A549, SPC-A1, NCI-H1299, SK-MES-1 etc.) down-regulated In a cohort of 140 NSCLC patients, decreased PANDAR expression was negatively correlated with greater tumor size and advanced TNM stage. Moreover, PANDAR could serve as an independent predictor for overall survival in NSCLC. PANDAR-mediated growth regulation is in part due to the transcriptional modulation of Bcl-2 by interacting with NF-YA, thus affecting NSCLC cell apoptosis. 25719249 2015 Low expression of long noncoding RNA PANDAR predicts a poor prognosis of non-small cell lung cancer and affects cell apoptosis by regulating Bcl-2. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 colorectal cancer C19.9 NA qPCR, RNAi, MTT assay etc. CRC tissues, cell lines (HCT116, HT29, SW480, DLD-1) up-regulated The expression level of PANDAR was higher in CRC tissues and cells compared with adjacent nontumor tissues and normal colonic cell line NCM460. PANDAR expression was significantly correlated with local invasion, lymph node metastasis and TNM stage. Furthermore, PANDAR knockdown significantly inhibited cell proliferation, cycle progression, migration and invasion of CRC in vitro. 28106228 2017 Expression of long non-coding RNA PANDAR and its prognostic value in colorectal cancer patients. PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. CRC tissues, cell lines (SW480, LoVo, HCT-116, SW620, HT29) up-regulated The expression level of PANDAR was higher in CRC tissues and cells. Patients with high PANDAR expression level had poorer overall survival than those with low PANDAR expression. Knockdown of PANDAR could inhibit cell growth, migration and invasion, arrest cell cycle as well as induce apoptosis of CRC cells in vitro study. In addition, PANDAR could affect epithelial-mesenchymal transition through inhibiting N-cadherin, vimentin, B-catenin, Snail and Twist expression and increasing the expression levels of E-cadherin. 27629879 2016 The high expression of long non-coding RNA PANDAR indicates a poor prognosis for colorectal cancer and promotes metastasis by EMT pathway. PART1 NA 25859 ENSG00000152931 NR_024617 GRCh38_5:60487713-60547657 colorectal cancer C19.9 NA qPCR, Western blot, luciferase reporter assay cell line (LoVo, SW620) up-regulated In the present study, we revealed that prostrate androgen-regulated transcript1 (PART-1) was highly expressed in colorectal cancer cells and tissues , and knockdown of PART-1 suppressed cell proliferation and metastasis, both in vitro and in vivo. In addition, PART-1 functioned as a ceRNA of DNMT3A,by sponging miR-143. Finally, PART-1 induced tumor progression by regulating DNMT3A. The Kaplan-Meier log-rank test was used to compare survival curves.Several studies have reported that miR-143 could regulate tumor progression through direct interaction with DNMT3A. As an enzyme modulating DNA methylation, DNMT3A can exert diverse epigenetic regulations. 28619512 2017 PART-1 functions as a competitive endogenous RNA for promoting tumor progression by sponging miR-143 in colorectal cancer. PART1 NA 25859 ENSG00000152931 NR_024617 GRCh38_5:60487713-60547657 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated the expression of PART1 was significantly up-regulated in 73.1% (152/208) stage I-III NSCLC specimens compared with adjacent normal tissues. high tissue PART1 expression indicated poor DFS in stage I-III NSCLC patients. PART1 may prove to be a promising biomarker for prediction of survival and tumor recurrence in stage I-III NSCLC. 28819376 2017 PART1 expression is associated with poor prognosis and tumor recurrence in stage I-III non-small cell lung cancer. PCA3 PCA3, DD3, NCRNA00019, PCAT3 50652 ENSG00000225937 NR_015342 GRCh38_9:76691980-76863307 prostate cancer C61.9 NA qPCR, western blot etc. cell lines differential expression Three proteins were found down-regulated and 7 proteins up -regulated in PC3PCA+ cells compared to PC3NC cells,including GRP78.Higher GRP78 was also found in PCa clinical specimens.This study confirmed that in PCa, PCA3 plays a pro-cancer role through promoting cell proliferation, migration and invasion while inhibiting cell apoptosis. This process might involve the up-regulation of GRP78.GRP78 was also reported to be preferentially expressed in the camptothecin (CPT)- resistant PC3 prostate cancer cell line in comparison to the CPT-sensitive LNCaP prostate cancer cell line, which indicated its involvement in chemotherapy resistant in PCa. 28739722 2017 GRP78 Participates in PCA3-regulated Prostate Cancer Progression. PCA3 PCA3, DD3, NCRNA00019, PCAT3 50652 ENSG00000225937 NR_015342 GRCh38_9:76691980-76863307 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. PCAN-1 XLOC_002996, lnc-AC069257.9.1-5 NA NA NA NA breast cancer C50 NA qPCR, RNAi etc. breast cancer tissues, cell line (MCF-7) up-regulated The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines. 27322459 2016 Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis. PCAN-4 NA NA NA NA NA breast cancer C50 NA qPCR, RNAi etc. breast cancer tissues, cell line (MCF-7) down-regulated The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines. 27322459 2016 Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis. PCAN-6 NA NA NA NA NA breast cancer C50 NA qPCR, RNAi etc. breast cancer tissues, cell line (MCF-7) up-regulated The qPCR results in pooled breast tumor samples (n = 5), pooled normal breast samples (n = 5) and MCF-7 cell lines. In all cases, the expression levels show statistically significant differential expression in the same directions as the RNA-Seq data, both between primary tumor and normal sample pools and between normal and MCF-7 cancer cell lines. 27322459 2016 Pan-Cancer Analyses Reveal Long Intergenic Non-Coding RNAs Relevant to Tumor Diagnosis, Subtyping and Prognosis. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 osteosarcoma NA M9180/3 qRT-PCR, Western blot, in vitro knockdown osteosarcoma tissues, osteosarcoma cell lines (LM7, KHOS, MG-63 and U2OS) up-regulated PCAT1 was upregulated in osteosarcoma tissues when compared to normal bone tissues. PCAT1 was also upregulated in osteosarcoma cell lines when compared to normal bone cell line. The upregulation of PCAT1 was significantly associated with advanced clinical stage, tumor metastasis and shorter overall survival in patients with osteosarcoma. 29430187 2018 The lncRNA PCAT1 is correlated with poor prognosis and promotes cell proliferation, invasion, migration and EMT in osteosarcoma. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 cervical cancer C53 NA qPCR, in vitro knockdown etc. cell lines (HeLa and C-33A), cervical cancer tissue down-regulated Decreased expression of lncRNA PCAT-1 could reduce the invasion ability. The up-regulation of lncRNA PCAT-1 was associated with poor prognosis of patients with cervical cancer. LncRNA PCAT-1 siRNA transfected into cervical cancer cell lines can effectively lower the expression of lncRNA PCAT-1, while lncRNA PCAT-1 expression can inhibit the proliferation, metastasis and invasion abilities of cervical cancer cells. 29687842 2018 LncRNA PCAT-1 regulates the proliferation, metastasis and invasion of cervical cancer cells. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 osteosarcoma NA M9180/3 qPCR, Western blot, in vitro knockdown, RIP OS tumor tissues, human OS cell lines (Saos-2, U2OS, MG-63 and 143B) up-regulated PCAT-1 expression was also upregulated in OS tissues,PCAT-1 could interact with EZH2, thereby repressing p21 expression. Additionally, rescue experiments indicated that PCAT-1 functioned as an oncogene partly via suppressing p21 in OS cells. 29291409 2017 Long noncoding RNA PCAT-1 acts as an oncogene in osteosarcoma by reducing p21 levels. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 gastric cancer C16 NA qPCR All cell lines (AGS, Mgastric cancer-803, Bgastric cancer-823, GES-1, MKN-45) up-regulated Our data suggested that PCAT-1 could play an oncogenic role in gastric cancer progression. Silencing PCAT-1 is a potential novel therapeutic approach for gastric cancer.Over-expression of PCAT-1 was correlated with poor overall survival in gastric cancer patients 28571676 2017 Long non-coding RNA PCAT-1 over-expression promotes proliferation and metastasis in gastric cancer cells through regulating CDKN1A. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues up-regulated The expression of all 18 candidate lncRNAs was evaluated by RT-qPCR, using 80 pairs of CRC and control tissue samples. Among these, eight lncRNAs (MALAT-1, NR_029373, NR_046321, NR_034119, GAS5, BANCR, NR_026817 and PCAT-1) were found significantly dysregulated in CRC tumor tissues compared with controls. 27591862 2016 Identification of long noncoding RNAs as potential novel diagnosis and prognosis biomarkers in colorectal cancer. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Our results showed that PCAT-1 expression in CRC tissues was significantly upregulated compared with the matched normal tissues and the overexpression of PCAT-1 was found in 64 % (62/81) of CRC. In addition, there was a significant association between PCAT-1 expression and distant metastasis. More important, CRC patients with PCAT-1 higher expression have shown significantly poorer overall survival than those with lower PCAT-1 expression. In conclusion, our results suggest that high expression of PCAT-1 is involved in CRC progression and could be a novel biomarker of poor prognosis in patient with colorectal cancer. 23640607 2013 Overexpression of long noncoding RNA PCAT-1 is a novel biomarker of poor prognosis in patients with colorectal cancer. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 gastric cancer C16 NA qPCR etc. GC tissues, cell lines (AGS, BGC-823, MKN-45, HGC-27, GES-1) up-regulated PCAT-1 is up-regulated in GC samples and cell lines.PCAT-1 expression was elevated in GC tissues and cell lines, and PCAT-1 levels were highly positively correlated with invasion depth (p < 0.001), TNM stages (p < 0.001) and lymphatic metastasis (p = 0.003).PCAT-1 may have potential roles as a biomarker and/or a therapeutic target in gastric cancer.The association between PCAT-1 expression and clinicopathological factors,as well as survival rates, was analyzed. 28742205 2017 Up-regulation of long non-coding RNA PCAT-1 correlates with tumor progression and poor prognosis in gastric cancer. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated Our data showed that PCAT-1 expression in HCC tissues was significantly increased compared with adjacent non-tumor tissues. Up-regulated expression of PCAT-1 was significantly associated with TNM stage and metastasis, but not other clinical parameters. 26097602 2015 Prognostic significance of long non-coding RNA PCAT-1 expression in human hepatocellular carcinoma. PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. PCAT-14 PCAT14 101978785 ENSG00000280623 NR_109832 GRCh38_22:23536881-23547797 prostate cancer C61.9 NA RNA-seq, qPCR, RNAi, ISH etc. prostate cancer tissues, cell lines (VCaP, LNCa) up-regulated An RNA in-situ hybridization (ISH) assay for PCAT14 distinguished benign vs malignant cases, as well as high vs low Gleason disease. PCAT14 is transcriptionally regulated by AR, and endogenous PCAT14 overexpression suppresses cell invasion. Thus, Using RNA-sequencing data we identify PCAT14, a novel prostate cancer and lineage-specific lncRNA. PCAT14 is highly expressed in low grade disease and loss of PCAT14 predicts for disease aggressiveness and recurrence. 27566105 2016 Identification and Validation of PCAT14 as Prognostic Biomarker in Prostate Cancer. PCAT-14 PCAT14 101978785 ENSG00000280623 NR_109832 GRCh38_22:23536881-23547797 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. hepatocellular carcinoma tissues, cell lines (Huh7, HCCLM3, HepG2, SMMC7721, PLC5, and QGY7701) up-regulated the lncRNA PCAT-14 is overexpressed in patients with hepatocellular carcinoma (HCC), and is associated with a poor prognosis after surgery. In addition, PCAT-14 inhibits miR-372 expression by inducing methylation of the miR-372 promoter. 28415780 2017 Long noncoding RNA PCAT-14 induces proliferation and invasion by hepatocellular carcinoma cells by inducing methylation of miR-372 PCAT29 PCAT29 104472713 ENSG00000259641 NR_126437 GRCh38_15:69592200-69695750 prostate cancer C61.9 NA qPCR, Western blot etc. cell lines (VCap, PC3M-luc, LNCaP etc.) down-regulated This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAIC and PCAT30, that are prognostic for a wide variety of cancer types.This study reveals a novel tumor suppressive locus encoding two hormone-regulated lncRNAs, DRAICand PCAT29, that are prognostic for a wide variety of cancer types. 25700553 2015 The lncRNA DRAIC/PCAT29 locus constitutes a tumor suppressive nexus. PCAT29 PCAT29 104472713 ENSG00000259641 NR_126437 GRCh38_15:69592200-69695750 prostate cancer C61.9 NA microarray, qPCR etc. cell lines (Glutamax(Invitrogen), LNCaP, DU145 etc.) down-regulated PCAT29 is suppressed by DHT and upregulated upon castration therapy in a prostate cancer xenograft model. PCAT29 knockdown significantly increased proliferation and migration of prostate cancer cells, whereas PCAT29 overexpression conferred the opposite effect and suppressed growth and metastases of prostate tumors in chick chorioallantoic membrane assays. Finally, in prostate cancer patient specimens, low PCAT29 expression correlated with poor prognostic outcomes. PCAT29 as an androgen-regulated tumor suppressor in prostate cancer. 25030374 2014 The lncRNA PCAT29 inhibits oncogenic phenotypes in prostate cancer. PCAT6 PCAT6, KDM5B-AS1, KDM5BAS1, PCAN-R1, ncRNA-a2, onco-lncRNA-96 100506696 ENSG00000228288 NR_046325 GRCh38_1:202810954-202812156 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated To identify lncRNAs that are critical to lung carcinogenesis, we selected three lncRNAs, CAR intergenic 10 (hereafter, CAR10), AK311218, and RP11-480I12.3, from the most up-regulated lncRNAs in the HPR NSCLCs (Table S3) and tested their expression by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The expression of these lncRNAs was consistent with the microarray analysis. 27322209 2016 Long non-coding RNA stabilizes the Y-box-binding protein 1 and regulates the epidermal growth factor receptor to promote lung carcinogenesis. PCAT6 PCAT6, KDM5B-AS1, KDM5BAS1, PCAN-R1, ncRNA-a2, onco-lncRNA-96 100506696 ENSG00000228288 NR_046325 GRCh38_1:202810954-202812156 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Both lncRNA showed positive correlation between gene expression and SCNA. The criteria of increasing expression from normal to primary to metastatic prostate cancer aimed to uncover lncRNA that may be important therapeutic targets for both primary and metastatic cancers. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. PCAT6 PCAT6, KDM5B-AS1, KDM5BAS1, PCAN-R1, ncRNA-a2, onco-lncRNA-96 100506696 ENSG00000228288 NR_046325 GRCh38_1:202810954-202812156 lung cancer C34 NA qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. lung cancer tissues, cell lines (H292, PC-9, CL1-5, H460, H1650, A549, H446, and H1975) up-regulated PCAT6 expression was significantly elevated in lung cancer cells compared to normal human bronchial epithelial (NHBE) cells, especially in CL1-5 and H446 cells. PCAT6 knockdown significantly inhibited cellular proliferation and metastasis, as well as induced early apoptosis of lung cancer cells. Molecular analysis revealed that PCAT6 regulated the expression of two pivotal cancer-related proteins, c-Myc and p53, in lung cancer cells. However, PCAT6 was not directly combined with c-Myc and p53 as confirmed by RNA immunoprecipitation. Finally, a retrospective study further revealed that PCAT6 negatively correlates with overall survival of lung cancer patients. 27458097 2016 Knockdown of Long Noncoding RNA PCAT6 Inhibits Proliferation and Invasion in Lung Cancer Cells. PCAT7 PCAT7, PCAN-R2 101928099 ENSG00000231806 NR_121566 GRCh38_9:94555054-94603990 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Both lncRNA showed positive correlation between gene expression and SCNA. The criteria of increasing expression from normal to primary to metastatic prostate cancer aimed to uncover lncRNA that may be important therapeutic targets for both primary and metastatic cancers. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. PCAT7 PCAT7, PCAN-R2 101928099 ENSG00000231806 NR_121566 GRCh38_9:94555054-94603990 nasopharyngeal cancer C11 NA qPCR, Western blot, Luciferase reporter assay Nasopharyngeal Carcinoma cell lines (SUNE-1, CNE-1, HNE-1, CNE2, C666-1, HONE-1) up-regulated Relative expression of PCAT7 expression in NPC cell lines and normal oral epidermal cell. Here, we discovered the novel LncRNA, prostate cancer associated transcript 7 (PCAT7), which was overexpressed and associated with worse prognosis in NPC. Decreased PCAT7 expression was found to significantly suppress tumor cell proliferation in vitro, and inhibited tumor growth and reduced the expression of proliferation antigen Ki67 in vivo. Rescue assay was performed to further confirm that PCAT7 contributed to the progression of NPC through regulating miR-134-5p/ELF2 signal pathway. .The Kaplan-Meier survival analysis indicated that PCAT7 high expression (red line, n=38) has a worse overall survival compared to the low expression subgroup (grey line, n=12)hese results indicated that PCAT7 might contribute to the tumor progression in NPC by functioning as a ceRNA to sponge miR-134-5p. 28728844 2017 Long non-coding RNA PCAT7 regulates ELF2 signaling through inhibition of miR-134-5p in nasopharyngeal carcinoma. PCAT7 PCAT7, PCAN-R2 101928099 ENSG00000231806 NR_121566 GRCh38_9:94555054-94603990 nasopharyngeal cancer C11 NA qPCR, Western blot, Luciferase reporter assay, RNAi etc. Nasopharyngeal Carcinoma cell lines (SUNE-1, CNE-1, HNE-1, CNE2, C666-1, HONE-1), Nasopharyngeal Carcinoma tissues up-regulated Relative expression of PCAT7 expression in NPC cell lines and normal oral epidermal cell. Here, we discovered the novel LncRNA, prostate cancer associated transcript 7 (PCAT7), which was overexpressed and associated with worse prognosis in NPC. Decreased PCAT7 expression was found to significantly suppress tumor cell proliferation in vitro, and inhibited tumor growth and reduced the expression of proliferation antigen Ki67 in vivo. Rescue assay was performed to further confirm that PCAT7 contributed to the progression of NPC through regulating miR-134-5p/ELF2 signal pathway. .The Kaplan-Meier survival analysis indicated that PCAT7 high expression (red line, n=38) has a worse overall survival compared to the low expression subgroup (grey line, n=12)hese results indicated that PCAT7 might contribute to the tumor progression in NPC by functioning as a ceRNA to sponge miR-134-5p. 28728844 2017 Long non-coding RNA PCAT7 regulates ELF2 signaling through inhibition of miR-134-5p in nasopharyngeal carcinoma. PCGEM1 PCGEM1, LINC00071, NCRNA00071, PCAT9 64002 ENSG00000227418 NR_002769 GRCh38_2:192749845-192776899 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. PDIA3P NA NA NA NA NA oral squamous cell carcinoma C06.9 M8070/3 qPCR, Luciferase reporter assay, RNAi oral squamous cell carcinoma tissues, cell lines (SCC4, SCC9, SCC1, SCC25, TU183, HSU3,FADU, OEC-M1, SNU1041,SCC15 and the NHOK) up-regulated PDIA3P was overexpressed in oral squamous cell carcinoma (OSCC) and decreased the survival rate of OSCC patients.silencing PDIA3P by small interfering RNA (siRNA) inhibited OSCC cell proliferation and repressed tumor growth and reduced the expression of proliferation antigen Ki-67 in-vivo. PDIA3P negatively regulated miR-185-5p in OSCC cells.silencing PDIA3P by siRNA suppressed proliferation via miR-185-5p in OSCC cells.silencing PDIA3P by siRNA inhibited CCND2 protein (no influence on mRNA levels) expression via miR-185-5p in OSCC cells, and CCND2 facilitated cell proliferation of SCC4 and SCC15 cells induced by sh-PDIA3P#1. 29246288 2017 The lncRNA PDIA3P Interacts with miR-185-5p to Modulate Oral Squamous Cell Carcinoma Progression by Targeting Cyclin D2. PEG10 PEG10, EDR, HB-1, MEF3L, Mar2, Mart2, RGAG3, RTL2, SIRH1 NA ENSG00000242265 NA GRCh38_7:94656325-94669695 hypopharyngeal squamous cell carcinoma C13 M8070/3 qPCR tumor tissue and para-carcinoma tissue, HSCC FaDu cell line. up-regulated In the in vitro experimental studies, enhanced expression of lncRNA PEG10 was significantly associated with increased proliferation, invasion and metastasis of FaDu cells. lncRNA PEG10 was upregulated in HSCC, and its overexpression in HSCC cells promoted an increase in the tumorigenic activities of proliferation, invasion and migration.A total of >75% of patients with HSCC have an advanced stage of the disease at the time of diagnosis (2), and the prognosis of these patients is poor with a 5-year overall survival rate of 30–35% (3–5). 28928830 2017 Overexpression of long noncoding RNA PEG10 promotes proliferation, invasion and metastasis of hypopharyngeal squamous cell carcinoma. PFKFB2 NA NA ENSG00000123836 NA GRCh38_1:207034366-207081024 glioblastoma NA M9440/3 qPCR etc. cell line (U251 and U87MG) differential expression lncRNA UCA1/miR-182 axis has been regarded as a nodal driver of glioma invasion mediated by GB-associated stromal cells (GASCs) and GASC-secreted chemokine CXCL14.In clinical specimens, CXCL14 upregulation in GASCs also correlated with poor prognosis. Notably, CXCL14-high GASCs mediated lncRNA UCA1 upregulation and miR-182 downregulation in glioma cells. Moreover, miR-182 directly bound to the fructose-2,6-biphosphatase PFKFB2.UCA1/miR-182 axis thereby modulated GASC-induced glycolysis in glioma cells. Overall, UCA1/miR-182/PFKFB2 axis modulates chemokine CXCL14 secretion, glycolysis and invasion of glioma cells in GASCs. 29655792 2018 Long non-coding RNA UCA1/miR-182/PFKFB2 axis modulates glioblastoma-associated stromal cells-mediated glycolysis and invasion of glioma cells. PlncRNA-1 CBR3-AS1, PlncRNA-1, PlncRNA1 100506428 ENSG00000236830 NR_038892 GRCh38_21:36131767-36175815 osteosarcoma NA M9180/3 qPCR, Western blot etc. osteosarcoma tissue, cell lines (Saos-2, MG-63, U-2 OS and HOS) up-regulated In our results, we found lncRNA CBR3-AS1 was highly-expressed in osteosarcoma tissues and cell lines, and associated with Enneking stage, distant metastasis and histological grade. Survival analysis indicated that the high-expression of lncRNA CBR3-AS1 was an independent poor prognostic factor for osteosarcoma patients. Loss-of-function studies showed knockdown of lncRNA CBR3-AS1 suppressed osteosarcoma cells proliferation, migration and invasion, and promotes cells apoptosis, but had no effect on cell-cycle distribution. There was no association between lncRNA CBR3-AS1 and CBR3 expression in osteosarcoma tissues, and knockdown of lncRNA CBR3-AS1 had no effect on CBR3 mRNA and protein expression osteosarcoma cells. 29554595 2018 LncRNA CBR3-AS1 predicts unfavorable prognosis and promotes tumorigenesis in osteosarcoma. PlncRNA-1 CBR3-AS1, PlncRNA-1, PlncRNA1 100506428 ENSG00000236830 NR_038892 GRCh38_21:36131767-36175815 colorectal cancer C19.9 NA Western blot etc. cell lines (SW480, SW620, HCT116, and HT29) up-regulated up-regulated PlncRNA-1 in CRC tissues and cells promoted cell proliferation by accelerating cell cycle process and inhibiting cell apoptosis in vitro, enhanced tumor growth and matastasis in vivo and was associated with cell migration and invasion, EMT process of CRC cells. In addition, PlncRNA-1 was a target of miR-204 and enhanced the expression of an endogenous miR-204 target, MMP9 in CRC cells.Furthermore, we found that PlncRNA-1 activates Wnt/B-catenin pathway through the miR-204 in CRC cells.the PlncRNA-1/miR-204/ Wnt/B-catenin regulatory network may shed light on tumorigenesis in CRC. PlncRNA-1 may act as a ceRNA to regulate the expression level of MMP9 in a miR-204 dependent manner. 29738066 2018 Long non-coding RNA PlncRNA-1 promotes cell proliferation and hepatic metastasis in colorectal cancer. PlncRNA-1 CBR3-AS1, PlncRNA-1, PlncRNA1 100506428 ENSG00000236830 NR_038892 GRCh38_21:36131767-36175815 glioma NA M9380/3 qPCR, Western blot etc. glioma tissues, cell lines (U87, U251, SHG139, SHG44, A172) up-regulated we firstly identified that PlncRNA-1 expression levels were prominently augmented in glioma patient tissues and glioma cell lines compared with adjacent noncancerous tissue and normal cells, respectively. Moreover, Kaplan-Meier survival analysis indicated that glioma patients with high PlncRNA-1 expression had shorter overall survival (OS) and progression-free survival (PFS) than those with low PlncRNA-1 expression. Furthermore, loss-of-function assay showed that PlncRNA-1 knockdown dramatically reduced cell proliferation, colony formation, and promoted apoptosis of glioma cell lines. In addition, overexpression of PlncRNA-1 promoted cell proliferation, stimulated cell colony formation, and inhibited cell apoptosis in NHA cells. Mechanically, our results showed that PlncRNA-1 significantly promoted activation of the Notch signal pathway through regulation of Notch-1, Jag-1, and Hes-1 expression. 29653367 2018 Upregulation of lncRNA PlncRNA-1 indicates the poor prognosis and promotes glioma progression by activation of Notch signal pathway. PlncRNA-1 CBR3-AS1, PlncRNA-1, PlncRNA1 100506428 ENSG00000236830 NR_038892 GRCh38_21:36131767-36175815 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. HCC tissues, cell lines (HCCLM3, Huh7, SK-Hep1, HepG2) up-regulated The results showed that the level of PlncRNA-1 expression was significantly increased in HCC tissues and significantly correlated with tumor size, vascular invasion and advanced TNM stage. Moreover, patients with high levels of PlncRNA-1 expression had relatively poor prognostic outcomes, serving as an independent prognostic factor for HCC. In vitro functional assays indicated that knockdown of PlncRNA-1 expression significantly reduced cell proliferation, migration and invasion by inhibiting the epithelial-mesenchymal transition (EMT) signaling. Animal model experiments confirmed the ability of PlncRNA-1 to promote tumor growth in vivo. 26906068 2016 Upregulation of Long Non-Coding RNA PlncRNA-1 Promotes Metastasis and Induces Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma. PlncRNA-1 CBR3-AS1, PlncRNA-1, PlncRNA1 100506428 ENSG00000236830 NR_038892 GRCh38_21:36131767-36175815 colorectal cancer C19.9 NA qPCR, Western blot, in vitro knockdown etc. CRC tissues, cell lines (SW480, DLD-1, HCT116, SW620, HcoEpiC) up-regulated High PlncRNA-1 expression was associated with depth of invasion, lymph node metastasis, and TNM stage of CRC patients. Kaplan-Meier curve analysis showed that patients with high PlncRNA-1 expression had a poor overall survival.PlncRNA-1 exerted its effects by targeting the PI3K/Akt signaling pathway in CRC. 28835319 2017 Long Noncoding RNA PlncRNA-1 Promotes Colorectal Cancer Cell Progression by Regulating the PI3K/Akt Signaling Pathway. POLR2E NA NA ENSG00000099817 NA GRCh38_19:1086579-1095380 papillary thyroid cancer NA M8260/3 qPCR etc. papillary thyroid carcinoma tissues differential expression The meta-analysis further revealed that POLR2E rs3787016T allele was associated with an increased cancer risk in Chinese population. Collectively, the POLR2E rs3787016 may be used as a genetic biomarker to predict cancer risk in Chinese population. 29724531 2018 Long non-coding RNA POLR2E rs3787016 is associated with the risk of papillary thyroid carcinoma in Chinese population. PRCAT17.3 NA NA NA NA NA prostate cancer C61.9 NA qPCR etc. prostate cancer tissues, cell line (PC3) up-regulated Our data revealed that the expression levels of PRCAT17.3 (P<0.0001) and PRCAT38 (P<0.0002) were significantly upregulated in human prostate cancer tissues, compared to BPH ones. Moreover, the altered expression was much higher for PRCAT17.3 (～2000 folds) than PRCAT38 (～50 folds). Moreover, real-time RT-PCR analyses on urine samples of prostate cancer patients revealed that prcat17.3 level is significantly elevated, (P<0.0197; AUC-ROC value of 0.72), compared to that of BPH patients. 29671889 2018 Two long non-coding RNAs, Prcat17.3 and Prcat38, could efficiently discriminate benign prostate hyperplasia from prostate cancer. PRCAT38 NA NA NA NA NA prostate cancer C61.9 NA qPCR etc. prostate cancer tissues, cell line (PC4) up-regulated Our data revealed that the expression levels of PRCAT17.3 (P<0.0001) and PRCAT38 (P<0.0002) were significantly upregulated in human prostate cancer tissues, compared to BPH ones. Moreover, the altered expression was much higher for PRCAT17.3 (～2000 folds) than PRCAT38 (～50 folds). 29671889 2018 Two long non-coding RNAs, Prcat17.3 and Prcat39, could efficiently discriminate benign prostate hyperplasia from prostate cancer. PRINS PRINS, NCRNA00074 100169750 NA NA NA adrenocortical carcinoma NA M8370/3 microarray, qPCR etc. ACC tissues down-regulated MALAT1, DLX6-AS1 and LOC100131320 were found in the microarray to be overexpressed in ACC. This was confirmed by qRT-PCR in the validation cohort, with these lncRNAs also overexpressed. CREM and PRINS expression was down-regulated in ACC by microarray and also by qRT-PCR. 25595289 2015 Long noncoding RNA profiles of adrenocortical cancer can be used to predict recurrence. PRINS PRINS, NCRNA00074 100169750 NA NA NA prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) down-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. PROM1 PROM1, AC133, CD133, CORD12, MCDR2, MSTP061, PROML1, RP41, STGD4 NA ENSG00000007062 NA GRCh38_4:15963076-16084378 head and neck squamous cell carcinoma C76.0 M8070/3 microarray, qPCR etc. blood differential expression To investigate the role of lncRNAs in HPV16 promoting MDSCs aggregation in HNSCC, we examined 4 lncRNAs (HOTAIR, PROM1, CCAT1 and MUC19) expression in 47 HPV-positive blood samples using qRT-PCR. It turns out that the expression of HOTAIR, PROM1, CCAT1, and MUC19 was negatively associated with the number of MDSCs in HPV-positive HNSCC. 28159935 2017 LncRNAs as an intermediate in HPV16 promoting myeloid-derived suppressor cell recruitment of head and neck squamous cell carcinoma. PTAF NA NA NA NA NA ovarian cancer C56.9 NA qPCR, Western blot, etc. ovarian cancer tissues, cell lines (SKOV3, A2780, OVCAR-3) up-regulated we provided evidence that the lncRNA PTAF-miR-25-SNAI2 axis controlled EMT in OvCa. Our results revealed that up-regulated PTAF induced elevated SNAI2 expression by competitively binding to miR-25, which in turn promoted OvCa cell EMT and invasion.The mesenchymal OvCa patients in the TCGA dataset with high PTAF expression showed a poorer prognosis than those with low PTAF expression. we found that miR-25 not only had binding sites within SNAI2, a key TF regulating EMT, and PTAF but also had an inverse expression relationship with both SNAI2 and PTAF. 29929545 2018 Systematic analyses reveal long non-coding RNA (PTAF)-mediated promotion of EMT and invasion-metastasis in serous ovarian cancer. PTENP1 PTENP1, PTEN-rs, PTEN2, PTENpg1, PTH2, psiPTEN 11191 ENSG00000237984 NA GRCh38_9:33673504-33677499 hepatocellular carcinoma C22.0 M8170/3 Western blots, qPCR, Luciferase reporter assay, RIP etc. HCC tissue, cell lines (Sk-Hep-1, SMMC-7721) up-regulated PTENP1 level in the HCC tissues was significantly lower compared with those in the adjacent normal tissues. And PTENP1 was able to repress cell invasion, metastasis, and proliferation capacity in HCC cell lines. The overexpression of PTENP1 inhibited HCC growth both in vitro and in vivo. There were a binding sequence and direct interaction between PTENP1 and miR-193a-3p. PTENP1 as an endogenous sponge interacted with miR-193a-3p, leading to regulate the downstream PTEN/Akt pathway. 29296207 2017 Long non-coding RNA PTENP1 interacts with miR-193a-3p to suppress cell migration and invasion through the PTEN pathway in hepatocellular carcinoma PTENP1 PTENP1, PTEN-rs, PTEN2, PTENpg1, PTH2, psiPTEN 11191 ENSG00000237984 NA GRCh38_9:33673504-33677499 breast cancer C50 NA qPCR breast cancer tissues, cell line (MCF10A, MCF-7 and MDA-MB231) down-regulated The expression of PTENP1 was significantly downregulated in both BC tissues and cell lines.Overexpressed PTENP1 could significantly increase the abilities of cell survival,colony forming, migration and invasion but decrease apoptosis in BC cell lines.PTENP1 performed a negative role in the development of BC via downregulating miR-19 through PTEN-PI3K/Akt pathway. 29212574 2017 Over-expression of long non-coding RNA PTENP1 inhibits cell proliferation and migration via suppression of miR-19b in breast cancer cells. PTTG3P PTTG3，rcPTTG1 26255 ENSG00000213005 NR_002734 GRCh38_8:66767400-66768005 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. hepatocellular carcinoma tissues, cell lines (HepG2 and Hep3B) We found that PTTG3P was frequently up-regulated in HCC and its level was positively correlated to tumor size, TNM stage and poor survival of patients with HCC. 29803224 2018 The long non-coding RNA PTTG3P promotes cell growth and metastasis via up-regulating PTTG1 and activating PI3K/AKT signaling in hepatocellular carcinoma PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. cell lines (HepG2, LM3, SMMC-7721) up-regulated We found that human lncRNA-hPVT1 was up-regulated in HCC tissues and that patients with higher lncRNA-hPVT1 expression had a poor clinical prognosis. The protumorigenic effects of lncRNA-hPVT1 on cell proliferation, cell cycling, and stem cell-like properties of HCC cells were confirmed both in vitro and in vivo by gain-of-function and loss-of-function experiments. Moreover, mRNA expression profile data showed that lncRNA-hPVT1 up-regulated a series of cell cycle genes in SMMC-7721 cells. Regulation of the lncRNA-hPVT1/NOP2 pathway may have beneficial effects in the treatment of HCC. 25043274 2014 Oncofetal long noncoding RNA PVT1 promotes proliferation and stem cell-like property of hepatocellular carcinoma cells by stabilizing NOP2. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 breast Cancer C50 NA qPCR breast cancer tissue down-regulated significant inverse correlations were found between CCAT2 expression and stage, as well as lymph node involvement. Besides, a significant inverse correlation was found between the relative MYC expression in tumor tissues compared with their corresponding ANCTs and disease stage.CCAT2 expression level was suggested as a predictor of metastasis and poor survival for a particular subgroup of breast cancer patients. 28480695 2017 Expression Study and Clinical Correlations of MYC and CCAT2 in Breast Cancer Patients PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 uveal melanoma C69.9 M8720/3 other OS tissues up-regulated high PVT1 expression group had a higher proportion of epithelioid cell dominant disease (a more malignant histological subtype than spindle cell dominant disease) and more cases of extrascleral extension (a risk factor for metastasis), PVT1 expression was strongly and negatively correlated with its methylation status.high PVT1 expression was an independent predictor of poor OS in patients with uveal melanoma.PVT1 expression is modulated by both DNA amplification and methylation and its expression might serve as a valuable and specific prognostic biomarker in terms of OS in uveal melanoma. 29244840 2017 High expression of lncRNA PVT1 independently predicts poor overall survival in patients with primary uveal melanoma. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 B-cell lymphoma NA M9591/3 qPCR, FISH, ISH etc. bone marrow, lymph node, pleural effusion differential expression In addition, not only MYC rearrangement but also PVT1 rearrangement may also be implicated in the disease development of HABCLs with 8q24 abnormalities. 23547836 2013 Deletion or methylation of CDKN2A/2B and PVT1 rearrangement occur frequently in highly aggressive B-cell lymphomas harboring 8q24 abnormality. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 cervical squamous cell carcinoma C53 M8070/3 qPCR, Western blot etc. cell lines (SiHa, C33A, Ect1/E6E7 and HCvEpC) up-regulated No significant differences in serum levels of PVT1 were detected among patients infected with different HPVs and HPV-negative patients. However, serum levels of PVT1 were significantly higher in all patient groups than in healthy control group. Serum level of PVT1 increased with the increased sizes of primary tumor. Serum PVT1 accurately predicted the disease and its prognosis. PVT1 siRNA silencing inhibited the proliferation of cancer cells and reduced the expression of TGF-B1, while PVT1 overexpression played an opposite role. LncRNA PVT1 promotes the growth HPV positive and negative cervical squamous cell carcinoma by inhibiting TGF-B1. 29760583 2018 LncRNA PVT1 promotes the growth of HPV positive and negative cervical squamous cell carcinoma by inhibiting TGF-B1. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 renal cancer C64.9 NA qPCR, Western blot, Luciferase reporter assay etc. cell lines (ACHN, 786-O) up-regulated Higher PVT1 expression correlated with advanced TNM stage, histological grade, and poor survival. PVT1 knockdown promoted apoptosis, inhibited renal cancer cell proliferation, decreased Mcl-1, and increased cleaved caspase-3 and cleaved PARP. PVT1 increased Mcl-1 mRNA levels in renal cancer cells by promoting mRNA stability without influencing its transcription. in vitro, the enhanced apoptosis arising from PVT1 suppression was attenuated by overexpressing Mcl-1. In addition, in vivo experiments showed that PVT1 knockdown repressed xenograft tumor growth, while Mcl-1 overexpression partially rescued xenograft tumor growth. These results indicate the PVT1/Mcl-1 pathway inhibits renal cancer cell apoptosis in vitro and in vivo. 29254209 2017 Long noncoding RNA PVT1 inhibits renal cancer cell apoptosis by up-regulating Mcl-1 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR etc. PDAC tissues up-regulated The study results showed that the PVT1 expression was significantly increased in PDAC tissues compared to adjacent nontumor tissues. The expression of PVT1 was associated with clinical stage and N-classification. Patients with high PVT1 expression level had shorter overall survival times compared to those with low PVT1 expression level. 25668599 2015 Increased expression of the lncRNA PVT1 is associated with poor prognosis in pancreatic cancer patients. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 lung cancer C34 NA Western blot, qPCR, luciferase assays cell lines (NCI-H1650, A549, SK-MES-1, NCIH1975,95D) up-regulated Taken together,lncRNA-PVT1 functions as a competitive endogenous RNA to regulate MMP9 expression through competitively binding the common microRNAs, miR-200a and miR-200b. These findings suggest that lncRNA-PVT1 could predispose NSCLC patients to metastases and may serve as a promising target for antimetastatic therapies. 28731781 2017 lncRNA-PVT1 Facilitates Invasion Through Upregulation of MMP9 in Nonsmall Cell Lung Cancer Cell. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 renal cell carcinoma C64.9 NA qPCR renal cell carcinoma tissues up-regulated PVT1 expression was positively associated with gender, tumor size,pT stage, TNM stage, and Fuhrman grade.patients with high PVT1 expression had shorter disease-free survival (DFS) and overall-survival (OS) than those with low PVT1 expression, and multivariate analysis identified PVT1 as an independent prognostic factor in ccRCC. 29081406 2017 Upregulation of long noncoding RNA PVT1 predicts unfavorable prognosis in patients with clear cell renal cell carcinoma. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 colon cancer C18 NA qPCR, Western blot, RIP colon cancer tissues, cell lines (HCT116, HT29, SW620, SW480, Caco2, NCM460, 293T) up-regulated PVT1 expression was significantly higher in tumor tissues than in peritumoral tissues, and was associated with lymph node metastasis, tumor stage and survival time of these patients.knockdown of PVT1 promoted tumor growth and invasion in vitro.PVT1 could promote metastasis and proliferation of colon cancer via suppressing miR-30d-5p/RUNX2 axis.Expression levels of PVT1 increased in colon cancer tissues and cell lines, and were associated with short disease-free survival of colon cancer patients. 29552759 2017 Long non-coding RNA PVT1 functions as an oncogene in human colon cancer through miR-30d-5p/RUNX2 axis. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 nasopharyngeal cancer C11 NA Microarray, qPCR, Western blot, in vitro knockdown NPC tissues, Human NPC cell lines (CNE2 and 5-8F) up-regulated PVT1 shows higher expression in NPCs than in normal nasopharyngeal epithelial tissue, and patients with NPCs who show higher expression of PVT1 have worse progression-free and overall survivals.Additionally, we observed that the proliferation of NPC cells decreased, and their rate of apoptosis increased; these results indicated that the knockdown of PVT1 expression in the NPC cells induced radiosensitivity. Further, we have shown that the knockdown of PVT1 expression can induce apoptosis in the NPC cells by influencing the DNA damage repair pathway after radiotherapy. 29445147 2018 Long non-coding RNA PVT1 predicts poor prognosis and induces radioresistance by regulating DNA repair and cell apoptosis in nasopharyngeal carcinoma. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 renal cell carcinoma C64.9 NA Microarray, qPCR, RNAi etc. renal cell carcinoma tissues up-regulated knockdown of DUXAP8 could impair RCC cells invasive ability in vitro. lots of lncRNAs expression levels are significantly associated RCC patients overall survival time, such as PVT1 and DUXAP8. 29152119 2017 A genome-wide comprehensively analyses of long noncoding RNA profiling and metastasis associated lncRNAs in renal cell carcinoma. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 diffuse glioma NA M8145/3 qPCR breast and ovarian cancer cell lines, glioma tumor tissue. up-regulated These results implied that these four lncRNAs might play important role in diffuse gliomas progression, particularly, PVT1 and HAR1A could be explored as promising biomarkers for diagnosis, prognosis and target therapy of diffuse gliomas.Kaplan-Meier survival curve and Cox regression analyses showed that glioma patients with high PVT1 expression or low HAR1A expression had poor survival outcome, aberrantly expressed PVT1 and HAR1A could be the independent prognosis biomarkers for glioma patients. LncRNA CYTOR was up-regulated in HCC tissues, circulating CYTOR were also highly expressed in plasma samples of HCC patients, and could serve as potential biomarker for diagnosis of HHC. High expression of PVT1 and CYTOR as well as low HAR1A and MIAT expression were associated with high Ki-67 level and more TP53 mutation. 29108264 2017 lncRNAs PVT1 and HAR1A are prognosis biomarkers and indicate therapy outcome for diffuse glioma patients PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 small cell lung cancer C56.9 M8441/3 qPCR, RNAi, Cell proliferation assay, Cell migration and invasion assay etc. SCLC tissues, cell lines (H446, H2227, 16HBE, BEAS-2B) up-regulated PVT1 expression was markedly higher in SCLC tissues and cell lines than in normal lung tissues and normal bronchial epithelial cell lines. High levels of PVT1 were positively associated with the status of clinical stage, lymph node metastasis, and distant metastasis in SCLC patients. Knocking down PVT1 expression significantly inhibited the SCLC cell migration and invasion in vitro. 27904703 2016 LncRNA PVT1 overexpression is a poor prognostic biomarker and regulates migration and invasion in small cell lung cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 thyroid cancer C73.9 NA qPCR, Western blot, RIP, ChIP etc. thyroid cancer tissues, cell lines (IHH-4, FTC-133, 8505C) up-regulated Compared to the controls, lncRNA PVT1 was significantly up-regulated in thyroid tissues, as well as in three kinds of tumor cell lines. Silenced PVT1 significantly inhibited thyroid cell line IHH-4, FTC-133, and 8505C cell proliferation and arrested cell cycle at G0/G1 stage and significantly decreased cyclin D1 and TSHR expressions. Moreover, lncRNA PVT1 could be enriched by EZH2, and silencing PVT1 resulted in the decreased recruitment of EZH2 26427660 2015 Long noncoding RNA PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulating thyroid-stimulating hormone receptor (TSHR) PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 ovarian cancer C56.9 NA qPCR etc. cell lines (A2780, DOV13, PA-1 etc.) up-regulated These results suggest that MYC and PVT1 contribute independently to ovarian and breast pathogenesis when overexpressed because of genomic abnormalities. They also suggest that PVT1-mediated inhibition of apoptosis may explain why amplification of 8q24 is associated with reduced survival duration in patients treated with agents that act through apoptotic mechanisms. 17908964 2007 Amplification of PVT1 contributes to the pathophysiology of ovarian and breast cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, Luciferase assays etc. clear cell renal cell carcinoma tissues, cell lines (293T, ACHN and HK-2) up-regulated Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression. 29156724 2017 lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 colorectal cancer C19.9 NA qPCR, Western blot etc. cell lines (HCT116, SW480, HT29, NCM460, SW620, CaCO2) up-regulated The present study demonstrated that the expression of PVT1 in CRC cell lines was higher than that in normal colon mucosal cell lines. Using GEO database analysis and the measurement of clinical samples, it was revealed that CRC patients with high PVT1 expression demonstrated poor OS. Multivariate analysis indicated that high PVT1 expression is an independent risk factor for patients with CRC. In addition, PVT1 knockdown suppressed the proliferation, invasion and metastasis of CRC cells in vitro, which were associated with decreasing vimentin, cyclin D1 and cyclin-dependent kinase 4 expression and enhanced E-cadherin expression. The results of the present study suggest that PVT1 may serve a critical role in CRC progression and metastasis and may serve as a potential prognostic biomarker for CRC. 29512788 2018 Upregulated plasmacytoma variant translocation 1 promotes cell proliferation, invasion and metastasis in colorectal cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, Western blot etc. renal cell carcinoma tissues, cell lines (786-O, Caki-1, ACHN, 769-P, and HK-2) up-regulated The expression of PVT1 in ccRCC was analyzed using reverse transcription-quantitative polymerase chain reaction, and it was revealed that PVT1 expression was upregulated in ccRCC tissues compared with that in normal adjacent tissues. Next, PVT1 expression from The Cancer Genome Atlas datasets was validated, and it was also revealed that the high expression of PVT1 was associated with advanced disease stage and a poor prognosis. Furthermore, the knockdown of PVT1 induced apoptosis by increasing the expression of poly ADP ribose polymerase and Bcl-2-associated X protein, and promoted cell cycle arrest at the G1 phase by decreasing the expression of cyclin D1. Study of the mechanism involved indicated that PVT1 promoted the progression of ccRCC partly through activation of the epidermal growth factor receptor pathway. 29725475 2018 Knockdown of long non-coding RNA PVT1 induces apoptosis and cell cycle arrest in clear cell renal cell carcinoma through the epidermal growth factor receptor pathway. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Among them, AFAP1-AS1, BCAR4, H19, HOXA-AS2, MALAT1 and PVT1 were significantly up-regulated, and ADAMTS9-AS2 was significantly down-regulated in cancer tissue samples. 27596298 2016 Differentially expressed long non-coding RNAs and the prognostic potential in colorectal cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 non small cell lung cancer C34 M8046/3 qPCR, Luciferase reporter assay, RIP cell lines (H1650, A549, H1975, and H358, BEAS-2B) up-regulated PVT1 knockdown remarkably inhibited cell viability, invasion and promoted apoptosis in NSCLC cells.PVT1 could directly interact with miR-497.Moreover, PVT1 overexpression reversed the inhibitory effect of miR-497 on cell viability, invasion and promotion effect on apoptosis of NSCLC cells. knockdown of PVT1 inhibited tumor growth in vivo and promoted miR-497 expression.In human gastric cancer, PVT1 expression was found to serve as an independent predictor for overall survival. 29133127 2017 Knockdown of LncRNA PVT1 inhibits tumorigenesis in non-small-cell lung cancer by regulating miR-497 expression. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 breast cancer C50 NA qPCR, Western blot, RIP etc. cell lines (BT549, MCF7, T47D, MDA-MB-231, MDA-MB-453, MDA-MB-468, MCF10A, and ZR-7530) up-regulated Here we report that the lncRNA PVT1 promotes KLF5/beta-catenin signaling to drive TNBC tumorigenesis. PVT1 is upregulated in clinical TNBC tumors. Using genetic approaches targeting PVT1 in TNBC cells, we found that PVT1 depletion inhibited cell proliferation, colony formation, and orthotopic xenograft tumor growth. Mechanistically, PVT1 binds with KLF5 and increases its stability via BAP1, which upregulates beta-catenin signaling, resulting in enhanced TNBC tumorigenesis. PVT1, KLF5, and beta-catenin were also revealed to be co-expressed in clinical TNBC samples. Our findings uncover a new singaling pathway to mediate TNBC, and provide PVT1 as a new target for improving treatment of TNBC. 29760406 2018 LncRNA PVT1 regulates triple-negative breast cancer through KLF5/beta-catenin signaling. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 breast cancer C50 NA qPCR, Western blotting etc. cell lines (MCF-7, BT474, ZR-75-1, SKBR3, MDA-MB-231) up-regulated PVT1 expression is upregulated in human breast cancer tissues and cell lines.And the elevation of PVT1 was correlated with poor prognosis in breast cancer patients. We also identified an interaction between SOX2 and PVT1, which promotes breast cancer growth and invasion through epithelial to mesenchymal transition. To further reveal the function of SOX2/ PVT1 in breast cancer, the MTT and invasion assay were performed through silencing of PVT1 or SOX2. We found that either knockdown PVT1 or blocking SOX2 can suppress breast cancer cell growth and invasion through inhibition of EMT. 28882595 2017 Upregulation of SOX2 activated LncRNA PVT1 expression promotes breast cancer cell growth and invasion PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot etc. NSCLC cell lines (A549, H157, H226, H460, HCC827) up-regulated Our results indicated that PVT1 expression was significantly increased in NSCLC tissues and cell lines, and its upregulation was associated with advanced T-stage and tumor-node-metastasis (TNM) stage and regional lymph node metastasis. PVT1 expression levels were robust in differentiating NSCLC tissues from controls 26493997 2015 Long non-coding RNA PVT1 as a novel biomarker for diagnosis and prognosis of non-small cell lung cancer PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 breast cancer C50 NA qPCR etc. cell lines (A2780, DOV13, PA-1 etc.) up-regulated These results suggest that MYC and PVT1 contribute independently to ovarian and breast pathogenesis when overexpressed because of genomic abnormalities. They also suggest that PVT1-mediated inhibition of apoptosis may explain why amplification of 8q24 is associated with reduced survival duration in patients treated with agents that act through apoptotic mechanisms. 17908964 2007 Amplification of PVT1 contributes to the pathophysiology of ovarian and breast cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 glioma NA M9380/3 qPCR, Western blot, RNAi clinical glioma tissues, cell lines (U87MG,U251,HEB) up-regulated he expression levels of both PVT1 and EZH2 were up-regulated in human glioma tissues and cell lines, and positively correlated with glioma malignancy.silencing of PVT1 expression resulted in decreased proliferation, increased apoptosis, and decreased migration and invasion.exogenous PVT1 led to increased EZH2 expression and increased proliferation and induced proliferation and invasion.long non-coding RNA PVT1 could be served as an indicator of glioma prognosis, and PVT1-EZH2 regulatory pathway may be a novel therapeutic target for treating glioma.high PVT1 expression levels correlated with patients’ poor overall survival. 29046366 2017 Long non-coding RNA PVT1 indicates a poor prognosis of glioma and promotes cell proliferation and invasion via target EZH2. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 prostate cancer C61.9 NA RNA-seq, qPCR, Western blot etc. prostate cancer tissues, cells lines (PC-3, DU145, 22RV1 and WPMY) up-regulated PVT1 promotes prostate cancer invasion and metastasis by modulating EMT.Furthermore,PVT1 can promote EMT by up-regulation of Twist1,a transcription factor associated with EMT.We then confirmed that PVT1 acts as a sponge for miRNA-186-5p and positively regulates Twist1 by a sponge effect.Therefore, this study has revealed a novel MECHANISM for the promotion of EMT in prostate cancer by PVT1.Our findings suggest that the PVT1/miR-186/Twist1 regulatory axis may be a new therapeutic target for prostate cancer. PVT1 can reduce the expression of miR-186 as ceRNA in PCa cell lines and promotes Twist1 expression by suppressing miR-186. 29452232 2018 Long noncoding RNA PVT1 promotes EMT via mediating microRNA-186 targeting of Twist1 in prostate cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 pancreatic cancer C25 NA qPCR etc. pancreatic carcinoma tissues, cell lines (PANC-1, AsPC-1 and HEK 293T) up-regulated PVT1 functions as an endogenous sponge by competing for miR-448 binding to regulate the miRNA target SERBP1,therefore,promotes the proliferation and migration of PC cells. 28657147 2018 LncRNA-PVT1 promotes pancreatic cancer cells proliferation and migration through acting as a molecular sponge to regulate miR-448. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 cervical cancer C53 NA qPCR, RNAi, Luciferase reporter assay, Cell proliferation assay etc. cervical cancer tissues, cell lines (HeLa, SiHa, Ect1/E6E7) up-regulated PVT1 was up-regulated in cervical cancer tissue and cell lines. After transfecting PVT1 siRNA, the proliferation, migration and invasion of cervical cancer cells were markedly decreased. Bioinformatics analysis revealed that miR-424 was potentially targeted by PVT1, which was confirmed by dual-luciferase reporter assay. Finally, miR-424 lower-expression could recover the tumor-suppressive effects of PVT1 knockdown in cervical cancer cell lines. 28276314 2017 Long Non-Coding RNA PVT1 Facilitates Cervical Cancer Progression Via Negative Regulating of miR-424. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 cervical cancer C53 NA qPCR, RNAi, Western blot, RIP, ChIP, RNA pull-down assay etc. cervical cancer tissues, cell lines (SiHa and HeLa) up-regulated Our results revealed that PVT1 is upregulated in cervical cancer tissues. Overexpression of PVT1 promotes cervical cancer cells proliferation, cell cycle progression and migration, and depletion of PVT1 inhibits cervical cancer cell proliferation, cell cycle progression, and migration. Mechanistically, we verified that PVT1 binds to EZH2, recruits EZH2 to the miR-200b promoter, increases histone H3K27 trimethylation level on the miR-200b promoter, and inhibits miR-200b expression. 27272214 2016 Long noncoding RNA PVT1 promotes cervical cancer progression through epigenetically silencing miR-200b. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 prostate cancer C61.9 NA qPCR, RNAi prostate cancer tissues, cell lines (BPH-1, PNT2, LNCaP, PC-3, and DU145) up-regulated PVT1 was overexpressed in prostate cancer tissues and cells. Higher levels of PVT1 indicated poorer overall survival and disease-free survival. A significant association was found between PVT1 expression and tumor stage.PVT1 knockdown significantly inhibited prostate cancer growth in vivo and in vitro and promoted cell apoptosis. PVT1 knockdown also significantly upregulated the expression of cleaved caspase-3 and cleaved caspase-9, but downregulated the expression of c-Myc in prostate cancer cell lines. 29050519 2017 LncRNA PVT1 predicts prognosis and regulates tumor growth in prostate cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 gastric cancer C16 NA qPCR, Western blot, RIP, ChIP, Luciferase reporter assay etc. cell lines (AGS, HGC27, NCI-N87, MKN45, MGC803, HEK-293T) up-regulated The lncRNA PVT1 was significantly upregulated in gastric cancer tissues compared with ANTs. High expression of PVT1 predicted poor prognosis in patients with gastric cancer. PVT1 enhanced gastric cancer cell proliferation and invasion in vitro and in vivoPVT1 directly bound FOXM1 protein and increased FOXM1 posttranslationally. Moreover, PVT1 is also a FOXM1-responsive lncRNA, and FOXM1 directly binds to the PVT1 promoter to activate its transcription. Finally, PVT1 fulfilled its oncogenic functions in a FOXM1-mediated manner. 27756785 2017 A Positive Feedback Loop of lncRNA-PVT1 and FOXM1 Facilitates Gastric Cancer Growth and Invasion. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 gastric cancer C16 NA qPCR etc. cell lines (SgC7901, BgC823, MgC803, AgS , MKN45 and gES1) up-regulated This study was to evaluate the expression of PVT1 in GC and further explore its clinical significance.Previous microarray datasets were analyzed to conduct a preliminary screening for candidate lncRNAs of gastric cancer biomarkers in human gastric cancer tissues. Expression levels of PVT1 in 111pairs of gastric cancer and adjacent normal tissues, gastric cancer cell lines and gastric cancer juices compared to their corresponding controls were detected by real-time quantitative RT-PCR assay. PVT1 might serve as a promising biomarker for early detection and prognosis prediction of gastric cancer. 26925791 2016 Aberrant expression of long noncoding RNA PVT1 and its diagnostic and prognostic significance in patients with gastric cancer PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 prostate cancer C61.9 NA RNA-seq, microarray, qPCR, RNAi, Northern blot etc. prostate cancer tissues, cell lines (LNCaP, CWR22Rv1, PC3 etc.) up-regulated Interestingly, nine out of these thirteen known cancer-related lncRNA showed significantly differential expression between tumor and normal prostate samples. Several lncRNA such as NEAT1, DANCR, HOTTIP, PRINS, and EGOT that have established functions in forming nuclear speckles, in development or in autoimmune disease, but were not previously known to be related to cancer, showed differential expression between tumor and normal prostate samples, suggesting their potential function in prostate cancer. 23728290 2013 Integrative genomic analyses reveal clinically relevant long noncoding RNAs in human cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 colorectal cancer C19.9 NA microarray, qPCR, RNAi, Western blot etc. CRC tissues, cell lines (RKO, HCT116 etc.) up-regulated CRC cells transfected with PVT-1 siRNA exhibited significant loss of their proliferation and invasion capabilities. In these cells, the TGFB1 signalling pathway and apoptotic signals were significantly activated. In addition, univariate and multivariate analysis revealed that PVT-1 expression level was an independent risk factor for overall survival of colorectal cancer patients. 24196785 2014 Amplification of PVT-1 is involved in poor prognosis via apoptosis inhibition in colorectal cancers. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. non-small cell lung cancer tissues, cell lines (A549, H157, HCC827, H838) differential expression PVT1 was negatively correlated with miR-195 expression in NSCLC tissues and associated with poor prognosis of NSCLC patients. Knockdown of PVT1 enhances radiosensitivity of NSCLC by sponging miR-195, providing a novel therapeutic target to improve radiotherapy efficiency in NSCLC. 28848163 2017 Knockdown of Lncrna PVT1 Enhances Radiosensitivity in Non-Small Cell Lung Cancer by Sponging Mir-195 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. NSCLC tissues, cell lines (A549, H157, H226, H460, and HCC827) up-regulated Our results indicated that PVT1 expression was significantly increased in NSCLC tissues and cell lines, and its upregulation was associated with advanced T-stage and tumor-node-metastasis (TNM) stage and regional lymph node metastasis. PVT1 expression levels were robust in differentiating NSCLC tissues from controls. The results of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony formation assays indicated that knockdown of PVT1 remarkably inhibited NSCLC cell proliferation, whereas overexpression of PVT1 significantly promoted cellular proliferation. In addition, PVT1 knockdown increased the number of cells in the G0/G1 phase and reduced the number of cells in the S phase, while overexpression of PVT1 could promote cell cycle progression. 26490983 2016 Long non-coding RNA PVT1 as a novel biomarker for diagnosis and prognosis of non-small cell lung cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, RIP, ChIP, Flow cytometry assay etc. NSCLC tissues, cell lines (PC-9, SPC-A1, H157, H1299, A549, and SK-MES-1) up-regulated Here, we found that PVT1 was upregulated in 105 human NSCLC tissues compared with normal samples. High expression of PVT1 was associated with a higher tumor-node-metastasis stage and tumor size, as well as poorer overall survival. Functional analysis revealed that knockdown of PVT1 inhibited NSCLC cell proliferation and induced apoptosis both in vitro and in vivo RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that PVT1 recruits EZH2 to the large tumor suppressor kinase 2 (LATS2) promoter and represses LATS2 transcription. Furthermore, ectopic expression of LATS2 increased apoptosis and repressed lung adenocarcinoma cell proliferation by regulating the Mdm2-p53 pathway. 26908628 2016 Long Noncoding RNA PVT1 Promotes Non-Small Cell Lung Cancer Cell Proliferation through Epigenetically Regulating LATS2 Expression. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell lines (Huh7, SK-hep1, SMMC-7721, HepG2, Hep3B, PLC/PRF/5, Bel-7402) up-regulated The relative expression levels of PVT1 were significantly higher in cancerous tissues compared with the corresponding non-cancerous tissues. Furthermore, overexpression of PVT1 was associated with a higher serum a-fetoprotein expression level and a higher recurrence rate. Kaplan-Meier analysis indicated that the patients with high PVT1 expression exhibited poor recurrence-free survival, and multivariate analysis demonstrated that high levels of PVT1 expression are an independent predictor for HCC recurrence. 25624916 2015 Long non-coding RNA PVT1 is associated with tumor progression and predicts recurrence in hepatocellular carcinoma patients. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 non small cell lung cancer C34 M8046/3 qPCR, RNAi etc. NSCLC tissues, cell lines (A549, H157, HEK-293T) up-regulated lncRNA PVT1 expression was significantly upregulated in NSCLC tissues and lung cancer cells. Increased PVT1 expression was significantly correlated with histological grade and lymph node metastasis. In addition, NSCLC patients with PVT1 higher expression have shown significantly poorer overall survival than those with lower PVT1 expression. In vitro assays our results indicated that knockdown of PVT1 inhibited cell proliferation, migration, and invasion. 25400777 2014 Increased expression of the lncRNA PVT1 promotes tumorigenesis in non-small cell lung cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, RIP etc. gastric cancer tissues, cell lines(GES-1, SGC-7901, BGC-823, MNK-45, AGS, SUN-638, HGC-27, and HUVEC) up-regulated We demonstrated that lncRNA PVT1 was upregulated and significantly associated with high-microvessel density and poor prognosis in gastric cancer. Through gain- and loss-of PVT1 expression, we found PVT1 could obviously induce angiogenesis within tumors, in addition to promoting tumor growth in vitro and in vivo. Mechanistically, PVT1 directly interacted with the signal transducer activator phospho-STAT3 in the nucleus, and increased its protein stability by protecting it from poly-ubiquitination and proteasome-dependent degradation. The binding of PVT1 activated the STAT3 signalling pathway, and successively elevated VEGFA expression to stimulate angiogenesis. The positive correlation of PVT1 and VEGFA expression was also verified in gastric cancer specimens, and high levels of PVT1 and VEGFA in combination frequently predicted shorter survival time. 29706652 2018 LncRNA PVT1 promotes angiogenesis via activating the STAT3/VEGFA axis in gastric cancer. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, Flow cytometry assay, Cell proliferation assay etc. gastric cancer tissues, cell lines (AGS, SGC-7901, BGC-823) up-regulated The higher expression of PVT1 was significantly correlated with deeper invasion depth and advanced TNM stage. Multivariate analyses revealed that PVT1 expression served as an independent predictor for overall survival. Further experiments demonstrated that PVT1 knockdown significantly inhibited the proliferation both in vitro and in vivo. Importantly, we also showed that PVT1 played a key role in G1 arrest. 25890171 2015 Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically regulating p15 and p16. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 pancreatic ductal adenocarcinoma NA M9380/3 qRT-PCR, Western blot assay, Luciferase reporter assay, RNA pull-down assay, RIP PDA cell lines (HPAF-II, PANC-1, SW1990, BxPC-3, MIA PaCa-2, Capan-2 and AsPC-1)The immortalized pancreatic ductal epithelial cell line H6C7, The cell line (HEK 293 T), PDA specimens and adjacent non-tumor tissues up-regulated PVT1 levels paralleled those of ULK1 protein in PDA cancer tissues. PVT1 promoted cyto-protective autophagy and cell growth by targeting ULK1 both in vitro and in vivo. Moreover, high PVT1 expression was associated with poor prognosis. Furthermore, we found that PVT1 acted as sponge to regulate miR-20a-5p and thus affected ULK1 expression and the development of pancreatic ductal adenocarcinoma. 30001707 2018 LncRNA PVT1 triggers Cyto-protective autophagy and promotes pancreatic ductal adenocarcinoma development via the miR-20a-5p/ULK1 Axis. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 ovarian cancer C56.9 NA qPCR, Cell proliferation assay, Flow cytometric assay, Luciferase reporter assay, etc. Three human OC cell lines (HEY, SKOV-3, OVCAR-3), normal human ovary cell line (IOSE80). OC tissues. up-regulated Taken together, our finding shows that PVT1 may be a novel biomarker for prognosis and a promising therapeutic target for OC.Patients were divided into high PVT1 expression group and low PVT1 expression group on the basis of the median of PVT1 expression levels in OC tissues. Kaplan-Meier survival analysis and log-rank test were used to evaluate the correlation between PVT1 expression levels and overall survival rate of OC patients. *P < 0.05, **P < 0.01.Mechanistically, miR-133a was identified to serve as a direct downstream target of PVT1 in OC. Knockdown of PVT1 inhibited cell proliferation, migration and invasion through negative regulating miR-133a in OC cells.The long non-coding RNA, plasmacytoma variant translocation 1 (PVT1), was reportedly to be highly expressed in a variety of tumors including ovarian cancer (OC). 29957467 2018 Long non-coding RNA PVT1 promotes cell proliferation and invasion through regulating miR-133a in ovarian cancer. RAD51-AS1 TODRA 100505648 ENSG00000245849 NR_040058 GRCh38_15:40686724-40695107 epithelial ovarian cancer C56.9 NA Microarray, qPCR, Western blot, Luciferase reporter assay etc. epithelial ovarian cancer tissues, cell lines (SKOV3, SKOV3.ip, HO8910 and HO8910-PM) up-regulated We verified RAD51-AS1 as a target of E2F1 under negative regulation in EOC. We then examined RAD51-AS1 expression in EOC samples using in situ hybridization (ISH). RAD51-AS1 was localized to the nucleus and found to be a critical marker for clinical features that significantly correlated with poor survival in EOC patients. RAD51-AS1 was also an independent prognostic factor for EOC. Overexpression of RAD51-AS1 promoted EOC cell proliferation, while silencing of RAD51-AS1 inhibited EOC cell proliferation, delayed cell cycle progression and promoted apoptosis in vitro and in vivo. RAD51-AS1 may participate in carcinogenesis via regulation of p53 and p53-related genes. Our study highlights the role of RAD51-AS1 as a prognostic marker of EOC. Survival analysis showed that EOC patients with high RAD51-AS1 expression levels had a significantly decreased overall survival (OS) than those with low RAD51-AS1 expression levels. 28667302 2017 E2F1-regulated long non-coding RNA RAD51-AS1 promotes cell cycle progression, inhibits apoptosis and predicts poor prognosis in epithelial ovarian cancer. RAMP2-AS1 RAMP2-AS1 100190938 ENSG00000197291 NR_024461 GRCh38_17:42753914-42761257 glioblastoma NA M9440/3 microarray, qPCR, Western blot, Flow cytometry assay, Cell proliferation assay etc. glioblastoma tissues, cell lines (U87 and U251) down-regulated lncRNA RAMP2-AS1 had significant decrease of expression in glioblastoma tissues and showed coexpressional relationship with NOTCH3, an important tumor promoter in many neoplastic diseases. Our follow up experiment indicated that (i) an overexpression of RAMP2-AS1 reduced glioblastoma cell proliferation in vitro and also reduced glioblastoma xenograft tumors in vivo; (ii) NOTCH3 and RAMP2-AS1 coexpression rescued the inhibitory action of RAMP2-AS1 in glioblastoma cells; and (iii) RNA pull-down assay revealed a direct interaction of RAMP2-AS1 with DHC10, which may consequently inhibit, as we hypothesize, the expression of NOTCH3 and its downstream signaling molecule HES1 in glioblastoma. 27784795 2016 The Potential Roles of Long Noncoding RNAs (lncRNA) in Glioblastoma Development. RBM5-AS1 RBM5-AS1, LUST 100775107 ENSG00000281691 NR_045388 GRCh38_3:50099603-50100988 colon cancer C18 NA qPCR, Cell transfection, Dual-luciferase reporter assay, Flow cytometry assay etc. cell lines (LS174T, SW480, HT-29, CaCo-2, DLD-1 and HCT 116) differential expression In this study, we report enrichment of the lncRNA RBM5-AS1/LUST during sphere formation of colon CIC. Its silencing impaired WNT signaling, whereas its overexpression enforced WNT signaling, cell growth, and survival in serum-free media. Mechanistic investigations showed that silencing or overexpression of RBM5-AS1 caused a respective loss or retention of B-catenin from TCF4 complexes bound to the WNT target genes SGK1, YAP1, and MYC Our work suggests that RBM5-AS1 activity is critical for the functional enablement of colon cancer stem-like cells. Furthermore, it defines the mechanism of action of RBM5-AS1 in the WNT pathway via physical interactions with B-catenin, helping organize transcriptional complexes that sustain colon CIC function. 27520449 2016 RBM5-AS1 Is Critical for Self-Renewal of Colon Cancer Stem-like Cells. RCCRT1 NA NA NA NA NA renal cell carcinoma C64.9 NA qPCR, RNAi etc. RCC tissues, cell lines (ACHN, A498) up-regulated Compared with adjacent noncancerous tissues, RCCRT1 is upregulated remarkably in RCC, particularly in high-grade RCC tissues. RCCRT1 is associated with clinicopathologic findings such as tumor size, pathologic T stage, tumor grade, lymph node metastasis, and distant metastasis. 25168566 2014 RCCRT1 is correlated with prognosis and promotes cell migration and invasion in renal cell carcinoma. RGMB-AS1 NA 503569 ENSG00000246763 NR_033932 GRCh38_5:98769618-98773469 hepatocellular carcinoma C22.0 M8170/3 qRT-PCR, Western blot hepatocellular carcinoma tissue, hepatocellular carcinoma cell lines (QGY-7703, HuH7, BEL-7402 and HepG2) down-regulated lncRNA RGMB-AS1 was low-expressed in hepatocellular carcinoma tissues and cell lines, and associated with clinical stage, tumor size and metastasis. Survival analysis indicated that lncRNA RGMB-AS1 high was an independent favorable prognostic factor for hepatocellular carcinoma patients. Gain-of-function studies showed up-regulated lncRNA RGMB-AS1 expression suppressed hepatocellular carcinoma cells proliferation, migration and invasion, and promoted cells apoptosis. There was a positively association between lncRNA RGMB-AS1 and RGMB in hepatocellular carcinoma tissues, and up-regulated lncRNA RGMB-AS1 expression increased RGMB mRNA and protein expressions in hepatocellular carcinoma cells. 29288973 2017 The clinical significance and biological function of lncRNA RGMB-AS1 in hepatocellular carcinoma. RGMB-AS1 NA 503569 ENSG00000246763 NR_033932 GRCh38_5:98769618-98773469 lung adenocarcinoma C34 M8140/3 microarray, qPCR, Western blot etc. lung adenocarcinoma tissues, cell lines (A549 and SPC-A-1) down-regulated We showed that upregulation of lncRNA RGMB-AS1 was significantly correlated with differentiation, TNM stage, and lymph node metastasis. In lung adenocarcinoma cells, downregulation of lncRNA RGMB-AS1 inhibited cell proliferation, migration, invasion, and caused cell cycle arrest at the G1/G0 phase. In vivo experiments showed that lncRNA RGMB-AS1 downregulation significantly suppressed the growth of lung adenocarcinoma. The expression of lncRNA RGMB-AS1 was inversely correlated with that of repulsive guidance molecule b (RGMB) in lung adenocarcinoma tissues, and UCSC analysis and fluorescence detection assay indicated that lncRNA RGMB-AS1 may be involved in the development of human lung adenocarcinoma by regulating RGMB expression though exon2 of RGMB. 26950071 2016 Long Noncoding RNA RGMB-AS1 Indicates a Poor Prognosis and Modulates Cell Proliferation, Migration and Invasion in Lung Adenocarcinoma RMRP RMRP, CHH, NME1, RMRPR, RRP2 6023 ENSG00000269900 NR_003051 GRCh38_9:35657751-35658018 glioma NA M9380/3 qPCR, RNAi etc. glioma tissues, cell line (U87, U251) up-regulated lncRNA RMRP might act as an oncogene and could be used as a therapeutic target for the treatment of glioma. Our findings provide an indepth insight into the role of lncRNA RMRP in glioma progression. 29181061 2017 Up-regulation of the long non-coding RNA RMRP contributes to glioma progression and promotes glioma cell proliferation and invasion RNCR3 LINC00599 157627 ENSG00000253230 NA GRCh38_8:9900064-9905366 glioma NA M9380/3 qPCR glioma tissues down-regulated Expression of lncRNAs MEG3, JPX, RNCR3, and ZFAS1 significantly differed between low and high malignancy grade. MEG3, JPX, RNCR3, and ZFAS1 showed significant decrease with tumour malignant progression. Expression of certain lncRNAs seems to be associated with patient's age at the time of diagnosis as correlation analysis showed moderate negative association for MEG3 (rs = 0.336, p = 0.009, R2 = 0.113), ZFAS1 (rs = 0.368, p = 0.004, R2 = 0.164), and RNCR3 (rs = 0.431, p = 0.001, R2 = 0.186). 29138748 2017 Identifying Novel Glioma-Associated Noncoding RNAs by Their Expression Profiles RNCR3 LINC00599 157627 ENSG00000253230 NA GRCh38_8:9900064-9905366 prostate cancer C61.9 NA qPCR, Luciferase reporter assay, Western blot, etc. 52 pairs of prostate cancer tissue, adjacent normal prostate tissue. The prostate epithelial cell line (RWPE-1), human prostate cancer cell lines (LNCaP, DU145, PC-3). up-regulated Our data revealed that RNCR3 functions as an tumor-promoting lncRNA in prostate cancer and may serve as a novel important biomarker for the diagnosis and treatment of prostate cancer. Upregulation of RNCR3 in prostate cancer cells compared with normal prostate epithelial cells RWPE-1. *P < 0.05. C. Kaplan-Meier survival curves for patients with prostate cancer tissues expressing low and high levels of RNCR3. We also confirmed that the oncogenic function of RNCR3 in prostate cancer are partly mediated by negative regulation of miR-185-5p targeted BRD8 ISO2. Moreover, knockdown of RNCR3 can also result to higher expression of IL-6, CCL2 and TNF-α in blood plasma, indicating that RNCR3 may have a biological function in immune system . 29887969 2018 Long non-coding RNA RNCR3 promotes prostate cancer progression through targeting miR-185-5p. RP11-119F7.4 RP11-119F7.5 NA NA NA GRCh38_10:68698500-68700794 gastric cancer C16 NA qPCR etc. gastric cancer tissues down-regulated RP11-119F7.4 expression was significantly downregulated in the gastric cancer tissues compared with the matched NATs and was significantly associated with the macroscopic type and Lauren grade. LncRNA RP11-119F7.4 may be involved in carcinogenesis and may prove useful as a biomarker for diagnosis and prognostic significance in patients with gastric cancer. 26170986 2015 Novel long non-coding RNA RP11-119F7.4 as a potential biomarker for the development and progression of gastric cancer. RP11-140I24 RP11-140I24.2 NA NA NA GRCh38_16:73293866-73294296 endometrial cancer NA M8380/3 microarray, qPCR etc. endometrial carcinoma tissues down-regulated Real-time PCR verified that 6 of the 7 lncRNAs are dramatically downregulated in EC, which is consistent with the microarray data. 27748922 2016 Distinct expression profile of lncRNA in endometrial carcinoma. RP11-169D4.1 RP11-169D4.2 101928555 ENSG00000227467 NR_126364 GRCh38_11:72584572-72587979 laryngeal squamous cell cancer C32.3 NA microarray, qPCR etc. LSCC tissues up-regulated AC026166.2-001 and RP11-169D4.1-001 were distinctly dysregulated, with AC026166.2-001 exhibiting lower expression in cancer tissues and RP11-169D4.1-001 higher expression. We verified that both AC026166.2-001 and RP11-169D4.1-001 were expressed at a lower level in cervical lymph nodes compared with paired laryngeal cancer tissues and paired normal tissues. RP11-169D4.1-001 levels were positively correlated with lymph node metastasis. 25243407 2014 Long non-coding RNA profiling in laryngeal squamous cell carcinoma and its clinical significance: potential biomarkers for LSCC. RP11-263F15.1 NA NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 Microarray, qPCR cancer tissues differential expression In conclusion, these data indicate that differentially expressed lncRNAs and mRNAs were involved in the carcinogenesis of PDAC, and RP11-263F15.1 may prove to be a potential biomarker for the diagnosis and prognostic prediction of PDAC.Pancreatic ductal adenocarcinoma (PDAC) remains one of the most devastating malignancies with a 5-year survival rate less than 5% 1. Early diagnosis in combination with comprehensive therapies including surgical resection, adjuvant chemotherapy and radiotherapy can increase the 5-year survival rate significantly 2. 28928863 2017 Microarray Analysis of the Expression Profile of Long Non-Coding RNAs Indicates lncRNA RP11-263F15.1 as a Biomarker for Diagnosis and Prognostic Prediction of Pancreatic Ductal Adenocarcinoma. RP1130-1 LINC02055, RP1130-1 107986980 ENSG00000254101 NR_147196 GRCh38_8:136530798-136984935 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell lines (HepG2, LO2, Huh7, and SMMC-7721) down-regulated Expression of LINC RP1130-1 was found to be markedly down-regulated in 51 HCC tissues compared to matching adjacent non-tumor liver tissues. The expression of LINC RP1130-1 was associated with clinical stage, the number of tumors, portal vein tumor thrombus (PVTT), and microvascular invasion (MVI). 27773892 2016 The significance of low levels of LINC RP1130-1 expression in human hepatocellular carcinoma. RP11-363E7.4 RP11-363E7.4 NA NA NA GRCh38_9:19453209-19455173 gastric cancer C16 NA qPCR etc. gastric cancer tissues down-regulated The expression of lncRNA RP11-363E7.4 was downregulated compared with that of paracarcinoma tissues in five GC samples. High expression of lncRNA RP11-363E7.4 was found to be correlated to better overall survival (OS) for GC patients. 29843141 2018 A Novel LncRNA-miRNA-mRNA Triple Network Identifies LncRNA RP11-363E7.4 as An Important Regulator of miRNA and Gene Expression in Gastric Cancer RP11-366H4.1.1 NA NA NA NA NA esophageal squamous cell cancer NA NA RNA-seq, Microarray, qRT-PCR, in vitro knockdown ESCC tissues, Human esophageal cancer cell lines (KYSE150,KYSE180, KYSE450, KYSE70, KYSE140 and TE3) up-regulated A novel three-lncRNA signature, comprised of RP11-366H4.1.1 (ENSG00000248370), LINC00460 (ENSG00000233532) and AC093850.2 (ENSG00000230838), was identified. The signature classified patients into high-risk and low-risk groups with different overall survival (OS) and disease-free survival (DFS). The signature indicates that patients in the high-risk group show poor OS and DFS, whereas patients with a low-risk group show significantly better outcome. The independence of the signature was validated by multivariable Cox regression analysis. GO and KEGG pathway analysis for 588 protein-coding genes-associated with the three lncRNAs indicated that the three lncRNAs were involved in tumorigenesis. In vitro assays further demonstrated that the three lncRNAs promoted the migration and proliferation of ESCC cells. 29409459 2018 A three-lncRNA signature predicts overall survival and disease-free survival in patients with esophageal squamous cell carcinoma. RP11-396F22.1 NA NA NA NA GRCh38_12:38906451-38909592 cervical cancer C53 NA Microarray, qPCR, in vitro knockdown etc. cell lines (SiHa, HeLa, C33a and Ms751) up-regulated RP11-396F22.1 might regulate Cpne8 expression via miRNA-32.Indeed, we found that knock down of RP11-396F22.1 significantly down regulated miRNA-32 expression 29636859 2018 Overexpression of long non-coding RNA RP11-396F22.1 correlates poor prognosis of patients with early-stage cervical cancer. RP11-436H11.5 NA NA NA NA GRCh38_5:124734618-124735175 renal cell carcinoma C64.9 NA qPCR, Luciferase reporter assay, Western blot etc. RCC tissues, cell lines (A498, 786-O, OSRC-2) up-regulated The results of survival analysis indicated that patients in the high lncRNA RP11-436H11.5 group presented significantly worse outcomes compared with those in the low lncRNA RP11-436H11.5 group. Downregulation of lncRNA RP11-436H11.5 suppressed RCC cell proliferation and invasion in vitro and in vivo. Luciferase reporter assay results demonstrated that lncRNA RP11-436H11.5 enhanced BCL-W expression by regulating miR-335-5p expression. LncRNA RP11-436H11.5 could function as a miR-335-5p decoy to derepress expression of BCL-W. LncRNA RP11-436H11.5 could function as a competing endogenous RNA to promote RCC cell proliferation and invasion, which might serve as a therapeutic application to suppress RCC progression. LncRNA RP11-436H11.5 may be a novel therapeutic target and prognostic marker in RCC. 29070041 2017 LncRNA RP11-436H11.5, functioning as a competitive endogenous RNA, upregulates BCL-W expression by sponging miR-335-5p and promotes proliferation and invasion in renal cell carcinoma RP11-466I1.1 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. hepatocellular carcinoma tissues up-regulated Results showed that RP11-466I1.1 was upregulated in HCC tissues (P < .01) and serum (P < .05). This study suggested that RP11-466I1.1 is distinctively expressed in HCC and may serve as a promising novel prognostic biomarker. 29790663 2018 A distinctively expressed long noncoding RNA, RP11‐466I1.1, may serve as a prognostic biomarker in hepatocellular carcinoma RP11-501O2 RP11-501O2.3 NA NA NA GRCh38_3:148160911-148226606 endometrial cancer NA M8380/3 microarray, qPCR etc. endometrial carcinoma tissues down-regulated Real-time PCR verified that 6 of the 7 lncRNAs are dramatically downregulated in EC, which is consistent with the microarray data. 27748922 2016 Distinct expression profile of lncRNA in endometrial carcinoma. RP11-528G1.2 RP11-528G1.2 NA NA NA GRCh38_1:160537073-160571458 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. RP1-153P14.5 RP1-153P14.5 NA NA NA GRCh38_6:37545145-37550860 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Cell proliferation assay, Cell migration assay etc. cell lines (HepG2, SMMC-7721 and HCCLM9) differential expression Knockdown of seven of the ten candidate lncRNAs significantly affected cell migration in at least one cell line; knockdown of three lncRNAs produced accordant alterations in cell migration in at least two cell lines by suppressing or promoting cell migration 28194035 2017 Recurrently deregulated lncRNAs in hepatocellular carcinoma. RP11-552M11.4 NA NA NA NA GRCh38_1:111438638-111441364 ovarian cancer C56.9 NA Microarray, qPCR, Western blot, Luciferase reporter assay ovarian cancer cell lines (SKOV3, A-2780) up-regulated Rescue experiment and luciferase reporter assay showed that lncRNA RP11-552M11.4 regulated SKOV3 cells functions through binding BRCA2. Further experiments in A-2780 cells also validated that lncRNA RP11-552M11.4 induced A-2780 cell proliferation while repressing apoptosis by targeting BRCA2. In addition, upregulation of lncRNA RP11-552M11.4 increased IOSE80 cell proliferation, migration and invasion while decreasing apoptosis. 29478268 2018 Long non-coding RNA RP11-552M11.4 promotes cells proliferation, migration and invasion by targeting BRCA2 in ovarian cancer. RP11-600K15.1 LINC01592 NA ENSG00000253658 NA GRCh38_8:68911803-69104190 endometrial cancer NA M8380/3 microarray, qPCR etc. endometrial carcinoma tissues down-regulated Real-time PCR verified that 6 of the 7 lncRNAs are dramatically downregulated in EC, which is consistent with the microarray data. 27748922 2016 Distinct expression profile of lncRNA in endometrial carcinoma. RP11-600K15.1 LINC01592 NA ENSG00000253658 NA GRCh38_8:68911803-69104190 esophageal squamous cell cancer NA NA RIP etc. esophageal cancer cell lines up-regulated Here, we describe a novel lncRNA POU6F2-AS2 specifically expressed in OSCC. POU6F2-AS2 is involved in the DNA damage response and regulates cells survival after ionizing radiation. POU6F2-AS2 interacts with Ybx1 protein and regulates its chromatin localization. 27033944 2016 Long noncoding RNA POU6F2-AS2 is associated with oesophageal squamous cell carcinoma RP11-643M14.1 RP11-643M14.1 NA NA NA GRCh38_15:62060503-62062434 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. RP11-766N7.4 LINC02231 109729131 ENSG00000248995 NR_146276 GRCh38_12:64920845-64982524 esophageal squamous cell cancer NA NA qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. ESCC tissues, cell lines (TE-13, TE-1, EC-1 and Eca-109) down-regulated RP11-766N7.4 was downregulated in ESCC tissues and cell lines and correlated with lymph node metastasis, tumor stage and survival rate. In addition, long noncoding RNA RP11-766N7.4 knockdown promoted cellular migration and invasion via inducing EMT process, and overexpression of long noncoding RNA RP11-766N7.4 inhibited cellular migration and invasion by suppressing EMT process. 28157654 2017 Long noncoding RNA RP11-766N7.4 functions as a tumor suppressor by regulating epithelial-mesenchymal transition in esophageal squamous cell carcinoma. RP11-789C1.1 LINC01612 101928223 ENSG00000250266 NR_125889 GRCh38_4:170273919-170283079 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues down-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. RP11-909B2.1 NA 400654 ENSG00000266952 NR_033983 GRCh38_18:64213082-64260055 colorectal cancer C19.9 NA qPCR etc. colorectal cancer tissues, cell line(RKO) down-regulated the three RNAs-based biomarker network (long non-coding intergenic RNA-[lncRNA RP11-909B2.1], Homo sapiens microRNA-595 [hsa-miRNA-595], and L3MBTL1 mRNA), had high sensitivity and specificity for discriminating CRC from healthy controls and also from benign colorectal neoplasm. The data suggest that among these three RNAs, serum lncRNA RP11-909B2.1 could be a promising independent prognostic factors in CRC.The circulatory RNA based biomarker panel can act as potential biomarker for CRC diagnosis and prognosis. 29737552 2018 Competing endogenous RNA network crosstalk reveals novel molecular markers in colorectal cancer. RP1-4514.2 NA NA NA NA NA prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (LNCaP) down-regulated Five lncRNAs, RP1-4514.2, SUZ12P1, SNHG5, LINC01138, and SNHG1, were down-regulated under DHT treatment. Five lncRNAs, KLKP1, LINC00969, LINC-PINT, TUG1 and MIR17HG, were up-regulated under DHT treatment. Notably, RP1-4514.2 and LINC01138 were induced and KLKP1 was reduced over 2 fold after AR silenced, suggesting the involvement of AR in androgen-mediated regulation of these lncRNAs expressions. 27556357 2016 Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer. RP1-4514.2 NA NA NA NA NA prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (WPMY-1, DU145, PC-3 and LNCaP) up-regulated To further validate the results, we examined the expression levels in 11 normal prostate tissues and 14 prostate cancer tissues with real-time PCR. All of these lncRNAs except LINC00969, were expressed significantly higher in prostate cancer samples compared with normal prostate tissues, which were consistent with the TCGA and microarray results. Then, the expression levels of ten lncRNAs were validated in the noncancerous prostatic cells WPMY-1 and four human prostate cancer cell lines by qRT-PCR. It turned out that most of the ten lncRNAs were up-regulated in prostate cancer cell lines and showed a similar expression pattern in patient samples. 27556357 2016 Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer. RP5-833A20.1 NFIA-AS1 645030 ENSG00000237853 NR_104180 GRCh38_1:61248945-61253510 glioma NA M9380/3 qPCR, Cell transfection, Western blot, Cell proliferation assay etc. glioma tissues, cell line (U251) down-regulated The expression of RP5-833A20.1 was downregulated, whereas the expression of NFIA was upregulated in glioma tissues, compared with corresponding adjacent nontumor tissues from 20 patients with glioma. The overexpression of RP5-833A20.1 inhibited proliferation and cell cycle progression, and induced apoptosis in the U251 cells. 27779670 2016 Long non-coding RNA RP5-833A20.1 inhibits proliferation, metastasis and cell cycle progression by suppressing the expression of NFIA in U251 cells. RPL34-AS1 FLJ37673, RP11-462C24.1 285456 ENSG00000234492 NR_026968 GRCh38_4:108538190-108620460 colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues down-regulated We found that RP11-462C24.1 expression level was lower in cancer tissues compared with adjacent normal samples. Furthermore, its expression level was lower in CRC patients with metastasis than those without metastasis. That is, RP11-462C24.1 expression level decreased as the malignant degree of CRC increased. In addition, low expression of RP11-462C24.1 significantly correlated with more distant metastasis. 24908062 2014 Low expression of novel lncRNA RP11-462C24.1 suggests a biomarker of poor prognosis in colorectal cancer. RPL34-AS1 FLJ37673, RP11-462C24.1 285456 ENSG00000234492 NR_026968 GRCh38_4:108538190-108620460 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues, cell lines (HCG-27, SGC-7901) down-regulated Linc00261, DKFZP434K028 and RPL34-AS1 had lower expression levels in gastric cancer tissues than the normal counterparts. In gastric cell lines, the three lncRNAs were also down-regulated compared with the respective normal gastric epithelial cell line GES-1. Moreover, the low expression levels of DKFZP434K028 and RPL34-AS1 positively correlated with the larger tumor size. 26237576 2015 Long non-coding RNA Linc00152 is involved in cell cycle arrest, apoptosis, epithelial to mesenchymal transition, cell migration and invasion in gastric cancer. RPLP0P2 RPLP0P2, RPLP0L2, RPLP0_3_1146 NA ENSG00000243742 NA GRCh38_11:61615036-61639449 lung adenocarcinoma C34 M8140/3 qPCR, Cell transfection, Cell migration and invasion assay etc. LAD tissues, cell lines (SPCA-1, NCI-H1299, A549, NCI-H441, LTEP-a2) down-regulated We found that RPLP0P2 expression was lower while LRRC10B mRNA level was higher in LAD than NT by qPCR. The expression of RPLP0P2 in lymph node metastasis of LAD group was significantly lower than LAD without lymph node metastasis group. Survival analysis showed that survival time of high expression of RPLP0P2 was significantly longer than low RPLP0P2 level in LAD patients. After RPLP0P2 was overexpressed, the proliferation rate, adhesion ability, S phase and G2/M phase cells and LRRC10B mRNA significantly reduced, while apoptosis and G0/G1 phase cells obviously increased, but migration ability and invasion did not significantly change. 27460542 2016 Low expression lncRNA RPLP0P2 is associated with poor prognosis and decreased cell proliferation and adhesion ability in lung adenocarcinoma. RUNDC3A-AS1 NA 101926996 ENSG00000267750 NR_110802 thyroid cancer C73.9 NA qPCR, Western blot, etc. cell lines (BHT101, BCPAP) up-regulated thyroid cancer patients with higher RUNDC3A-AS1 or lower FOXD-AS1 expression levels had shorter OS time, 29923329 2018 Identification of differential expressed lncRNAs in human thyroid cancer by a genome-wide analyses. SBDSP1 SBDSP1, SBDSP NA ENSG00000225648 NA GRCh38_7:72829425-72836701 colorectal cancer C19.9 NA qPCR etc. CRC tissues down-regulated Our study is the frst to demonstrate that higher SBDSP1 can predict poor prognosis for patients with CRC. It seems that SBDSP1 is a potential prognostic predictor in CRC. 28975982 2017 Increased expression of long non-coding RNA SBDSP1 correlates with poor survival in colorectal cancer SBF2-AS1 NA 283104 ENSG00000246273 NR_036485 GRCh38_11:9758292-9811319 lung adenocarcinoma C34 M8140/3 qPCR etc. NSCLC tissues up-regulated 4 lncRNAs were also selected and validated by qRT-PCR in 20 pairs of lung cancer tissues and adjacent tissues. Expression patterns of all 4 lncRNAs were consistent with our analysis results, showing the analysis results were solid. 26918601 2016 Comprehensive analysis of lncRNA expression profiles and identification of functional lncRNAs in lung adenocarcinoma. SBF2-AS1 NA 283104 ENSG00000246273 NR_036485 GRCh38_11:9758292-9811319 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated The expression of SBF2-AS1 was higher in NSCLC tissues compared with adjacent non-tumor tissues. Additionally, high expression level of SBF2-AS1 was significantly associated with NSCLC histological grade, and lymph node metastasis. Furthermore, a higher SBF2-AS1 expression was demonstrated to be associated with poor overall survival times in NSCLC patients. 27460731 2016 Over-expression of lncRNA SBF2-AS1 is associated with advanced tumor progression and poor prognosis in patients with non-small cell lung cancer. SchLAH STEAP4, STAMP2, SchLAH, TIARP, TNFAIP9 79689 ENSG00000127954 NA GRCh38_7:88270892-88306891 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. HCC tissues, cell lines (HepG2, Hep3B, SMMC7721, Huh7) down-regulated SchLAH was generally downregulated in HCC. Overexpression of SchLAH inhibited the migration and lung metastasis of HCC cells. Knockdown of SchLAH pool promoted the migration of HCC cells. RNA pull-down and RNA immunoprecipitation assays demonstrated SchLAH physically interacted with fused in sarcoma (FUS). PCR array analysis showed that RhoA and Rac1 were the downstream effector molecules of SchLAH during HCC metastasis. 28196303 2017 Long noncoding RNA SchLAH suppresses metastasis of hepatocellular carcinoma through interacting with fused in sarcoma. SChLAP1 SCHLAP1, LINC00913, PCAT11, PCAT114 101669767 ENSG00000281131 NR_104323 GRCh38_2:180692104-180916939 prostate cancer C61.9 NA microarray, ISH etc. prostate cancer tissues up-regulated SChLAP1 expression increases with prostate cancer progression, and high SChLAP1 expression by ISH is associated with poor outcome after radical prostatetcomy in patients. This study highlights SChLAP1 as a novel lncRNA that promotes tumor cell invasion and metastasis, and associates with lethal disease. 25499224 2014 A Novel RNA In Situ Hybridization Assay for the Long Noncoding RNA SChLAP1 Predicts Poor Clinical Outcome After Radical Prostatectomy in Clinically Localized Prostate Cancer. SChLAP1 SCHLAP1, LINC00913, PCAT11, PCAT114 101669767 ENSG00000281131 NR_104323 GRCh38_2:180692104-180916939 prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues up-regulated The long non-coding RNA SChLAP1 was identified as the highest-ranked overexpressed gene in cancers with metastatic progression. Validation in three independent cohorts confirmed the prognostic value of SChLAP1 for metastatic progression. On multivariate modelling, SChLAP1 expression (high vs low) independently predicted metastasis within 10 years. We identified and validated high SChLAP1 expression as significantly prognostic for metastatic disease progression of prostate cancer. 25456366 2014 RNA biomarkers associated with metastatic progression in prostate cancer: a multi-institutional high-throughput analysis of SChLAP1. SDPR-AS NA NA NA NA NA renal cell carcinoma C64.9 NA qPCR etc. renal cell carcinoma tissues, cell lines (HKC, OS-RC-2, 786-O, 769-P, Caki-1, Caki-2 and ACHN) down-regulated We uncovered the downregulated expressions of both lncRNA SDPR-AS and its protein-coding gene, SDPR, in RCC tissues compared to the matched normal tissues. Furthermore, SDPR-AS and SDPR expressions were positively correlated. Overexpression and knockdown experiments suggested that SDPR-AS and SDPR were coregulated in RCC cell lines. In addition, overexpression of SDPR-AS suppressed cell migration and invasion, but not cell growth. Furthermore, expression of SDPR-AS was associated with tumor differentiation and lymphatic metastasis. Kaplan-Meier survival and log-rank tests demonstrated the association of elevated expression of SDPR-AS with increased overall survival. In conclusion, our results suggest that the SDPR-AS may serve as a prognostic biomarker and therapeutic target of RCC. 28790838 2017 Downregulation of lncRNA SDPR-AS is associated with poor prognosis in renal cell carcinoma. SERHL NA NA ENSG00000172250 NA GRCh38_22:42500579-42512560 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. hepatocellular carcinoma tissues, cell lines (MHCC97L, SMCC-7721, Huh-7, MHCC97H and LO3) up-regulated We totally identified a set of four lncRNAs(MIR100HG, SERHL, CTD-2574D22.4 and SNHG21) that were significantly correlated with patient's survival. We then measured the expression levels of these four lncRNAs using TCGA data, and found that it was significant. 29684484 2018 Characterization of long non-coding RNAs to reveal potential prognostic biomarkers in hepatocellular carcinoma. SFTA1P SFTA1P, SFTPF NA ENSG00000225383 NA GRCh38_10:10784437-10794980 gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissues, cell lines (BGC823 and SGC7901 and GES-1) down-regulated We report that a pseudogene-derived lncRNA named surfactant associated 1, pseudogene (SFTA1P), which is 693-nt long, was significantly down-regulated in GC tissues compared with that in the adjacent normal tissues. In addition, decreased SFTA1P expression was strongly correlated with advanced tumor lymph node metastasis (TNM) stage, larger tumor size, lymphatic metastasis, and poor prognosis of patients with GC. Moreover, gain-of-function experiments revealed that the overexpression of SFTA1P inhibits cell proliferation, migration, and invasion, thus verifying the tumor inhibitory role of SFTA1P in GC. Furthermore, we investigated the potential action mechanism of SFTA1P. Our results showed that down-regulation of SFTA1P may be associated with decreased TP53 expression. 29523596 2018 The pseudogene-derived long non-coding RNA SFTA1P suppresses cell proliferation, migration, and invasion in gastric cancer. SFTA1P SFTA1P, SFTPF NA ENSG00000225383 NA GRCh38_10:10784437-10794980 lung adenocarcinoma C34 M8140/3 qPCR, Cell transfection, Cell migration and invasion assay etc. LAD tissues, cell lines (A549, H1975, SPC-A1, PC9, H1299, H1650, and SK-MES-1) down-regulated SFTA1P expression was down-regulated in all LUAD cell lines compared with HBE. In addition, gain-of-function studies including growth curves, migration, invasion assays, and in vivo studies were performed to verify the tumor suppressor role of SFTA1P in non-small cell lung cancer. 28231733 2017 The pseudogene-derived long noncoding RNA SFTA1P is down-regulated and suppresses cell migration and invasion in lung adenocarcinoma. Skp2 SKP2, FBL1, FBXL1, FLB1, p45 NA ENSG00000145604 NA GRCh38_5:36151989-36184319 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. NSCLC tissues, NSCLC cell lines (ATCC, Rockville, MD, USA) differential expression These data suggest that the Skp2 may be regulated by Meg3 at post-transcriptional level. Bioinformatics analyses showed that miR-3163 bound to 3'-UTR of Skp2 mRNA in NSCLC cells to inhibit its translation, which was supported by luciferase reporter assay. Meg3 augmented the effects of miR-3163 on Skp2 mRNA, possibly through binding-induced function enhancement, which was supported by the double fluorescent in situ hybridization showing co-localized intracellular Meg3 and miR-3163 signals in NSCLC cells. The miR-3163 levels in NSCLC were not different from in NT, suggesting that the regulation of Skp2 in NSCLC by miR-3163 may require coordination of Meg3 26482610 2015 Skp2 regulates non-small cell lung cancer cell growth by Meg3 and miR-3163 SLCO4A1-AS1 SLCO4A1-AS1 100127888 ENSG00000232803 NR_024470 GRCh38_20:62663019-62666724 colorectal cancer C19.9 NA microarray, qPCR etc. cell lines (HCT116, RKO, HT29, HCT15, Lovo, Caco-2, SW480 and SW620) up-regulated We randomly selected three lncRNAs that were significantly up-regulated in tumors compared with normal tissues according to the above RNA-Seq data analysis for experimental validation (SNHG15, MAFG-AS1 and SLCO4A1-AS1). In agreement with these findings, the q-PCR results confirmed the changes in expression patterns for the three lncRNAs in all eight CRC cell lines. 27147563 2016 Integrative analysis reveals clinical phenotypes and oncogenic potentials of long non-coding RNAs across 15 cancer types. SLINKY NA NA NA NA NA kidney cancer C64 NA qPCR, RIP Clear cell renal cell carcinoma cell lines up-regulated In ccRCC cell lines, SLINKY knockdown reduced cancer cell proliferation (with cell-cycle G1 arrest) and induced transcriptome changes enriched for cell proliferation and survival processes. Notably, the genes affected by SLINKY knockdown in cell lines were themselves prognostic and correlated with SLINKY expression in the ccRCC patient samples. 28423633 2017 Novel lincRNA SLINKY is a prognostic biomarker in kidney cancer SMARCC2 NA NA ENSG00000139613 NA GRCh38_12:56162983-56189567 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (AGS, SGC-7901, MKN-45,BGC-823, HGC-27), gastric cancer tissues up-regulated LncRNA SMARCC2 inhibits the expression of miR-551b-3p through binding to its mRNA response elements in gastric cancer cells. Overexpression of LncRNA SMARCC2 enhances the proliferation and migration of gastric cancer cells, while inhibition of LncRNA SMARCC2 does the opposite. TMPRSS4 is a direct target gene of miR-551b-3p. We conclude that miR-551b-3p functions as a tumour suppressor gene in gastric cancer, and its function is regulated by LncRNA SMARCC2/miR-551b-3p/TMPRSS4 axis. 29337109 2018 Molecular mechanisms of lncRNA SMARCC2/miR-551b-3p/TMPRSS4 axis in gastric cancer. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62852252-62855488 astrocytoma NA M9400/3 qPCR etc. astrocytoma tissues up-regulated Our analysis ultimately generated a list of 7 lncRNAs that were differentially expressed in astrocytomas in comparison to the NAT samples. Among these lncRNAs, ENST00000244906, ENST00000545440, NR_002809 and ENST00000436616 were shown to be upregulated by a factor greater than twofold, whereas 3 lncRNAs, XLOC_010967, BC002811 and ASO1937, were shown to be downregulated by a factor greater than twofold. 26252651 2016 The Use of Three Long Non-Coding RNAs as Potential Prognostic Indicators of Astrocytoma. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 neuroblastoma NA M9500/3 qPCR cell lines (SK-N-DZ, SK-N-SH, SK-N-BE(2)-C) up-regulated In conclusion, our study unveils that SNHG1 is up-regulated by MYCN amplification and could be a potential prognostic biomarker for high-risk NB intervention. Kaplan-Meier analysis shows that higher expression of SNHG1 is significantly associated with poor patient survival. 27517149 2016 Co-expression analysis identifies long noncoding RNA SNHG1 as a novel predictor for event-free survival in neuroblastoma SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 laryngeal squamous cell cancer C32.3 NA qPCR, Western blot, RNAi etc. laryngeal carcinoma tissues up-regulated SNHG1 knockdown could significantly inhibit the proliferation of laryngeal carcinoma HEp-2 cells. Flow cytometry showed that transfection with si-SNHG1 could promote the apoptosis of HEp-2 cells.SNHG1 knockdown could inhibit invasion and migration of HEp-2 cells through inhibiting the epithelial-mesenchymal transition (EMT) process and expressions of matrix metalloproteinase-2 (MMP-2) and MMP-9 in cells. 29565491 2018 Up-regulation of long non-coding RNA SNHG1 contributes to proliferation and metastasis in laryngeal squamous cell carcinoma. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 osteosarcoma NA M9180/3 qPCR, Luciferase reporter assay, Western blot osteosarcoma tissues, cell lines (MG-63, U2OS,Saos-2,SOSP-9607, hFOB 1.19) up-regulated high SNHG1 expression predicts poor overall survival of OS patients.Knockdown of SNHG1 inhibited cell growth and metastasis of OS in-vitro and in-vivo. there was reciprocal repression between SNHG1 and miR-326 which act as a tumor suppressor in OS cells, and exhibiting a strong negative relationship between SNHG1 and miR-326 expression in OS tissues. SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS. 29115574 2017 Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 nasopharyngeal cancer C11 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (HEK293T , N69, CNE,HNE-1), NPC tissues up-regulated Down-regulation of SNHG1 facilitated the expression of miR-145-5p and further suppressed the level of NAUK1 in CNE and HNE-1 cells. Silencing of SNHG1, up-regulation of miR-145-5p and inhibition of NAUK1 by relative transfection all attenuated the aggressiveness of CNE and HNE-1 cells both in vivo and in vitro. Moreover, the impaired cell migration and invasion by SNHG1 siRNA could be rescued by cotransfection of miR-145-5p in CNE and HNE-1 cells. LncRNA SNHG1 promoted the expression of NUAK1 by down-regulating miR-145-5p and thus promoted the aggressiveness of nasopharyngeal carcinoma cells through AKT signalling pathway and induced epithelial-mesenchymal transition (EMT). 29575772 2018 LncRNA SNHG1 functions as a ceRNA to antagonize the effect of miR-145a-5p on the down-regulation of NUAK1 in nasopharyngeal carcinoma cell SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 glioma NA M9380/3 qPCR etc. glioma tissues, cell lines (U251 and U87) up-regulated SNHG1 expression was measured in glioma tissues and cell lines.The association between SNHG1 expression in tissues and clinicopathological characteristics and prognosis in glioma patients was also explored. SNHG1 was highly expressed in glioma tissues, and its upregulation was closely related to old age.ectopic expression of SNHG1 enhanced cell proliferation and cell invasion and reduced cell apoptosis in vitro, while SNHG1 knockdown reversed these effects. High expression of SNHG1 correlates with large tumor size, poor differentiation, aggressive BCLC stage and poor prognosis of HCC patients. High expression of SNHG1 also exacerbates HCC cell proliferation, invasion, and migration in vitro via suppression of miR-195 and p53.SNHG1 promoted cell proliferation via proto-oncogene CST3 upregulation by acting as a non-degradable sponge for the tumor suppressor miR-338 in esophageal cancer cells. 28501778 2017 Upregulation of the long non-coding RNA SNHG1 predicts poor prognosis, promotes cell proliferation and invasion, and reduces apoptosis in glioma. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 gastric cancer C16 NA qPCR, Western blot etc. gastric tissue, cell lines (NCI-N87, MKN-45) up-regulated The expression of lncRNA SNHG1 in gastric cancer tissues was significantly higher than that in adjacent tissues and was correlated with TNM stage, T stage, and lymph node metastasis. The survival time of patients with higher expression level of lncRNA-SNHG1 was significantly lower than that of the lower expression level. LncRNA-SNHG1 accelerated the proliferation of gastric cancer cells obviously and increased the expression of DNMT1. 28754593 2017 LncRNA-SNHG1 contributes to gastric cancer cell proliferation by regulating DNMT1 SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 esophageal cancer C15 NA qPCR, Western blot esophageal squamous cell cancertissues, cell lines (Eca109 and TE-1) up-regulated increased lncRNA SNHG1 expression levels markedly correlated with lymph node etastasis, depth of invasion, TNM stage and reduced over survival time in ESCC patients.knockdown of lncRNA SNHG1 could inhibit cell proliferation and cell invasion capacity and cell Epithelial-Mesenchymal Transition (EMT) phenomenon by up-regulation E-cadherin and down-regulating Vimentin and N-cadherin in ESCC cells.knockdown of SNHG1 suppressed the Notch signaling pathway by reducing the Notch1 and Hes-1 expression levels in ESCC cells. 29081407 2017 Downregulation of SNHG1 suppresses cell proliferation and invasion by regulating Notch signaling pathway in esophageal squamous cell cancer. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. liver cancer tissues, cell lines (SMMC-7721, MHCC97H, HCCLM3 and HepG2) up-regulated we found SNHG1 was upregulated in HCC tissues in comparison with adjacent liver tissues in both publicly available microarray data and our own cohort. High SNHG1 expression was correlated with large tumor size, poor differentiation, and aggressive BCLC stage. Kaplan-Meier survival analysis demonstrated that high SNHG1 expression predicts poor prognosis of HCC patients. Gain-of-function and loss-of function experiments showed that SNHG1 promotes HCC cells proliferation, cell cycle progression, and inhibits HCC cells apoptosis. Further experiments revealed that SNHG1 promotes HCC cells proliferation through inhibiting p53 and p53-target genes expression 27133041 2016 Long noncoding RNA SNHG1 predicts a poor prognosis and promotes hepatocellular carcinoma tumorigenesis SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. NSCLC tissues, cell lines (A549, SPC-A1, H23 and NCI-H520) up-regulated SNHG1 was up-regulated in non-small cell lung cancer (NSCLC) tissues and cell lines. Furthermore,SNHG1 inhibition suppressed NSCLC cell proliferation both in vitro and in vivo. We also found that miR-101-3p could act as a target of SNHG1 in NSCLC and the inhibition of NSCLC progression induced by SNHG1 knockdown required the activity of miR-101-3p.In addition,we identified that SOX9 acted as a target of miR-101-3p,and SOX9 played the oncogenic role in NSCLC by activating Wnt/B-catenin signaling pathway. 28147312 2017 Upregulated lncRNA SNHG1 contributes to progression of non-small cell lung cancer through inhibition of miR-101-3p and activation of Wnt/B-catenin signaling pathway. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (LNCaP) down-regulated Five lncRNAs, RP1-4514.2, SUZ12P1, SNHG5, LINC01138, and SNHG1, were down-regulated under DHT treatment. Five lncRNAs, KLKP1, LINC00969, LINC-PINT, TUG1 and MIR17HG, were up-regulated under DHT treatment. Notably, RP1-4514.2 and LINC01138 were induced and KLKP1 was reduced over 2 fold after AR silenced, suggesting the involvement of AR in androgen-mediated regulation of these lncRNAs expressions. 27556357 2016 Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (WPMY-1, DU145, PC-3 and LNCaP) up-regulated To further validate the results, we examined the expression levels in 11 normal prostate tissues and 14 prostate cancer tissues with real-time PCR. All of these lncRNAs except LINC00969, were expressed significantly higher in prostate cancer samples compared with normal prostate tissues, which were consistent with the TCGA and microarray results. Then, the expression levels of ten lncRNAs were validated in the noncancerous prostatic cells WPMY-1 and four human prostate cancer cell lines by qRT-PCR. It turned out that most of the ten lncRNAs were up-regulated in prostate cancer cell lines and showed a similar expression pattern in patient samples. 27556357 2016 Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 colorectal cancer C19.9 NA qPCR, Western blot colorectal cancer tissues, cell lines (LOVO and HCT116) up-regulated SNHG1 expression was correlated with advanced colorectal cancer stage and tumor recurrence.SNHG1 promoted cell proliferation by acting as a sponge of miR-145, a well known tumor suppressor of colorectal cancer.colorectal cancer patients with higher expression of SNHG1 had a worse prognosis.SNHG1 may act as a potential therapeutic target for the treatment of colorectal cancer. 29416759 2017 SNHG1 promotes cell proliferation by acting as a sponge of miR-145 in colorectal cancer. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 colorectal cancer C19.9 NA qPCR, Western blot colorectal cancer tissues, cell lines (CCC-HIE-2,SW480, HCT116, HT-29, LOVO, CaCO-2) up-regulated SNHG1 expression levels were upregulated aberrantly in colorectal cancer tissues and colorectal cancer cell lines. patients with high SNHG1 expression level had poorer overall survival (OS) and progression-free survival (PFS) than those with low SNHG1 expression.increased SNHG1 expression was proved to be an independent unfavorable prognostic indicator for CRC.SNHG1 silencing inhibited the growth and metastasis and induced apoptosis of CRC cell lines.SNHG1 may induce the activation of the WNT/B-catenin pathway through regulating B-catenin expression and transcription factor-4 (TCF-4), cyclin D1 and MMP-9. 29340086 2017 Up-regulation of lncRNA SNHG1 indicates poor prognosis and promotes cell proliferation and metastasis of colorectal cancer by activation of the Wnt/B-catenin signaling pathway. SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 23642 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 cholangiocarcinoma NA M810/3 qPCR, RNA-seq, Microarray, RIP, ChIP, Western blot, Flow cytometry assay, CCA cell lines (HuCCT, RBE). normal HIBEpiC. 92 pairs of cancer and 91 normal tissue samples. up-regulated These data verified a major function of the epigenetic regulation of SNHG1 in CCA oncogenesis, in addition to its likely function as a target for CCA interruption.To summarize, as suggested by our research works, the regulatory mechanism in the tumorigenesis of SNHG1, by which SNHG1 could promote malignancy of CCA through regulating the transcription of CDKN1A epigenetically in the nucleus, facilitates cell survival and metastasis of CCA. SNHG1 epigenetically silenced CDKN1A transcription through EZH2-mediated H3K27me3 demethylation. 29970899 2018 Epigenetic silencing of tumor suppressor gene CDKN1A by oncogenic long non-coding RNA SNHG1 in cholangiocarcinoma. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 cervical cancer C53 NA qPCR, Luciferase reporter assay cervical cancer tissues, cell lines (C33A, ME-180, CaSki, HeLa and SiHa, NC104) up-regulated NHG12 was found to be abnormally elevated in human cervical cancer tissues compared with paired adjacent normal tissues.high SNHG12 expression in tumor tissues was significantly correlated with vascular involvement,lymph node metastasis,advanced FIGO stage and poor prognosis.the knockdown of SNHG12 was found to inhibit proliferation,migration and invasion of cervical cancer cells in vitro, and silencing SNHG12 was shown to suppress tumor growth in a nude mouse model. SNHG12 functioned as an endogenous sponge for miR-424-5p, thereby downregulating the expression of miR-424-5p in cervical cancer.the inhibition of miR-424-5p in SNHG12-depleted cells partially reversed the effects on cervical cancer cell apoptosis, adhesion and invasion. 29533945 2018 Upregulation of Long Non-Coding RNA Small Nucleolar RNA Host Gene 12 Contributes to Cell Growth and Invasion in Cervical Cancer by Acting as a Sponge for MiR-424-5p. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 glioma NA M9380/3 Microarray, qPCR, Western blot, in vitro knockdown, RIP cell lines (U87, U251), glioma tissues up-regulated Long non-coding RNA (lncRNA) dysregulation is involved in tumorigenesis and regulation of diverse cellular processes in gliomas.SNHG12 significantly inhibited malignant biological behaviors of glioma cells. miR-195, downregulated in glioma tissues and cells, significantly impaired the malignant progression of glioma cells.TDP43 upregulated miR-195 in an SNHG12-dependent manner. SNHG12 and miR-195 were in an RNA-induced silencing complex (RISC).Inhibition of SNHG12 combined with restoration of miR-195 robustly reduced tumor growth in vivo. SOX5 was overexpressed in glioma tissues and cells.miR-195 targeted SOX5 3' UTR in a sequence-specific manner. Gelsolin was activated by SOX5. More importantly, SOX5 activated SNHG12 promoter and upregulated its expression, forming a feedback loop. 29499929 2017 Inhibition of TDP43-Mediated SNHG12-miR-195-SOX5 Feedback Loop Impeded Malignant Biological Behaviors of Glioma Cells. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc. HCC tissues, cell line (SK-Hep1) up-regulated SNHG12 was significantly higher in the HCC tissues than that in the adjacent normal tissues.There were direct interactions between miR-199a/b-5p and the binding site of SNHG12.SNHG12 functioned as an endogenous sponge for miR-199a/b-5p to regulate the expression of MLK3 and affect the NF-kB pathway. 28073380 2017 Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) promotes tumorigenesis and metastasis by targeting miR-199a/b-5p in hepatocellular carcinoma. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 papillary thyroid cancer NA M8260/3 qPCR, Western blot, in vitro knockdown etc. cell lines (K1, BCPAP, TPC-1, Nthy-ori3-1), PTC tissue up-regulated The SNHG12 expression is relatively high in PTC tissues and cells. In-vivo/in-vitro experiments prove that SNHG12 can promote the proliferation and metastasis of PTC cells through influencing the Wnt/B-catenin signaling pathway. 29630517 2018 LncRNA SNHG12 promotes the proliferation and metastasis of papillary thyroid carcinoma cells through regulating wnt/B-catenin signaling pathway. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Flow cytometry assay, MTT assay etc. CRC tissues, cell lines (SW480, LOVO, HCT116, HT29) up-regulated Increased levels of SNHG12 were observed in CRC tissues and in CRC cells. SNHG12 promoted the cell proliferation of CRC cells. In addition, SNHG12 overexpression boosted the cell cycle progression of SW480 cells transfected with pcDNA-SNHG12 and SNHG12 knockdown inhibited the cell cycle progression of HT29 cells transfected with si-SNHG12. SNHG12 also inhibited the cell apoptosis of CRC cells. We also found that SNHG12 increased the expression of cell cycle-related proteins and suppressed the expression of caspase 3. 28225893 2017 LncRNA SNHG12 promotes cell growth and inhibits cell apoptosis in colorectal cancer cells. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 breast cancer C50 NA qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay, Cell proliferation assay etc. TNBC tissues, cell lines (MDA-MB-231 and BT-549) up-regulated SNHG12 is upregulated in TNBC. Mechanistic investigations show that SNHG12 is a direct transcriptional target of c-MYC. Silencing SNHG12 expression inhibits TNBC cells proliferation and apoptosis promotion, whereas SNHG12 overexpression has the opposite effect. In addition, we reveal that SNHG12 may promote cells migration by regulating MMP13 expression. 28337281 2017 C-MYC-induced upregulation of lncRNA SNHG12 regulates cell proliferation, apoptosis and migration in triple-negative breast cancer. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 non small cell lung cancer C34 M8046/3 qPCR, Western blot NSCLiver Cancer tissue, NSCLiver Cancer cell line (A549 )and DDP-resistant cell line A549/DDP up-regulated Overall, our study is the first to identify a SNHG12-miR-181a-MAPK/Slug axis to elucidate in part how SNHG12 exert functions in NSCLC MDR, providing a novel therapeutic target to overcome MDR in NSCLC. 29137407 2017 LncRNA SNHG12 contributes to multidrug resistance through activating the MAPK/Slug pathway by sponging miR-181a in non-small cell lung cancer. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown GC tissues, human gastric cancer cell lines (SGC7901, NCI-N87 and AGS ) up-regulated SNHG12 was significantly overexpressed in GC. Additionally, inhibition of SNHG12 in GC cell lines SGC-7901 and AGS suppressed cell growth, colony formation, proliferation and invasion. MicroRNA-320,a putative target gene of SNHG12, was inversely correlated with SNHG12 expression in GC tissues and cell lines. In addition,the present study determined that miR-320 was directly regulated by SNHG12 and suppression of miR-320 expression reversed the inhibitory effects of SNHG12 siRNA on GC cell proliferation and invasion. 29207106 2017 LncRNA SNHG12 regulates gastric cancer progression by acting as a molecular sponge of miR-320. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP osteosarcoma tissues, osteosarcoma cell lines (143B, U2OS, MG63 and HOS) up-regulated SNHG12 was significantly upregulated in both osteosarcoma tissues and cell lines and osteosarcoma patients with high levels of SNHG12 tended to have a poor prognosis. Dual-luciferase reporter and RIP assays were conducted to confirm that SNHG12 functioned as a ceRNA, modulating the expression of Notch2 by sponging miR-195-5p in osteosarcoma. 29229388 2017 LncRNA SNHG12 promotes tumorigenesis and metastasis in osteosarcoma by upregulating Notch2 by sponging miR-195-5p. SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 85028 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 glioma C34 M8140/3 qRT-PCR, RIP, RNA pull-down analysis, Western blot analysis Primary tumor samples and matched adjacent non-carcinoma tissues, The normal human skin fibroblast HF cell line and the glioma cell lines, ( U87, LN229, U373 and U251 ) up-regulated SNHG12 was significantly upregulated in glioma tissues and cell lines.The silencing of SNHG12 expression by RNA interference led to a reduced viability and mobility, and in an increased apoptosis of human glioma cells.SNHG12 was associated with and was stabilized by HuR. 30015836 2018 Long non-coding RNA SNHG12 promotes the proliferation and migration of glioma cells by binding to HuR. SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 glioma NA M9380/3 qPCR, Western blot, RIP etc. cell lines (hCMECs/D3) up-regulated SNHG15 is highly expressed in glioma-induced endothelial cells while miR-153 is lowly expressed in glioma-induced endothelial cells.SNHG15 negatively regulates the expression of miR-153 and miR-153 negatively regulates the expression of VEGFA and Cdc42, which in turn affects glioma vascular endothelial cell proliferation, migration and tube formation in vitro. Therefore, we suggest that SNHG15 and miR-153 are novel targets for glioma anti-angiogenesis therapy. 29048682 2017 SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153 SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 colon cancer C18 NA RNA-seq, qPCR etc. cell lines (HEK-293T, SW1116, HCT116, SW480, and SW620) down-regulated Slug is a fast-turnover transcription factor critical for controlling cell fate and cancer cell invasion and metastasis. LncRNA SNHG15 transcription is upregulated in a variety of human cancers according to The Cancer Genome Atlas. Ectopic expression of SNHG15 promoted colon cancer cell migration in vitro, accelerated xenografted tumor growth in vivo, and elevated levels of SNHG15 were associated with poor prognosis for colon cancer patients. Mechanistically, SNHG15 maintains Slug stability in living cells by impeding its ubiquitination and degradation through interaction with the zinc finger domain of Slug. 29604394 2018 Long non-coding RNA SNHG15 interacts with and stabilizes transcription factor Slug and promotes colon cancer progression. SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 colorectal cancer C19.9 NA microarray, qPCR etc. cell lines (HCT116, RKO, HT29, HCT15, Lovo, Caco-2, SW480 and SW620) up-regulated We randomly selected three lncRNAs that were significantly up-regulated in tumors compared with normal tissues according to the above RNA-Seq data analysis for experimental validation (SNHG15, MAFG-AS1 and SLCO4A1-AS1). In agreement with these findings, the q-PCR results confirmed the changes in expression patterns for the three lncRNAs in all eight CRC cell lines. 27147563 2016 Integrative analysis reveals clinical phenotypes and oncogenic potentials of long non-coding RNAs across 15 cancer types. SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated The lncRNA SNHG15 expression was significantly upregulated in tumor tissues compared with that in adjacent non-tumor tissues. It is also proved that lncRNA SNHG15 expression was associated with histological grade, TNM stage, and vein invasion. 27212162 2016 Long noncoding RNA SNHG15, a potential prognostic biomarker for hepatocellular carcinoma. SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 gastric cancer C16 NA qPCR, RNAi, Western blot etc. gastric adenocarcinoma cancer cell lines (SGC7901, BGC823, MGC803, AGS, MKN45, GES-1) up-regulated We identified a novel lncRNA SNHG15, whose expression was upregulated in tumor tissues in 106 patients with gastric cancer (GC) compared with those in the adjacent normal tissues. Furthermore, increased SNHG15 expression was positively correlated with invasion depth, advanced tumor node metastasis (TNM) stage, and lymph node metastasis. SNHG15 levels were robust in differentiating GC tissues from controls. Kaplan-Meier analysis demonstrated that elevated SNHG15 expression contributed to poor overall survival and disease-free survival of patients. A multivariate survival analysis also indicated that SNHG15 could be an independent prognostic marker. Furthermore, knockdown of SNHG15 expression by siRNA could inhibit cell proliferation and invasion and induce apoptosis, while ectopic expression of SNHG15 promoted cell proliferation and invasion in GC cells partly via regulating MMP2 and MMP9 protein expression 26662309 2015 Upregulated expression of long noncoding RNA SNHG15 promotes cell proliferation and invasion through regulates MMP2/MMP9 in patients with GC SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (A549, H460, SK-MES-1, Calu-3,NHBE, HEK-293T), NSCLC tissue up-regulated LncRNA SNHG15 was significantly upregulated in NSCLC tissue samples and cells, and its overexpression was associated with poor prognosis of NSCLC patients. In vitro, loss-of-functional cellular experiments showed that SNHG15 silencing significantly inhibited the proliferation, promoted the apoptosis, and induced the cycle arrest at G0//G1 phase. In vivo, xenograft assay showed that SNHG15 silencing suppressed tumor growth of NSCLC cells. Besides, SNHG15 silencing decreased CDK14 protein expression both in vivo and vitro. Bioinformatics tools and luciferase reporter assay confirmed that miR-486 both targeted the 3'-UTR of SNHG15 and CDK14 and was negatively correlated with their expression levels. In summary, our study conclude that the ectopic overexpression of SNHG15 contribute to the NSCLC tumorigenesis by regulating CDK14 protein via sponging miR-486, providing a novel insight for NSCLC pathogenesis and potential therapeutic strategy for NSCLC patients. 29630731 2018 Long non-coding RNA SNHG15 promotes CDK14 expression via miR-486 to accelerate non-small cell lung cancer cells progression and metastasis. SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 breast cancer C50 NA RT-PC, Western blot, Luciferase reporter assay, in vitro knockdown Primary cancer tissues, breast cancer cell lines (MCF-7, BT-20, ZR-75-1, MDA-MB-231) up-regulated SNHG15 downregulation suppressed cell migration and invasion in MCF-7 and BT-20 cells, and inhibited epithelial-mesenchymal transition (EMT).In mechanism, we found that SNHG15 acted as a competing endogenous RNA to sponge miR-211-3p,which was downregulated in breast cancers and inhibited cell proliferation and migration. Our results showed that there was a negative correlation between SNHG15 and miR-211-3p expression in breast cancer patients. 29217194 2017 Long noncoding RNA SNHG15 promotes human breast cancer proliferation, migration and invasion by sponging miR-211-3p. SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay etc. OS tissues, cell lines (143B, U2OS, HOS, MG63, and SaOS2) up-regulated up-regulation of SNHG15 was inversely correlated with miR-141 expression in OS tissues.SNHG15 could directly interact with miR-141 and regulate its expression.SNHG15 contributes to proliferation, invasion, migration and autophagy in OS by negatively regulating miR-141,providing a new potential target and prognostic biomarker for the treatment of OS. 28720111 2017 LncRNA SNHG15 contributes to proliferation, invasion and autophagy in osteosarcoma cells by sponging miR-141. SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 pancreatic cancer C25 NA Western blot, RIP pancreatic cancer tissues, PC cell lines. up-regulated Our results reported that SNHG15 could act as an oncogene in PC, revealing its potential value as a biomarker for early detection and individualized therapy.Compared with the steadily increasing survival rates in some cancers, colorectal cancer is characterized by a poor prognosis, which limits the 5-year relative survival to only 8 %. 29137412 2017 Long non-coding RNA SNHG15 inhibits P15 and KLF2 expression to promote pancreatic cancer proliferation through EZH2-mediated H3K27me3 SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 non small cell lung cancer C34 M8046/3 qPCR, western blot lung cancer tissues, cell lines (PC9, H1703, SK-MES-1, SPC-A1 and A549) up-regulated The expression of SNHG15 in lung cancer tissues is significantly higher than that in para-carcinoma tissues, the prognosis of patients accompanied with a high expression of SNHG15 is poor 29771418 2018 Long non-coding RNA SNHG15 indicates poor prognosis of non-small cell lung cancer and promotes cell proliferation and invasion SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 100507246 ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 colorectal cancer C19.9 NA qPCR, RNAi etc. CRC tissues, cell lines (LoVo, Caco-2, DLD1, SW620, SW480, HCT8, HCT116 etc.) down-regulated In this study, we demonstrated that ncRAN expression is significantly down-regulated in tumor tissue and CRC cell lines compared with adjacent normal tissue and a normal intestinal mucous cell line. Reduced expression of ncRAN was detected in poorly differentiated or undifferentiated tumors and in tumors with liver metastases. Kaplan-Meier analysis indicated that patients with lower ncRAN expression have a worse overall survival. 24519959 2014 Down-regulation of ncRAN, a long non-coding RNA, contributes to colorectal cancer cell migration and invasion and predicts poor overall survival for colorectal cancer patients. SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 100507246 ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 bladder cancer C67 NA qPCR etc. bladder cancer tissues, cell lines (RT4, T24, J82 etc.) up-regulated Expression of ncRAN was significantly higher in bladder cancers compared with normal tissues and in invasive tumor compared with superficial ones. Consistently, ncRAN expressed significantly higher in invasive bladder tumor cell lines (5637, T24, J82) than that in superficial tumor cell line (RT4). Overexpression of ncRAN in RT4 cells significantly enhanced cell proliferation, migration, and invasion. Silencing of ncRAN improved chemotherapy sensitivity in 5637 cells. 21147498 2011 ncRAN, a newly identified long noncoding RNA, enhances human bladder tumor growth, invasion, and survival. SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 100507246 ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 glioma NA M9380/3 qPCR, Luciferase reporter assay, Western blot brain glioma tissues, cell lines (NHAs, U251, H4, SW1783 and LN229) up-regulated SNHG16 was highly expressed in glioma tissues and cell lines, which was related to poorer clinicopathologic features and shorter survival time. Knockdown of SNHG16 inhibits the viability and induces apoptosis of glioma cells. Further investigation revealed that SNHG16 could up-regulate the expression of miR-4518 targeted gene PRMT5 via acting as an endogenous sponge of miR-4518.SNHG16 also affects the expression of Bcl-2 family proteins and the activation of PI3K/Akt signaling pathway. the overall survival rate was lower in the high SNHG12 expression group than in the low SNHG12 expression group 29529599 2018 LncRNA SNHG16 Functions as an Oncogene by Sponging MiR-4518 and Up-Regulating PRMT5 Expression in Glioma. SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 100507246 ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 cervical cancer C53 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP cervical cancer tissues, Cervical cancer cell lines (HeLa, CaSki, SiHa, and C33A) up-regulated miR-216-5p could interact with SNHG16 and there existed a negative correlation between the expression levels of miR-216-5p and SNHG16 in cervical cancer specimens. SNHG16 directly targeted miR-216-5p by harboring the binding sites of microRNA in the SNHG16 sequence.Additionally, bioinformatics analysis provided an evidence that ZEB1 was a potential target of miR-216-5p. 29126969 2017 SNHG16/miR-216-5p/ZEB1 signal pathway contributes to the tumorigenesis of cervical cancer cells. SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 100507246 ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 ovarian cancer C56.9 NA qPCR, Western blot, in vitro knockdown tumor tissues, ovarian cancer cells (SKOV-3, ES2, HO8910, OMC685) up-regulated the expression of SNHG16 in ovarian cancer was significantly higher than that in normal tissues, and the difference was statistically significant. Compared with patients with lower expression of SNHG16, patients with higher expression of SNHG16 had higher tumor stage, high rate of distant metastasis and low overall survival rate. Compared with the negative control si-NC group, the cell proliferation, invasion and migration ability in SNHG16 knockdown group (si-SNHG16) significantly decreased. Western Blot showed that after knockdown of SNHG16, expressions of P-AKT and MMP9 decreased significantly, while there was no significant change in the total AKT level. 29461589 2018 Long non-coding RNA SNHG16 promotes cell growth and metastasis in ovarian cancer. SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 100507246 ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 bladder cancer C67 NA qPCR, Western blot, RNA immunoprecipitation bladder cancer tissues, bladder cancer cells (T-24, BIU87, and 5637) up-regulated the level of SNHG16 was evidently enhanced both in tissues and cell lines of bladder cancer. Patients with highly expressed SNHG16 suffered from poor overall survival. Multivariable Cox proportional hazards regression analysis implied that highly expressed SNHG16 could be used as an independent prognostic marker. It could be known from functional assays that silenced SNHG16 impaired cell proliferation, owing to the effects of SNHG16 on cell cycle and apoptosis. Finally, mechanism experiments revealed that SNHG16 could epigenetically silence the expression of p21. 29234154 2017 LncRNA-SNHG16 predicts poor prognosis and promotes tumor proliferation through epigenetically silencing p21 in bladder cancer. SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 100507246 ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 esophageal squamous cell cancer NA NA qPCR, Western blot, Flow Cytometry, Luciferase Assay, etc. ESCC tissues, cell lines (TE-13, TE-1,EC-1, Eca-109, HEEC) up-regulated Kaplan-Meier assay showed that the survival time of patients with high SNHG16 expression was significantly shorter than those with low SNHG16 expression (p = 0.0017). Loss-of-function experiments revealed that knockdown of SNHG16 suppressed proliferation and invasion and induced apoptosis of ESCC cells. Mechanistically, Wnt/B-catenin signaling pathways were actively modulated by SNHG16 in ESCC cells. 29949155 2018 LncRNA SNHG16 predicts poor prognosis in ESCC and promotes cell proliferation and invasion by regulating Wnt/β-catenin signaling pathway. SNHG17 NA 388796 ENSG00000196756 NR_015366 GRCh38_20:38420588-38435353 colorectal cancer C19.9 NA qPCR, RIP, Western blot etc. cell lines (DLD1, HCT116, SW480, LOVO) up-regulated SNHG17 was upregulated in CRC tissues, and that its overexpression was significantly correlated with tumor size, TNM stage, and lymph node metastasis in CRC patients. Moreover, SNHG17 knockdown significantly inhibited the proliferation of CRC cells, and induced cell cycle G1/G0 phase arrest and cell apoptosis. Consistent with these findings, SNHG17 silencing inhibited tumor growth in vivo. Mechanistic studies revealed the capability of lncRNA SNHG17 to epigenetically suppress P57 by binding to enhancer of zeste homolog 2 (a key component of polycomb repressive complex 2) in CRC cells, and quantitative real-time polymerase chain reaction assays demonstrated that SNHG17 expression levels were inversely correlated with those of P57 in CRC tissues. Furthermore, rescue experiments confirmed that SNHG17 exerted oncogenic functions partly through regulating P57 expression. 28933484 2017 Long non-coding RNA SNHG17 is an unfavourable prognostic factor and promotes cell proliferation by epigenetically silencing P57 in colorectal cancer SNHG18 SNHG18 100505806 ENSG00000250786 NR_045196 GRCh38_5:9546200-9550609 glioma NA M9380/3 microarray, qPCR, RNAi, Western blot, ISH etc. cell lines (M059K, M059J, U87 and U251) up-regulated The expression of SNHG18 was remarkably upregulated in clinical glioma tissues compared with normal brain tissues. SNHG18 expression was associated with the clinical tumor grade and correlated negatively with isocitrate dehydrogenase 1 mutation. In addition, knockdown of SNHG18 with short hairpin RNA suppressed the radioresistance of glioma cells, and transgenic expression of SNHG18 had the opposite effect. 27788958 2016 Upregulation of Long Noncoding RNA Small Nucleolar RNA Host Gene 18 Promotes Radioresistance of Glioma by Repressing Semaphorin 5A. SNHG20 SNHG20, C17orf86, LINC00338, NCRNA00338, SCARNA16HG 654434 ENSG00000234912 NR_027058 GRCh38_17:77086716-77094990 cervical cancer C53 NA qPCR etc. cervical cancer tissue, cell lines (HeLa, SiHa, C33A, SW756, and ME-180) up-regulated SNHG20 expression was significantly increased in cervical cancer. MiR-140-5p acted as a downstream target of SNHG20. SNHG20 inhibition or miR-140-5p overexpression reduced cervical cancer cells proliferation and invasion ability. Furthermore, we identified that ADAM10 could act as a potential target of miR-140-5p. MEK/ERK signaling could be inhibited by miR-140-5p mimics in cervical cancer cells. In addition, ADAM10 overexpression abrogated the effect of miR-140-5p mimics on cervical cancer cells proliferation and invasion. 29604594 2018 LncRNA SNHG20 promotes cell proliferation and invasion via miR-140-5p-ADAM10 axis in cervical cancer. SNHG20 SNHG20, C17orf86, LINC00338, NCRNA00338, SCARNA16HG 654434 ENSG00000234912 NR_027058 GRCh38_17:77086716-77094990 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. lung tissues, cell lines (PC9, SPC-A1, NCIH1975, H1299, A549) up-regulated SNHG20 was upregulated in non-small cell lung cancer (NSCLC) tissues compared with normal samples.Higher SNHG20 expression was significantly associated with advanced tumor, lymph node and metastases (TNM) stage and tumor size, as well as poorer overall survival.Moreover, knockdown of SNHG20 repressed NSCLC cell proliferation, migration and induced cell apoptosis.Mechanistic investigations revealed that SNHG20 could interact with EZH2(enhancer of zeste homolog 2),thereby repressing P21 expression. Furthermore, rescue experiments indicated that SNHG20 functioned as an oncogene partly via repressing p21 in NSCLC cells. Taken together, our findings demonstrate that SNHG20 is a new candidate for use in NSCLC diagnosis, prognosis and therapy. 28981099 2017 Long non-coding RNA SNHG20 promotes non-smallcell lung cancer cell proliferation and migration byepigenetically silencing of P21 expression SNHG20 SNHG20, C17orf86, LINC00338, NCRNA00338, SCARNA16HG 654434 ENSG00000234912 NR_027058 GRCh38_17:77086716-77094990 gastric cancer C16 NA qPCR, Western blot, RIP etc. gastric cancer cell lines (Bgastric cancer823, Sgastric cancer-7901, MKN45), hepatocarcinoma tissues up-regulated Thus, the results showed that SNHG20 acted as an oncogene in GC and targeting SNHG20 may serve as a therapeutic target for GC. The western-blotting results showed that knockdown of SNHG20 significantly inhibited the expression levels of transcription factor Twist1 and EMT maker Vimentin, but upregulating the E-cadherin expression in MKN45 cells.LncRNAs could regulated cancer cells phenotypes through regulating target gene expression by different mechanisms, including chromatin modification, genomic imprinting, RNA decay and sponging miRNAs [20]. 29113337 2017 Long noncoding RNA SNHG20 promotes gastric cancer progression by inhibiting p21 expression and regulating the GSK-3B/ B-catenin signaling pathway. SNHG20 SNHG20, C17orf86, LINC00338, NCRNA00338, SCARNA16HG 654434 ENSG00000234912 NR_027058 GRCh38_17:77086716-77094990 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. CRC tissues, cell lines (HCT8, HT29, HCT116, SW480, LOVO) up-regulated The results suggested that SNHG20 expression was significantly upregulated in CRC tissues compared to corresponding normal tissues from 107 CRC patients. High expression of SNHG20 was remarkably associated with advanced TNM stage in patients with CRC. Multivariate analyses unraveled that SNHG20 expression was an independent prognostic factor for overall survival in CRC patients. Further functional assays revealed that knockdown of SNHG20 suppressed cell proliferation, invasion and migration, and cell cycle progression in CRC cells. Moreover, SNHG20 regulated cell growth through modulation of a series of cell cycle-associated genes. 27543107 2016 Increased long noncoding RNA SNHG20 predicts poor prognosis in colorectal cancer. SNHG20 SNHG20, C17orf86, LINC00338, NCRNA00338, SCARNA16HG 654434 ENSG00000234912 NR_027058 GRCh38_17:77086716-77094990 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. hepatocellular carcinoma tissues, cell lines (MHCC97L, SMCC-7721, Huh-7, MHCC97H and LO5) up-regulated We totally identified a set of four lncRNAs(MIR100HG, SERHL, CTD-2574D22.4 and SNHG23) that were significantly correlated with patient's survival. We then measured the expression levels of these four lncRNAs using TCGA data, and found that it was significant. 29684484 2018 Characterization of long non-coding RNAs to reveal potential prognostic biomarkers in hepatocellular carcinoma. SNHG20 SNHG20, C17orf86, LINC00338, NCRNA00338, SCARNA16HG 654434 ENSG00000234912 NR_027058 GRCh38_17:77086716-77094990 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RIP, CCK-8 assay etc. HCC tissues, cell lines (MHCC97L, SMCC-7721, MHCC97H and Huh-7) up-regulated SNHG20 was significantly up-regulated in HCC tissues. In vitro, loss-function assays revealed that knockdown of SNHG20 inhibited cell proliferation and invasion, whereas, gain-of-function promoted cell proliferation and invasion. Furthermore, knockdown of SNHG20 inhibited ZEB1, ZEB2, N-cadherin and Vimentin expression and up-regulated the E-cadherin expression in HCC cells. Mechanistic investigation revealed that SNHG20 could bind to enhancer of zeste homolog 2 (EZH2) and regulated E-cadherin expression. 28282787 2017 Long non-coding RNA SNHG20 predicts a poor prognosis for HCC and promotes cell invasion by regulating the epithelial-to-mesenchymal transition. SNHG20 SNHG20, C17orf86, LINC00338, NCRNA00338, SCARNA16HG 654434 ENSG00000234912 NR_027058 GRCh38_17:77086716-77094990 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi etc. HCC tissues, cell lines (HL-7702, MHCC-97H, HepG2, SK-Hep-1, SMMC-7721 etc.) up-regulated Our results showed that the expression of SNHG20 was remarkably up-regulated in HCC tissues compared with adjacent non-tumor liver tissues from 49 fresh HCC samples (cohort 1) detected by quantitative reverse-transcription polymerase chain reaction. 27053960 2016 Up-regulation of LncRNA SNHG20 Predicts Poor Prognosis in Hepatocellular Carcinoma SNHG3 SNHG3, NCRNA00014, RNU17C, RNU17D, U17HG, U17HG-A, U17HG-AB 8420 ENSG00000242125 NR_002909.1 GRCh38_1:28505980-28510892 colorectal cancer C19.9 NA qPCR, Luciferase reporter assay, RIP, Western blot Human colorectal cancer cell lines (HT29, HCT116, SW480, LoVo) up-regulated SNHG3 promoted CRC progression via sponging miR-182-5p and upregulating c-Myc and its target genes.The results confirmed that SNHG3 was markedly upregulated in CRC.Notably, Kaplan-Meier analysis and log-rank test demonstrated that patients with overexpression of SNHG3 had poorer overall survival time than those with low expression of SNHG3.HOTAIR expression levels were significantly positively correlated with hepatocellular carcinoma (HCC) recurrence and metastasis and with the overall survival time of patients with HCC. 28731158 2017 The long non-coding RNA SNHG3 functions as a competing endogenous RNA to promote malignant development of colorectal cancer. SNHG3 SNHG3, NCRNA00014, RNU17C, RNU17D, U17HG, U17HG-A, U17HG-AB 8420 ENSG00000242125 NR_002909.1 GRCh38_1:28505980-28510892 hepatocellular carcinoma C22.0 M8170/3 RNA-seq, qPCR, ISH etc. HCC tissues up-regulated Our results showed that the expression level of SNHG3 was significantly upregulated in HCC tissues compared with paired noncancerous tissues from 51 HCC patients, increased SNHG3 expression is associated with malignant status and poor prognosis in HCC patients. 26373735 2015 SNHG3 correlates with malignant status and poor prognosis in hepatocellular carcinoma. SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 387066 ENSG00000203875 NR_003038 GRCh38_6:85660950-85678736 bladder cancer C67 NA qPCR, Western blot, in vitro knockdown BC tissues, Bladder cancer cell lines (SW780, UMUC3, 5637, T-24) up-regulated SNGH5 was found upregulated in BC tissues and cell lines and a high level of SNGH5 was correlated with a poor prognosis. Silencing SNHG5 inhibited the proliferation ability of BC cells and such a function was attributed to its influence on cells cycle and apoptosis. 29434891 2017 lncRNA SNHG5 is associated with poor prognosis of bladder cancer and promotes bladder cancer cell proliferation through targeting p27. SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 387066 ENSG00000203875 NR_003038 GRCh38_6:85660950-85678736 gastric cancer C16 NA RIP etc. Fresh GC tissues down-regulated SNHG5 exerted its function through interacting with MTA2, preventing the translocation of MTA2 from the cytoplasm into the nucleus. SNHG5 overexpression led to significant increases in the acetylation levels of histone H3 and p53, indicating that SNHG5 might affect acetylation by trapping MTA2 in the cytosol, thereby interfering with the formation of the nucleosome remodeling and histone deacetylation complex. This study is the first to demonstrate that SNHG5 is a critical and powerful regulator that is involved in GC progression through trapping MTA2 in the cytosol. 27065326 2016 Long non-coding RNA SNHG5 suppresses gastric cancer progression by trapping MTA2 in the cytosol SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 387066 ENSG00000203875 NR_003038 GRCh38_6:85660950-85678736 prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (LNCaP) down-regulated Five lncRNAs, RP1-4514.2, SUZ12P1, SNHG5, LINC01138, and SNHG1, were down-regulated under DHT treatment. Five lncRNAs, KLKP1, LINC00969, LINC-PINT, TUG1 and MIR17HG, were up-regulated under DHT treatment. Notably, RP1-4514.2 and LINC01138 were induced and KLKP1 was reduced over 2 fold after AR silenced, suggesting the involvement of AR in androgen-mediated regulation of these lncRNAs expressions. 27556357 2016 Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer. SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 387066 ENSG00000203875 NR_003038 GRCh38_6:85660950-85678736 prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (WPMY-1, DU145, PC-3 and LNCaP) up-regulated To further validate the results, we examined the expression levels in 11 normal prostate tissues and 14 prostate cancer tissues with real-time PCR. All of these lncRNAs except LINC00969, were expressed significantly higher in prostate cancer samples compared with normal prostate tissues, which were consistent with the TCGA and microarray results. Then, the expression levels of ten lncRNAs were validated in the noncancerous prostatic cells WPMY-1 and four human prostate cancer cell lines by qRT-PCR. It turned out that most of the ten lncRNAs were up-regulated in prostate cancer cell lines and showed a similar expression pattern in patient samples. 27556357 2016 Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer. SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 387066 ENSG00000203875 NR_003038 GRCh38_6:85660950-85678736 acute myeloid leukemia NA M9861/3 qPCR blood up-regulated SNHG5 upregulation more frequently occurred in AML patients with advanced FAB classification (p<0.005) and unfavorable cytogenetics (p=0.001). overall patient survival for those with high plasma SNHG5 expression was significantly shorter than those patients with low SNHG5 expression. 29917184 2018 Long noncoding RNA SNHG5 is up-regulated and serves as a potential prognostic biomarker in acute myeloid leukemia. SNHG6 SNHG6, HBII-276HG, NCRNA00058, U87HG 641638 ENSG00000245910 NR_002599 GRCh38_8:66921684-66926398 gastric cancer C16 NA qPCR, Western blot etc. gastric tumor tissue, cell lines (MGC-803, AGS, SGC-7901, BGC-823) up-regulated SNHG6 was overexpressed in gastric cancer tissues and cell lines.In summary,our findings demonstrated that SNHG6 acted as an oncogene in gastric cancer cells through regulating miR-101-3p/ZEB1 at a post-transcriptional level and silencing expression at a transcriptional level by recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p27. High expression levels of SNHG6 wereassociated with invasion depth, lymph node metastasis, distant metastasis and tumor/node/metastasis (TNM) stage, and predicted poor prognosis. 28683446 2017 LncRNA SNHG6 is Associated with Poor Prognosis of Gastric Cancer and Promotes Cell Proliferation and EMT through Epigenetically Silencing p27 and Sponging miR-101-3p SNHG6 SNHG6, HBII-276HG, NCRNA00058, U87HG 641638 ENSG00000245910 NR_002599 GRCh38_8:66921684-66926398 glioblastoma NA M9440/3 qPCR, Western blot etc. glioblastoma tissue, cell lines (U87, U251, SHG44, U373-MG) up-regulated In this study, the high expression of SNHG6 was tested in both glioma tissues and glioma cells. The correlation between expression levels of SNHG6 and the overall survival of glioma patients was demonstrated by using Kaplan Meier method analysis. Next, gain of function assays revealed that overexpression of SNHG6 can promote the formation of malignant phenotype of 1800 cell. However, results of loss-of-function assays revealed that silenced SNHG6 exerted the inhibitory function on glioma cell growth. Flow cytometric analysis was performed in glioma cells to detect the anti-oncogenic effects of silenced SNHG6 on cell cycle and apoptosis. Finally, we identified that p21 was involved in glioma cell proliferation after SNHG6 was downregulated. 29579705 2018 LncRNA SNHG6 acts as a prognostic factor to regulate cell proliferation in glioma through targeting p21. SNHG6 SNHG6, HBII-276HG, NCRNA00058, U87HG 641638 ENSG00000245910 NR_002599 GRCh38_8:66921684-66926398 colorectal cancer C19.9 NA qRT-PCR, in vitro knockdown CRC tissues, cell lines (HCT116 and LoVo) up-regulated SNHG6 was up-regulated more than 1.5-fold in 50.0% (37/74) of CRC tissues compared with paired NCTs (P<0.0001). High level of SNHG6 expression was strongly associated with advanced tumor stage (P=0.026) and predicted poor prognosis of CRC (P=0.0215). Furthermore, SNHG6 knockdown by siRNA could inhibit cell proliferation, cell cycle progression, and induce apoptosis. 29506878 2017 Up-regulated expression of SNHG6 predicts poor prognosis in colorectal cancer. SNHG6 SNHG6, HBII-276HG, NCRNA00058, U87HG 641638 ENSG00000245910 NR_002599 GRCh38_8:66921684-66926398 glioma NA M9380/3 qPCR etc. glioma tissues, cell lines (U87, U251, LN229, and T98G) up-regulated The expression of lncRNA SNHG6 was positively correlated with the malignancy and poor prognosis of glioma patients. Our study provides novel insights into the functions of lncRNA SNHG6/miR-101-3p axis in the tumorigenesis of glioma. 29799357 2018 Long non-coding RNA SNHG6 promotes glioma tumorigenesis by sponging miR-101-3p SNHG7 SNHG7, NCRNA00061 84973 ENSG00000233016 NR_003672 GRCh38_9:136721366-136728184 prostate cancer C61.9 NA qPCR, Western blot etc. prostate cancer tumor tissue, cell lines (LNCaP, VCaP, 22RV1, DU145, PC-3) up-regulated SNHG7 expression was significantly up-regulated in prostate cancer tissue and cell lines.Besides, the overexpression of SNHG7 was closely correlated with the poor prognosis. In vitro and in vivo,SNHG7 knockdown markedly inhibited prostate cancer proliferation and cycle-related protein (CDK4, CDK6, Cyclin D1), induced cell cycle arrest at G0/G1 phase and suppressed tumor growth. Moreover, miR-503 was predicted by bioinformatics tools and validated using luciferase reporter assay to both directly inhibited SNHG7 and Cyclin D1 expression by targeting their RNA 3'-UTR. We found that lncRNA SNHG7 acts a ceRNA for miR-503 and harbors miR-503 to positively regulates Cyclin D1 expression. 29571017 2018 Long noncoding RNA SNHG7 accelerates prostate cancer proliferation and cycle progression through cyclin D1 by sponging miR-503. SNHG7 SNHG7, NCRNA00061 84973 ENSG00000233016 NR_003672 GRCh38_9:136721366-136728184 glioblastoma NA M9440/3 Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown Glioblastoma tissue, human GBM cell lines (A172, U87, T98G and SHG44) up-regulated the expression of SNHG7 was significantly upregulated in GBM tissues and cell lines compared with non-cancerous brain tissues. Furthermore,SNHG7 knockdown remarkably suppressed the proliferation, migration and invasion of A172 and U87-cells while inducing their apoptosis. Subsequently, SNHG7 knockdown significantly inhibited tumor growth and metastasis in-vivo by using xenograft experiments in nude mice.SNHG7 directly inhibited miR-5095,which targeted the 3'UTR of CTNNB1 mRNA and subsequently downregulated the Wnt/B-catenin signaling pathway in GBM. Using rescue experiments, we demonstrated that SNHG7 promoted the proliferation, migration and invasion of GBM cells through the inhibition of miR-5095 and concomitant activation of Wnt/B-catenin signaling pathway. 29360452 2018 Long noncoding RNA SNHG7 promotes the progression and growth of glioblastoma via inhibition of miR-5095. SNHG7 SNHG7, NCRNA00061 84973 ENSG00000233016 NR_003672 GRCh38_9:136721366-136728184 osteosarcoma C61.9 NA qRT-PCR, Luciferase reporter assay, Western blot analysis The OS cell lines (MG63, SaOS2, HOS, and 143B) and human osteoblastic cell line (hFOB1.19), The OS tissues and corresponding relative normal tissues up-regulated the LncRNA SNHG7 is upregulated during the development of OS via inhibition of tumor suppressor miR-34s signals. 29989838 2018 Long Noncoding RNA SNHG7 Promotes the Tumor Growth and Epithelial-to-Mesenchymal Transition via Regulation of miR-34a Signals in Osteosarcoma. SNHG7 SNHG7, NCRNA00061 84973 ENSG00000233016 NR_003672 GRCh38_9:136721366-136728184 colorectal cancer C19.9 NA Microarray, qPCR, RIP, Luciferase reporter assay, Western blot, etc. CRC cell lines (caco2, SW480, SW620, Hct116, LoVo). human normal colon epithelial cell line (FHC). CRC tissues, adjacent tissues. down-regulation SNHG7 expression showed a high fold (SW620/SW480) in CRC microarrays. The CRC patients with high expression of SNHG7 had a significantly poor prognosis. Furthermore, SNHG7 promoted CRC cell proliferation, metastasis, mediated cell cycle, and inhibited apoptosis. SNHG7 and GALNT7 were observed for co-expression by CNC analysis, and a negative correlation of SNHG7 and miR-34a were found by competing endogenous RNA (ceRNA) analysis. The CRC-related SNHG7 and miR-34a might be implicated in CRC progression via GALNT7, suggesting the potential usage of SNHG7/miR-34a/GALNT7 axis in CRC treatment.The survival curves were calculated using the Kaplan-Meier method, and the differences were assessed by a log-rank test. 29970122 2018 Long non-coding RNA-SNHG7 acts as a target of miR-34a to increase GALNT7 level and regulate PI3K/Akt/mTOR pathway in colorectal cancer progression. SNHG7 SNHG7, NCRNA00061 84973 ENSG00000233016 NR_003672 GRCh38_9:136721366-136728184 colorectal cancer C19.9 NA qPCR, Western blot, Dual luciferase reporter assays, RIP, etc. colorectal cancer tissues, cell lines (SW480, SW620, LOVO, HCT-116, FHC) up-regulated SNHG7 overexpression promoted the proliferation, migration, and invasion of CRC cell lines. SNHG7 directly interacted with miR-216b and downregulation of miR-216b reversed efficiently the suppression of GALNT1 induced by SNHG7 siRNA. Kaplan?Meier survival analysis showed that high expression of SNHG7 was associated with CRC poor overall survival. 29915311 2018 LncRNA SNHG7 sponges miR-216b to promote proliferation and liver metastasis of colorectal cancer through upregulating GALNT1. SNHG8 SNHG8, LINC00060, NCRNA00060 100093630 ENSG00000269893 NR_003584 GRCh38_4:118278709-118279823 endometrial cancer NA M8380/3 qPCR, Western blot, Luciferase reporter assay etc. cell line (Ishikawa, Japan, HEC1-A, HEC1-B, AN3CA, RL95-2), EC tissue up-regulated SNHG8 expression in endometrial carcinoma tissue was significantly higher than that in normal endometrium.After transfection with SNHG8 siRNA,the cell viability of AN3CA cells decreased, whereas the activity of Ishikawa was increased after transfection with SNHG8 overexpression plasmid.SNHG8 was bound to miR-152 and miR-152 targeted on c-MET. In addition, miR-152 mimics inhibited the expression of c-MET, and the inhibitory effect was reversed after SNHG8 overexpression. Silencing SNHG8 reduced c-MET expression, and c-MET expression was reversed after addition of miR-152 inhibitor. 29630089 2018 LncRNA SNHG8 participates in the development of endometrial carcinoma through regulating c-MET expression by miR-152 SOX2 NA NA ENSG00000181449 NA GRCh38_3:181711924-181714436 breast cancer C50 NA qPCR, Western blotting etc. cell lines (MCF-7, BT474, ZR-75-1, SKBR3, MDA-MB-231) up-regulated An interaction between SOX2 and PVT1, which promotes breast cancer growth and invasion through epithelial to mesenchymal transition. To further reveal the function of SOX2/ PVT1 in breast cancer, the MTT and invasion assay were performed through silencing of PVT1 or SOX2. We found that either knockdown PVT1 or blocking SOX2 can suppress breast cancer cell growth and invasion through inhibition of EMT. 28882595 2017 Upregulation of SOX2 activated LncRNA PVT1 expression promotes breast cancer cell growth and invasion SOX21-AS1 NA 100507533 ENSG00000227640 NR_046514 GRCh38_13:94712716-94716246 colorectal cancer C19.9 NA qPCR, Luciferase reporter assay, RIP colorectal cancer tissues, cell lines (HT29, HCT8, LS513, SW620 and HCT116,FHC) up-regulated lncRNA SOX21-AS1 expression was significantly over-expressed in CRC tissue samples and cells. The aberrant over-expression of SOX21-AS1 indicated poor prognosis of CRC patients. SOX21-AS1 silencing inhibited the proliferation, invasion, and decreased the tumor growth of CRC cells.miR-145 was proved to be the target of SOX21-AS1,besides, myosin VI (MYO6) was found to be one of the targets of miR-145.the tumorigenic effect of lncRNA SOX21-AS1 in CRC cells via targeting miR-145/MYO6, providing a novel insight for CRC carcinogenesis. 29217166 2017 Long non-coding RNA SOX21-AS1 sponges miR-145 to promote the tumorigenesis of colorectal cancer by targeting MYO6. SOX21-AS1 NA 100507533 ENSG00000227640 NR_046514 GRCh38_13:94712716-94716246 lung adenocarcinoma C34 M8140/3 qPCR, Western blot etc. non-small cell lung cancer tissues, NSCLC adenocarcinoma cell lines (A549, SPC-A1, NCI-H1299, NCI-H1650, PC9, and H1975), NSCLC squamous carcinomas cell lines (H1703, SK-MES-1 and H226) up-regulated Higher expression levels of SOX21-AS1 positively correlated with tumor size and advanced tumor–node–metastasis (TNM) stage. Multivariate analyses indicated that SOX21-AS1 expression could serve as an independent prognostic factor for overall survival of LUAD. 28873379 2017 A Novel Long Non-Coding RNA, SOX21-AS1, Indicates a Poor Prognosis and Promotes Lung Adenocarcinoma Proliferation SOX21-AS1 NA 100507533 ENSG00000227640 NR_046514 GRCh38_13:94712716-94716246 hepatocellular carcinoma C22.0 M8170/3 qPCR, RIP, Western blot etc. hepatocellular carcinoma tissues, cell line (Hep3B, LM3, MHHC97H,HepG2, Huh7 and LO2) up-regulated We detected the high expression level of SOX21-AS1 in tumor tissues and cell lines through performing qRT-PCR analysis. The prognostic value of SOX21-AS1 was identified. Moreover, the biological effects of SOX21-AS1 on HCC cell activities were evaluated by functional assays, such as MTT, colony formation assay and transwell assay. As a result, silenced SOX21-AS1 suppressed cell proliferation and metastasis, resulted in cell cycle arrest, and induced apoptosis in hepatocellular carcinoma. Mechanically, RIP was conducted to prove that SOX21-AS1 could bind with EZH2. ChIp assay was carried out and manifested that SOX21-AS1 epigenetically silenced p21 via recruiting EZH2 to the promoter of p21. Finally, rescue assays were designed and carefully conducted to investigate whether SOX21-AS1 can interact with p21 to affect hepatocellular carcinoma progression. Kaplan Meier method analyzed that HCC patients with high levels of SOX21-AS1 expression indicated the short survival time in comparison with those with low levels of SOX21-AS1 expression. 29772433 2018 LncRNA SOX21-AS1 is associated with progression of hepatocellular carcinoma and predicts prognosis through epigenetically silencing p21. SOX2OT SOX2-OT, NCRNA00043, SOX2OT 347689 ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 glioblastoma NA M9440/3 qPCR, Western blot, in vitro knockdown, Luciferase reporter assay etc. cell lines (U87, U251) up-regulated Knockdown of SOX2OT significantly increased the expression of miR-194-5p and miR-122 in GSCs.SOX2OT bound to both miR-194-5p and miR-122. SOX3 and TDGF-1 were up-regulated in human glioma tissues and GSCs. Knockdown of SOX3 inhibited the proliferation, migration and invasion of GSCs, promoted GSCs apoptosis, and decreased TDGF-1 mRNA and protein expression through direct binding to the TDGF-1 promoter. Over-expression of miR-194-5p and miR-122 decreased the mRNA and protein expression of SOX3 by targeting its 3’UTR. Furthermore, SOX3 knockdown also inhibited the SOX2OT expression through direct binding to the SOX2OT promoter and formed a positive feedback loop. 29132362 2017 Knockdown of SOX2OT inhibits the malignant biological behaviors of glioblastoma stem cells via up-regulating the expression of miR-194-5p and miR-122 SOX2OT SOX2-OT, NCRNA00043, SOX2OT 347689 ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 osteosarcoma NA M9180/3 qPCR, Western Blot etc. cell lines (Saos-2, MG-63, U-2 OS, MNNG/HOS) up-regulated lncRNA SOX2-OT expression was increased in osteosarcoma tissues and cell lines, and associated with malignant status and overall survival in osteosarcoma patients. LncRNA SOX2-OT positively regulated SOX2 expression in osteosarcoma cells and positively associated with SOX2 expression in osteosarcoma tissues. The rescued-function studies suggested that SOX2 is necessary for lncRNA SOX2-OT induced osteosarcoma cells migration, invasion, and expression of cancer stem cell biomarkers. In conclusion, lncRNA SOX2-OT is a prognostic biomarker for osteosarcoma patients and serves an oncogenic role to regulate osteosarcoma cells migration, invasion, and expression of cancer stem cell biomarkers. 28960757 2017 LncRNA SOX2-OT Is a Novel Prognostic Biomarker for Osteosarcoma Patients and Regulates Osteosarcoma Cells Proliferation and Motility Through Modulating SOX2 SOX2OT SOX2-OT, NCRNA00043, SOX2OT 347689 ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 gastric cancer C16 NA qPCR etc. gastric cancer tissues down-regulated Sox2ot expression levels were decreased in cancerous tissues compared to their corresponding non-cancerous controls. Sox2ot expression was associated with T stage, distant metastasis and differentiation. 27874951 2016 High expression of long noncoding RNA Sox2ot is associated with the aggressive progression and poor outcome of gastric cancer. SOX2OT SOX2-OT, NCRNA00043, SOX2OT 347689 ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 lung squamous cell carcinoma C34 M8070/3 qPCR, RNAi, Western blot, RIP etc. cell lines (A549, HCC827, SK-MES-1, NCI-H1299 etc.) up-regulated Sox2ot exprssion in lung cancer is significantly higher and promotes cancer cell proliferation. Sox2ot plays an important role in regulating lung cancer cell proliferation, and may represent a novel prognostic indicator for the disease. 24927902 2014 A long noncoding RNA Sox2ot regulates lung cancer cell proliferation and is a prognostic indicator of poor survival. SOX2OT SOX2-OT, NCRNA00043, SOX2OT 347689 ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 cholangiocarcinoma NA M810/3 qPCR, in vitro knockdown etc. cell line (RBE, QBC939, HIBEC), CCA tissues up-regulated Upregulation of Sox2ot significantly associated with lymph node invasion , TNM stage and postoperative recurrence . 29246536 2017 Overexpressed long noncoding RNA Sox2ot predicts poor prognosis for cholangiocarcinoma and promotes cell proliferation and invasion. SOX2OT SOX2-OT, NCRNA00043, SOX2OT 347689 ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi etc. HCC tissues, cell lines (HepG2, SMMC-7721) up-regulated lncRNA Sox2ot expression level was significantly higher in HCC tissues compared with adjacent non-tumor tissues. High expression of lncRNA Sox2ot was associated with histological grade, TNM stage, and vein invasion. 26097588 2015 Up-regulation of long non-coding RNA Sox2ot promotes hepatocellular carcinoma cell metastasis and correlates with poor prognosis. SOX2OT SOX2-OT, NCRNA00043, SOX2OT 347689 ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RNAi HCC tissue , adjacent normal tissue. human HCC cell lines (MHCC97H, SMMC-7721). normal liver cell line(LO2). up-regulated Furthermore, it was demonstrated that knockdown of lncRNA Sox2ot downregulated the mRNA and protein expression of Twist1 and N-cadherin, but upregulated the E-cadherin expression levels in MHCC97H and SMCC-7721 cells. Thus, it was indicated that lncRNA Sox2ot may be a novel predictive biomarker and a potential therapeutic target for HCC. Association between lncRNA Sox2ot expression and vein invasion. Kaplan-Meier survival analysis and the log-rank test were performed to analyze the DFS and OS time of patients with HCC in higher and lower lncRNA Sox2ot expression groups. 29963193 2018 Upregulation of lncRNA Sox2ot indicates a poor prognosis for patients with hepatocellular carcinoma and promotes cell invasion. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA cholangiocarcinoma NA M810/3 qPCR, Western blot, Luciferase reporter assay, RIP etc. cholangiocarcinoma tissues, cell lines (HIBEC, CCLP-1, HuCCT1, Huh-28, KMBC and QBC939) up-regulated SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally,SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold.Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p. 29642935 2018 SP1-induced upregulation of lncRNA SPRY4-IT1 exerts oncogenic properties by scaffolding EZH2/LSD1/DNMT1 and sponging miR-101-3p in cholangiocarcinoma. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR etc. pancreatic ductal adenocarcinoma tissues, cell lines (BxPC3, Capan-2, PANC1 and SW1990) down-regulated SPRY4-IT1 was abnormally upregulated in PDAC tissues and cell lines,and this overexpression is closely associated poor clinical outcomes including advanced tumor stages, low differentiation grade and worse overall survival. Tumor stage and differentiation grade was closely correlated with SPRY4-IT1 expression. Additionally, decreased SPRY4-IT1 contributed to tumor suppressive effect through attenuating cell growth, clonogenic ability and facilitating apoptosis via Bcl-2/caspase-3 pathway in PANC1 and Capan-2 cells.Furthermore,the xenograft study confirmed the tumor proliferation-promoting role of SPRY4-IT1 in PANC1 cells. 29551494 2018 Upregulated long non-coding RNA SPRY4-IT1 predicts dismal prognosis forpancreatic ductal adenocarcinoma and regulates cell proliferation and apoptosis. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA thyroid cancer C73.9 NA qPCR, Western blot TC tissues, thyroid squamous cell carcinoma cell line (SW579), papillary TC cell lines (K1 and TPC-1) up-regulated the level of SPRY4-IT1 was significantly upregulated in TC tissues and cell lines, which was correlated with poor prognosis. And cellular experiments exhibited that silenced SPRY4-IT1 inhibited the proliferative and migratory abilities of TC cells. Mechanism assays noted that silenced SPRY4-IT1 could increase the levels of transforming growth factor-B1 (TGF-B1) and p-Smad2/3 and function mediated by si-SPRY4-IT1 could be rescued by the interference of TGF-B1. 29234152 2017 LncRNA SPRY4-IT was concerned with the poor prognosis and contributed to the progression of thyroid cancer. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA lung adenocarcinoma C34 M8140/3 qPCR cell lines (H23, H1299, A549 and SPC-A1) up-regulated The results showed that SPRY4-IT1 was significantly up-regulated in LUAD tissues. Further analysis indicated that LUAD patients with high SPRY4-IT1 expression have significantly poorer overall survival in Chinese LUAD patients. 28881629 2017 Up-regulation of long non-coding RNA SPRY4-IT1 promotes tumor cell migration and invasion in lung adenocarcinoma SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA glioma NA M9380/3 qPCR etc. glioma tissues up-regulated The expression level of SPRY4-IT1 was significantly higher in glioma in comparison to normal matched tissue. Furthermore, lncRNA SPRY4-IT1 was associated significantly with WHO grade and tumor size. A significant difference was found that glioma patients with high SPRY4-IT1 expression level had distinctly shorter OS than patients with low SPRY4-IT1 expression level. 27460732 2016 Long noncoding RNA SPRY4-IT1 is a prognostic factor for poor overall survival and has an oncogenic role in glioma. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA ovarian cancer C56.9 NA qPCR, Western blot etc. ovarian cancer tissues, cell lines(IOSE80 , SKOV3, HO8910, ES-2 and CAOV3) down-regulated We quantified the expression level of SPRY4-IT1 in ovarian cancer patients and found its downregulation in ovarian cancer tissues compared to the adjacent normal tissues. Patients with lower SPRY4-IT1 expression were associated with a relatively poor prognosis. In consistency, the expression of SPRY4-IT1 was found to be reduced in four human ovarian cancer cell lines compared to normal ovarian epithelial cells. The cell proliferation was reduced following SPRY4-IT1 overexpression in SKOV3/HO8910 cells based on 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assays. The SPRY4-IT1 overexpression also dramatically arrested cell cycle and promoted cell apoptosis. Both wound-healing and transwell-based assays demonstrated that cell migration and invasion were inhibited following SPRY4-IT1 overexpression. 28691641 2018 Decreased long non-coding RNA SPRY4-IT1 contributes to ovarian cancer cell metastasis partly via affecting epithelial-mesenchymal transition. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated Up-regulated level of SPRY4-IT1 was detected in pathologic tissues of CRC patients compared with adjacent normal tissues. The relative expression of SPRY4-IT1 was associated with the tumor size, the depth of invasion, lymph node invasion, distant invasion, and tumor stage. 28099409 2017 Up-Regulated Expression of SPRY4-IT1 Predicts Poor Prognosis in Colorectal Cancer. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA ovarian cancer C56.9 NA qPCR, RNAi, Flow cytometry assay, Cell proliferation assay etc. ovarian cancer tissues, cell lines (OVCAR-3, SKOV3, A2780, HO-8910, Caov3, and CP70) up-regulated SPRY4-IT1 expression is significantly upregulated in ovarian tumor tissues and OC cell lines in comparison with adjacent non-tumor control tissues and the human ovarian immortalized nontumorigenic ovarian surface epithelial (IOSE), respectively. Also, knockdown of lncRNA SPRY4-IT1 inhibited the proliferation of OC cells by CCK-8 assay and clonogenic assay and arrested cell cycle at a G0/G1 stage in OC cells. 28129625 2017 Upregulation of the long non-coding RNA SPRY4-IT1 indicates a poor prognosis and promotes tumorigenesis in ovarian cancer. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA bladder cancer C67 NA qPCR, RNAi etc. bladder cancer tissues, cell lines (J82, T24, SW780, SV-40 etc.) up-regulated SPRY4-IT1 levels were highly positively correlated with histological grade, tumor stage, and lymph node metastasis and reduced overall survival. A multivariate analysis showed that SPRY4-IT1 expression is an independent prognostic factor of overall survival in patients with UCB. 25973088 2015 Increased expression of SPRY4-IT1 predicts poor prognosis and promotes tumor growth and metastasis in bladder cancer. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA gastric cancer C16 NA qPCR, RNAi, Western blot etc. gastric cancer tissues, cell lines (AGS, BGC-823, HGC-27, SGC-7901, MGC80-3, MKN-45) up-regulated SPRY4-IT1 expression was elevated in GC tissues and cell lines, and SPRY4-IT1 levels were highly positively correlated with tumor size, invasion depth, distant metastasis, TNM stage, and reduced overall survival (OS) and disease-free survival (DFS). SPRY4-IT1 may regulate the proliferation, migration, and invasion ability of GC cells, partially through regulation of cyclin D1, MMP2, and MMP9 expression. 25835973 2015 Long noncoding RNA SPRY4-IT1 predicts poor patient prognosis and promotes tumorigenesis in gastric cancer. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot hepatocellular carcinoma tissues, cell lines (MHCC97L, MHCC97H, HepG2 and SMMC7721, HL7702) up-regulated high expression of SPRY4-IT1 was associated with poor 5-year overall survival in the HCC patient cohort.the expression of SPRY4-IT1 was significantly correlated with TNM stage in HCC patients. knock-down of SPRY4-IT1 suppressed cell proliferation, colony formation, cell invasion and migration in HCC cells.knock-down of SPRY4-IT1 induced cell cycle arrest at G0/G1 phase and induced apoptosis. knock-down of SPRY4-IT1 also suppressed the mRNA and protein expression of estrogen-related receptor a (ERRa).knock-down of ERRa inhibited cell proliferation, colony formation, cell invasion and migration in HCC cells. More importantly, ERRa overexpression antagonized the effects of SPRY4-IT1 knock-down on cell proliferation, colony formation, cell invasion and migration in HCC cells. 29214989 2017 Long non-coding RNA SPRY4-IT1 promotes development of hepatic cellular carcinoma by interacting with ERRa and predicts poor prognosis. SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 100642175 ENSG00000281881 NR_131221 NA colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. CRC tissues, cell lines (HT-29, HCT-116, and SW-480) up-regulated Herein, we are the first to report that the SPRY4-IT1 was significantly upregulated in CRC tissues, serum, and cells. Higher SPRY4-IT1 expression was markedly associated with advanced Tumor Node Metastasis (TNM) stage in a cohort of 84 CRC patients. Further in vitro experiments revealed that knockdown of SPRY4-IT1 inhibited the proliferation, migration, and invasion of CRC cells and induced cell cycle arrestment. Moreover, we confirmed that the expression of epithelial-mesenchymal transition-related genes was modulated through alteration of SPRY4-IT1 expression. 27621655 2016 Long noncoding RNA SPRY4-IT1 promotes malignant development of colorectal cancer by targeting epithelial-mesenchymal transition. SSTR5-AS1 NA 146336 ENSG00000261713 NR_027242 GRCh38_16:1064093-1078731 neuroendocrine prostate cancer NA NA RNA-seq, Microarray, qPCR etc. neuroendocrine prostate cancer tissues up-regulated Top candidate lncRNAs FENDRR, H19, LINC00514, LINC00617, and SSTR5-AS5 identified in this study are implicated in the development of NEPC. 29757368 2018 The long noncoding RNA landscape of neuroendocrine prostate cancer and its clinical implications. STARD13 STARD13, ARHGAP37, DLC2, GT650, LINC00464 NA ENSG00000133121 NA GRCh38_13:33103135-33350630 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. HCC tissues, cell lines (HepG2, Huh7, L02) down-regulated STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival.Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy. 27844181 2017 STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas. SUMO1P3 NA NA ENSG00000235082 NA GRCh38_1:160317403-160317706 gastric cancer C16 NA qPCR etc. gastric cancer tissues up-regulated The results showed that SUMO1P3 was significantly up-regulated in gastric cancer tissues compared with paired-adjacent nontumorous tissues. Its expression level was significantly correlated with tumor size, differentiation, lymphatic metastasis, and invasion. We found that SUMO1P3 is up-regulated in gastric cancer and may be a new tumor marker for the diagnosis of gastric cancer. 23996296 2013 Up-regulation of SUMO1 pseudogene 3 (SUMO1P3) in gastric cancer and its clinical association. SUMO1P3 NA NA ENSG00000235082 NA GRCh38_1:160317403-160317706 colon cancer C18 NA qPCR, Western blot colon cancer tissues, cell lines (HT29, HCT116, SW480, SW620, and LoVo, NCM460 and HUVECs) up-regulated The upregulation of SUMO1P3 was positively correlated with the advanced histological stages, metastases, angiogenesis and poor prognosis of colon cancer patients. SUMO1P3 knockdown repressed the proliferation, migration,invasion, and pro-angiogenesis of colon cancer cells in vitro. SUMO1P3 silencing reduced the growth, liver metastasis, and vascularization of colon cancer in vivo. SUMO1P3 depletion decreased the levels of cyclin D1, Vimentin, and VEGFA while increased E-cadherin expression in xenograft tumor tissues.the patients with high levels of SUMO1P3 had shorter survival rates than those with low levels of SUMO1P3. 29312498 2017 LncRNA SUMO1P3 drives colon cancer growth, metastasis and angiogenesis. SUMO1P3 NA NA ENSG00000235082 NA GRCh38_1:160317403-160317706 hepatocellular carcinoma C22.0 M8170/3 qPCR, etc. hepatocellular carcinoma tissues, cell lines (MHCC97L, SMMC7721, HuH-7, HepG2, Hep-3B, HL-7702) up-regulated SUMO1P3 was highly expressed in HCC patients with higher TNM stage. We concluded that the knockdown of SUMO1P3 repressed tumor growth, invasion, promoted apoptosis. Following SUMO1P3 knockdown, the survival fraction of SMMC7721 and Hep-3B cells (Fig.?5b) 2?weeks after radiation exposure was significantly reduced compared to the sh-NC group, 29905911 2018 Knockdown of SUMO1P3 represses tumor growth and invasion and enhances radiosensitivity in hepatocellular carcinoma. TC0100223 NA NA NA NA NA epithelial ovarian cancer C56.9 NA microarray, qPCR etc. epithelial ovarian cancer tissues, cell lines (SKOV3 etc.) down-regulated Notably, three candidates (TC0100223, TC0101686 and TC0101441) were aberrantly expressed in ERa-positive compared to ERa-negative EOC tissues, showing correlations with some malignant cancer phenotypes such as advanced FIGO stage and/or high histological grade. Furthermore, multivariate analysis indicated that TC0101441 was an independent prognostic factor for overall survival. 24481591 2014 Expression and clinical significance of estrogen-regulated long non-coding RNAs in estrogen receptor a-positive ovarian cancer progression. TC0101441 NA 101929441 ENSG00000230550 NR_123739 GRCh38_1:204141408-204143009 epithelial ovarian cancer C56.9 NA microarray, qPCR etc. epithelial ovarian cancer tissues, cell lines (SKOV3 etc.) up-regulated Notably, three candidates (TC0100223, TC0101686 and TC0101441) were aberrantly expressed in ERa-positive compared to ERa-negative EOC tissues, showing correlations with some malignant cancer phenotypes such as advanced FIGO stage and/or high histological grade. Furthermore, multivariate analysis indicated that TC0101441 was an independent prognostic factor for overall survival. 24481591 2014 Expression and clinical significance of estrogen-regulated long non-coding RNAs in estrogen receptor a-positive ovarian cancer progression. TC0101686 NA NA NA NA NA epithelial ovarian cancer C56.9 NA microarray, qPCR etc. epithelial ovarian cancer tissues, cell lines (SKOV3 etc.) down-regulated Notably, three candidates (TC0100223, TC0101686 and TC0101441) were aberrantly expressed in ERa-positive compared to ERa-negative EOC tissues, showing correlations with some malignant cancer phenotypes such as advanced FIGO stage and/or high histological grade. Furthermore, multivariate analysis indicated that TC0101441 was an independent prognostic factor for overall survival. 24481591 2014 Expression and clinical significance of estrogen-regulated long non-coding RNAs in estrogen receptor a-positive ovarian cancer progression. TCONS_00017817 RP11-124O11.1, LOC101929445 NA NA NA NA esophageal squamous cell cancer NA NA microarray, qPCR etc. ESCC tissues down-regulated Therefore, we chose 10 significant differentially expressed lncRNAs randomly from microarray results. 27035335 2016 Microarray expression profile analysis of aberrant long non-coding RNAs in esophageal squamous cell carcinoma. TCONS_00027978 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR hepatocellular carcinoma tissues down-regulated the TCONS_00027978 expression level was significantly decreased in HCC tissues compared with matched normal tissues (p < 0.01).TCONS_00027978 was positively associated with TNM stage,lymph node metastasis and histologic grade in HCC patients.low levels of TCONS_00027978 expression were associated with poorer overall survival and disease-free survival.TCONS_00027978 expression was an independent poor prognostic factor for HCC patients. 29271999 2017 Expression of lncRNA TCONS_00027978 in hepatocellular carcinoma and its influence on prognosis and survival. TDRG1 TDRG1, LINC00532 NA NA NA NA esophageal squamous cell cancer NA NA qPCR, Cell proliferation assay etc. ESCC tissues, cell lines (TE1, TE13, T.Tn, Yes-2, and Eca109) up-regulated The expression level of lincRNA-NR_024015 in ESCC tumor tissues was significantly higher than that in corresponding normal tissues and rs8506 genotype has a genotype-specific effect on lincRNA-NR_024015 expression. Furthermore, rs8506 G to A variant might influence lincRNA-NR_024015 expression and function by disrupting the binding of hsa-miR-526b to the site. High expression level of lincRNA-NR_024015 and rs8506 A allele were associated with poor ESCC patients' survival. 27583835 2016 A genetic polymorphism at miR-526b binding-site in the lincRNA-NR_024015 exon confers risk of esophageal squamous cell carcinoma in a population of North China. TINCR TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16 NA ENSG00000223573 NA GRCh38_19:5558167-5578349 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. HCC tissues, cell line (HUH7) up-regulated TINCR was significantly up-regulated in HCC. the associations of TINCR with clinicopathological characteristics, disease-free survival (DFS) and overall survival (OS) of patients were further evaluated. high TINCR expression was significantly correlated with tumor size,tumor differentiation status, TNM stage, and vascular invasion. TINCR was demonstrated as a direct target of miR-137 and miR-133a, and was suppressed by miR-137/miR-133a. 28546230 2017 TINCR expression is associated with unfavorable prognosis in patients with hepatocellular carcinoma. TINCR TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16 NA ENSG00000223573 NA GRCh38_19:5558167-5578349 non small cell lung cancer C34 M8046/3 Microarray, qPCR, RNAi, RIP etc. cell lines (MRC-5, PC9, H1299, H522, A549, 95D,95C and H2172), 293T cell,NSCLC tissues up-regulated TINCR can interact with BRAF to facilitate its kinase activity, thereby leading to activation of oncogenic mitogen-activated protein kinase (MAPK) pathway. 29427662 2018 TINCR facilitates non-small cell lung cancer progression through BRAF-activated MAPK pathway. TINCR TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16 NA ENSG00000223573 NA GRCh38_19:5558167-5578349 gastric cancer C16 NA qPCR, Western blot, Luciferase report assay etc. GC tissues, cell lines (KATO III, NCI-N87, HGC-27, and SNU-1) up-regulated miR-375 level decreased and TINCR level increased in tumor tissues.TINCR was a target of miR-375 and inhibited its expression in GC cells.Furthermore,the low expression of TINCR increased cell apoptosis and inhibited the proliferation of GC cells,while the downregulation of miR-375 reversed the function.In particular,TINCR could negatively regulate the miR-375 expression and increased the PDK1 expression in GC cells.Finally,tumor growth suppression was retarded with miR-375 downregulated in TINCR knockdown of GC cell xenografts. 28744139 2017 The long noncoding RNA, TINCR, functions as a competing endogenous RNA to regulate PDK1 expression by sponging miR-375 in gastric cancer. TP53TG1 TP53TG1, LINC00096, NCRNA00096, P53TG1, P53TG1-D, TP53AP1 11257 ENSG00000182165 NR_015381 GRCh38_7:87325225-87345515 colon cancer C18 NA microarray, qPCR, RNA pull-down assay etc. cell line (HCT-116) down-regulated Herein, we have identified a p53-induced lncRNA, TP53TG1, that undergoes cancer-specific promoter hypermethylation-associated silencing. In vitro and in vivo assays identify a tumor-suppressor activity for TP53TG1 and a role in the p53 response to DNA damage. Importantly, we show that TP53TG1 binds to the multifaceted DNA/RNA binding protein YBX1 to prevent its nuclear localization and thus the YBX1-mediated activation of oncogenes. TP53TG1 epigenetic inactivation in cancer cells releases the transcriptional repression of YBX1-targeted growth-promoting genes and creates a chemoresistant tumor. 27821766 2016 Epigenetic inactivation of the p53-induced long noncoding RNA TP53 target 1 in human cancer. TP53TG1 TP53TG1, LINC00096, NCRNA00096, P53TG1, P53TG1-D, TP53AP1 11257 ENSG00000182165 NR_015381 GRCh38_7:87325225-87345515 gastric cancer C16 NA microarray, MSP-PCR, Immunohistochemistry etc. gastric cancer tissues, cell lines (MKN-45, MKN-7, TGBC11TKB, KATO-III, SNU-1 and GCIY) differential expression We found TP53TG1 hypermethylation in 26% (45 of 173) of the gastric neoplasms studied. Presence of TP53TG1 hypermethylation was significantly associated with shorter progression-free survival. 27821766 2016 Epigenetic inactivation of the p53-induced long noncoding RNA TP53 target 1 in human cancer. TP73-AS1 TP73-AS1, KIAA0495, PDAM 57212 ENSG00000227372 NR_033708 GRCh38_1:3735601-3747336 glioblastoma multiforme NA M9440/3 qPCR, RNAi, MTT assay etc. cell line (U87) differential expression Knockdown of TP73-AS1 could not only reduce the expression of RFX1, an mRNA of this triplet, but also induce apoptosis in U87 cells. 28168356 2017 Identifying survival-associated modules from the dysregulated triplet network in glioblastoma multiforme. TP73-AS1 TP73-AS1, KIAA0495, PDAM 57212 ENSG00000227372 NR_033708 GRCh38_1:3735601-3747336 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay hepatocellular carcinoma tissues, cell lines (HCCLM3, MHCC97L, SMMC7722, Hep3B and HepG2) up-regulated TP73-AS1 was upregulated in HCC tissues and cell lines. High TP73-AS1 expression was correlated with worse clinicopathological features, poorer prognosis and shorter survival. In HCC tissues, miR-200a was down-regulated while HMGB1 and RAGE were up-regulated; TP73-AS1 was inversely correlated with miR-200a, while positively correlated with HMGB1 and RAGE, respectively. 28403886 2017 The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through miR-200a-dependent HMGB1/RAGE regulation TP73-AS1 TP73-AS1, KIAA0495, PDAM 57212 ENSG00000227372 NR_033708 GRCh38_1:3735601-3747336 bladder cancer C67 NA qPCR, Western blot etc. bladder cancer tissues, cell lines (T24, 5637, SW780, BIU87, J82 and HT1376) down-regulated We identified that the expression level of TP73-AS1 was significantly down-regulated in bladder cancer tissues and cells compared to adjacent non-tumor tissues. Kaplan-Meier survival analysis found that patients with low TP73-AS1 expression level had shorter overall survival and progression-free survival than those with high TP73-AS1 expression. Moreover, we showed that overexpression of TP73-AS1 could inhibit cell growth, arrest cell cycle, reduce cell migration and invasion, and promote cell apotosis in vitro study. In addition, overexpression of TP73-AS1 diminished epithelial-mesenchymal transition (EMT) through inhibiting the expression of vimentin, snail, MMP-2, and MMP-9 and upregulating the expression levels of E-cadherin. 29625110 2018 LncRNA TP73-AS1 predicts the prognosis of bladder cancer patients and functions as a suppressor for bladder cancer by EMT pathway. TP73-AS1 TP73-AS1, KIAA0495, PDAM 57212 ENSG00000227372 NR_033708 GRCh38_1:3735601-3747336 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell line (U118, U251, SNB119, LN229,SHG-44), brain glioma tissues up-regulated TP73-AS1 was specifically upregulated in brain glioma tissues and cell lines,and was associated with poorer prognosis in patients with glioma. TP73-AS1 knocking down suppressed human brain glioma cell proliferation and invasion in vitro, as well as HMGB1 protein.MiR-142 has been reported to play a pivotal role in cancers,here we observed that TP73-AS1 and miR-142 could negatively regulate each other. Results from luciferase assays suggested that TP73-AS1 might compete with HMGB1 for miR-142 binding.Further,HMGB1/RAGE was involved in TP73-AS1/miR-142 regulation of glioma cell proliferation and invasion. In glioma tissues, TP73-AS1 and HMGB1 expression was up-regulated, whereas miR-142 expression was down-regulated. Data from the present study revealed that TP73-AS1 promoted the brain glioma growth and invasion through acting as a competing endogenous RNA (ceRNA) to promote HMGB1 expression by sponging miR-142. 28379612 2018 The Long Non-Coding RNA TP73-AS1 Interacted With miR-142 to Modulate Brain Glioma Growth Through HMGB1/RAGE Pathway TP73-AS1 TP73-AS1, KIAA0495, PDAM 57212 ENSG00000227372 NR_033708 GRCh38_1:3735601-3747336 ovarian cancer C56.9 NA qPCR, Western blot, etc. ovarian cancer tissues, cell lines (OVCA429, OVCA433, SKOV3, HOSE) up-regulated upregulation of TP73-AS1 was associated with poor prognosis. overexpression of TP73-AS1 promoted cell proliferation, invasion, and migration of OVCA429 cells. TP73-AS1 overexpression enhanced the expression of MMP2 and MMP9 in ovarian cancer cells. 29904939 2018 The lncRNA TP73-AS1 promotes ovarian cancer cell proliferation and metastasis via modulation of MMP2 and MMP9. TP73-AS1 TP73-AS1, KIAA0495, PDAM 57212 ENSG00000227372 NR_033708 GRCh38_1:3735601-3747336 osteosarcoma NA M9180/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. osteosarcoma tissues, cell line (MG-63, SW1353, Saos-2, HOS and U2OS) up-regulated TP73-AS1 expression was significantly increased in OS tissues and cell lines. High TP73-AS1 expression was associated with poor overall survival of OS patients. TP73-AS1 knockdown suppressed OS cells proliferation and invasion in vitro as well as tumor growth in vivo. Furthermore, we identified that miR-142 could act as a direct target for TP73-AS1 and miR-142 inhibition reversed the suppression of OS cells proliferation and invasion induced by TP73-AS1 knockdown. In addition, we showed that TP73-AS1 could function as a sponge of miR-142 to positively regulate Rac1 in OS cells. 29864904 2018 Knockdown of long non-coding RNA TP73-AS1 inhibits osteosarcoma cell proliferation and invasion through sponging miR-142. TPT1-AS1 TPT1-AS1 100190939 ENSG00000170919 NR_024458 GRCh38_13:45341345-45393413 glioma NA M9380/3 microarray, qPCR etc. glioma tissues down-regulated The expression of four lncRNAs in different grades showed that AGAP2-AS1, LINC01198 and MIR155HG were increased with tumor grade, while TPT1-AS1 was decreased. Knockdown of AGAP2-AS1 can inhibit the cell proliferation, migration and invasion, while increase the apoptosis cell rates in vitro. 27764782 2016 LncRNA profile study reveals four-lncRNA signature associated with the prognosis of patients with anaplastic gliomas. TRPM2-AS TRPM2-AS, TRPM2-AS1 101928607 ENSG00000230061 NR_109964 GRCh38_21:44414588-44425272 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissue, cell lines (HCCLM3, Huh7, SMMC-7721, SKHep1, HepG2) up-regulated The expression of TRPM2-AS was higher in most HCC tissues and was significantly correlated with tumor size, AJCC stage, tumor differentiation, and the prognosis of HCC patients. Interfering TRPM2-AS expression using siRNA significantly inhibited cell proliferation and promoted cell apoptosis in two HCC cell lines. 29081064 2017 Long non-coding RNA TRPM2-AS as a potential biomarker for hepatocellular carcinoma TRPM2-AS TRPM2-AS, TRPM2-AS1 101928607 ENSG00000230061 NR_109964 GRCh38_21:44414588-44425272 prostate cancer C61.9 NA microarray, qPCR etc. cell line (PC3) differential expression This essential role, coupled to the TRPM2-AS low-expression levels in healthy tissues, makes this ncRNA a suitable therapeutic target for further clinical studies. To get insights into the survival mechanism controlled by this molecule, we ablated its expression in prostate cancer cells and performed a genome-wide analysis of the transcripts differentially regulated in dying cells. 26484139 2014 Expression-profiling of apoptosis induced by ablation of the long ncRNA TRPM2-AS in prostate cancer cell. TUBA4B TUBA4B, TUBA4 NA ENSG00000243910 NA GRCh38_2:219253243-219272188 ovarian cancer C56.9 NA qPCR, Western blot, RNAi etc. cell lines (A2780, IGROV1,SKOV3, OVCAR3, HOSE 6.3), ovarian cancer tissues down-regulated The expression of lncRNA TUBA4B was significantly decreased in epithelial ovarian cancer tissue specimens. The low lncRNA TUBA4B level was closely related with pathological grade, FIGO stage and lymph node metastases, and serum CA125 level. Enforced expression of lncRNA TUBA4B obviously reduced the proliferation of SKOV3 cells, and attenuated the activation of ERK and Akt signaling pathways. Overexpression of lncRNA TUBA4B inhibits the proliferation of ovarian cancer cells. LncRNA TUBA4B may be an important target for therapeutic intervention in ovarian cancer. 28578489 2018 Downregulation of lncRNA TUBA4B is Associated with Poor Prognosis for Epithelial Ovarian Cancer TUBA4B TUBA4B, TUBA4 NA ENSG00000243910 NA GRCh38_2:219253243-219272188 non small cell lung cancer C34 M8046/3 qPCR, Cell proliferation assay etc. NSCLC tissues, cell lines (SPCA-1, NCI-H1299, A549, NCI-H441, LTEP-a2) down-regulated We found TUBA4B was lower expressed in NSCLC and five cell lines. The lower expression of TUBA4B was remarkably correlated with advanced TNM stage and lymph node metastasis and served as a predictor for overall survival of NSCLC. 27411923 2016 Low Expression LncRNA TUBA4B is a Poor Predictor of Prognosis and Regulates Cell Proliferation in Non-Small Cell Lung Cancer. TUC338 NA 102157401 ENSG00000282977 NR_109828 GRCh38_12:53464468-53465057 lung cancer C34 NA qPCR, Western blot lung cancer tissues, cell lines (A549, H1755, SK-MES-1, H1299) up-regulated the expression of TUC338 was correlated with the overall survival, tumor size and lymph node metastasis in patients, but not with age and gender.the activity of lung cancer cells was decreased, as well as the invasion ability after interference with TUC338.TUC338 can promote the development of lung cancer through regulating MAPK pathway. 29424901 2018 LncRNA TUC338 promotes invasion of lung cancer by activating MAPK pathway. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 intrahepatic cholangiocarcinoma C22 M8160/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (HuH28, HuCCT1, RBE, HCCC-9810) up-regulated In this study, we investigated the role of TUG1 in the pathogenesis of intrahepatic cholangiocarcinoma (ICC).TUG1 is upregulated in ICC samples, which correlates with poor prognosis and adverse clinical pathological characteristics. Knockdown of TUG1 inhibited the proliferation, motility, and invasiveness of cultured ICC cells, and decreased tumor burden in a xenograft mouse model. When we explored the mechanisms underlying these effects, we found that TUG1 acts as an endogenous competing RNA (ceRNA) that ‘sponges’ miR-145, thereby preventing the degradation of Sirt3 mRNA and increasing expression of Sirt3 and GDH proteins. Accordingly, glutamine consumption, a-KG production, and ATP levels were dramatically decreased by TUG1 knockdown in ICC cells, and this effect was reversed by miR-145 inhibition. These findings indicate that the TUG1/miR-145/Sirt3/GDH regulatory network may provide a novel therapeutic strategy for treatment of ICC. 29371936 2017 LncRNA TUG1 sponges miR-145 to promote cancer progression and regulate glutamine metabolism via Sirt3/GDH axis TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 clear cell renal cell carcinoma C64.9 M8005/0 qPCR etc. ccRCC tissues up-regulated The relative level of TUG1 was significantly higher in ccRCC tissues compared to the adjacent non-tumor tissues. Furthermore, TUG1 was associated significantly with histological grade, tumor stage, lymph node metastasis and distant metastasis. 28121352 2017 Prognostic significance of overexpressed long non-coding RNA TUG1 in patients with clear cell renal cell carcinoma. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 malignant melanoma NA M8720/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (A375, WM35, SK-MEL-5, SK-MEL-2), malignant melanoma tissues up-regulated Downregulation of either TUG1 or AEG1 suppressed cell growth and metastasis.miR-129-5p can bind directly to AEG1 and TUG1 can directly sponge miR-129-5p.Inhibition of TUG1 expression suppressed the expression of Bcl-2, MMP-9, and cyclin D1, and raised the level of cleaved caspase3 by modulating AEG1 level in melanoma cells. Inhibition of TUG1 reduced the growth of tumors in vivo and improved the chemosensitivity of A375 cells to cisplatin and 5-FU.Reduction of TUG1 level suppressed cell growth and metastasis by regulating AEG1 expression mediated by targeting miR-129-5p. 29543785 2018 Long Noncoding RNA Taurine-Upregulated Gene1 (TUG1) Promotes Tumor Growth and Metastasis Through TUG1/Mir-129-5p/Astrocyte-Elevated Gene-1 (AEG-1) Axis in Malignant Melanoma. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 thyroid cancer C73.9 NA qPCR, Western blot etc. thyroid cancer tissues, cell lines (ATC, SW1736, KAT18, FTC, FTC133, HGC-27) up-regulated TUG1 contributes to the progression of thyroid cancer cells through regulating miR-145/ZEB1 signal pathway.LncRNA TUG1 was found to be up-regulated in thyroid cancer tissues and thyroid cancer cells compared with that in the human normal breast epithelial cell HGC-27.Increased lncRNA TUG1 expression was found to significantly promote tumor cell proliferation,and facilitate cell invasion,while down-regulated TUG1 could obviously inhibit cell proliferation,migration/invasion and reverse EMT to MET.These results indicated that TUG1 may contribute to the progression of thyroid cancer cells by function as a ceRNA competitive sponging miR-145,and that lncRNA TUG1 is associated with tumor progression in thyroid cancer cells. 28645161 2017 LncRNA TUG1 influences papillary thyroid cancer cell proliferation, migration and EMT formation through targeting miR-145. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 epithelial ovarian cancer C56.9 NA qPCR, Western blot etc. epithelial ovarian cancer tissues, cell line (SKOV3) up-regulated LncRNA TUG1 expression was higher in tumor tissue compared to paired adjacent tissue, and it was positively correlated with pathological grade, tumor size and FIGO stage . Kaplan-Meier curve showed that lncRNA TUG1 high expression was associated with worse OS . Multivariate Cox analysis indicated that lncRNA TUG1 high expression (vs. low expression) was independently predictive factor for shorter OS. In vitro, cells proliferation was promoted after treatment with lncRNA TUG1 mimic and was suppressed after treatment with lncRNA TUG1 inhibitor. In addition, cells apoptosis rate was decreased in lncRNA TUG1 mimic group compared to NC1 mimic, and increased in lncRNA TUG1 inhibitor group compared to NC2 inhibitor.In conclusion, lncRNA TUG1 is positively correlated with advanced disease and poor prognosis, and it promotes cells proliferation and inhibits cells apoptosis in EOC cells. 29742691 2018 Long non-coding RNA taurine-upregulated gene 1 predicts unfavorable prognosis, promotes cells proliferation, and inhibits cells apoptosis in epithelial ovarian cancer. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 cholangiocarcinoma NA M810/3 qPCR, Western blot etc. CCA tissues, cell lines (QBC939, Huh-28, HuCCT1, KMBC, CCLP-1, HCCC-9810 and RBE) up-regulated up-regulation of TUG1 in both CCA tissues and cell lines. overexpression of TUG1 is linked to tumor size (p=0.005), TNM stage (p=0.013), postoperative recurrence (p=0.036) and overall survival (p=0.010) of CCA patients. TUG1 may be a rational CCA-related prognostic factor and therapeutic target. 29029475 2017 The prognostic potential and carcinogenesis of long non-coding RNA TUG1 in human cholangiocarcinoma. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 breast cancer C50 NA qPCR, Western blotting etc. cell lines (MDA-MB-231, MDA-MB-453, MDAMB-468, T-47D, MCF-7, ZR-75, SK-BR-3) down-regulated TUG1 overexpression significantly suppressed cell proliferation by causing cell cycle arrest and inducing apoptosis in breast cancer cells, while TUG1 knockdown caused increased cell growth via promoting cell cycle progression and regulating the expression of cyclinD1 and CDK4. Further functional assays indicated that TUG1 overexpression significantly promoted cell migration and invasion while TUG1 knockdown had the opposite effects. Our findings indicate that the lncRNA TUG1 is a tumor suppressor in breast cancer, and may serve as a novel prognostic biomarker and potential therapeutic target for patients with breast cancer. 28950664 2017 Downregulation of the long non-coding RNA TUG1 is associated with cell proliferation, migration, and invasion in breast cancer TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 pancreatic cancer C25 NA qPCR, Western blot, Luciferase reporter assay, RIP pancreatic tumor tissues, cell lines (PANC-1, AsPC-1, HEK 293T) up-regulated TUG1 was overexpressed in PC tissues and cell lines, and high expression of TUG1 predicted poor prognosis. at least partially, by functioning as an endogenous ‘sponge’ and competing for miR-382 binding to the miRNA target EZH2. 28813705 2017 The Lncrna-TUG1/EZH2 Axis Promotes Pancreatic Cancer Cell Proliferation, Migration and EMT Phenotype Formation Through Sponging Mir-382 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 cervical cancer C53 NA qPCR, Western blot etc. cervical cancer tissues, cell lines (HeLa, CaSki) up-regulated TUG1 expression was upregulated in cervical cancer tissues and correlated with advanced clinical features and poor overall survival.In addition, our results indicated that TUG1 could act as an endogenous sponge by directly binding to miR-138-5p and suppressed miR-138-5p expression. 29029428 2017 Long non-coding RNA TUG1 promotes cervical cancer progression by regulating the miR-138-5p-SIRT1 axis TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues down-regulated The lncRNAs HOTAIR, H19 and MALAT1 were up-regulated, while PANDAR and TUG1 were down-regulated in NSCLC cancer tissues compared with the corresponding adjacent normal tissue. 28121347 2017 The use of lncRNA analysis for stratification management of prognostic risk in patients with NSCLC. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 urothelial cancer NA M8120/3 qPCR urothelial carcinoma tissues, cell lines (VM-CUB1, SW-1710, HT-1376, 5637, and BFTC-905) differential expression Altered expression of individual lncRNAs was associated with overall survival, but not consistently between both patient cohorts. Interestingly, lower expression of TUG1 in a subset of UC patients with muscle-invasive tumours was significantly correlated with worse OS in both cohorts. 28430799 2017 Diagnostic and prognostic value of long noncoding RNAs as biomarkers in urothelial carcinoma TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 oral squamous cell carcinoma C06.9 M8070/3 qPCR, Western blot, Luciferase reporter assay Both tumors, OSCC cell lines (HN4, HN6, SCC-25, CAL-27, NHOK) up-regulated In conclusion, our data revealed that TUG1 confers oncogenic function in OSCC and TUG1/miR-219/FMNL2 axis may be a novel therapeutic strategy in this disease.Clinically, the expression of TUG1 and FMNL2 were increased, but miR-219 was decreased in primary tumors compared to non-tumor tissues. Both the upregulated TUG1, and FMNL2 and the downregulated miR-219 was associated with advanced stage of OSCC and poor overall survival.Increasing evidences indicated that the dysregulated lncRNAs and miRNAs were correlated with tumor progression and cancer-related cellular process, including proliferation, apoptosis, migration, and invasion. 28979812 2017 Long non-coding RNA TUG1 promotes progression of oral squamous cell carcinoma through upregulating FMNL2 by sponging miR-219 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. cell lines (A549, SK-MES-1, NCI-H1299 etc.) down-regulated TUG1, recruiting and binding to polycomb repressive complex 2 (PRC2), is generally downregulated in NSCLC tissues. Interestingly, inhibition of TUG1 could upregulate homeobox B7 (HOXB7) expression; ChIP assays demonstrated that the promoter of HOXB7 locus was bound by EZH2 (enhancer of zeste homolog 2), a key component of PRC2, and was H3K27 trimethylated. This TUG1-mediated growth regulation is in part due to specific modulation of HOXB7, thus participating in AKT and MAPK pathways. Together, these results suggest that p53-regulated TUG1 is a growth regulator, which acts in part through control of HOXB7. The p53/TUG1/PRC2/HOXB7 interaction might serve as targets for NSCLC diagnosis and therapy. 24853421 2014 P53-regulated long non-coding RNA TUG1 affects cell proliferation in human non-small cell lung cancer, partly through epigenetically regulating HOXB7 expression. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 bladder cancer C67 NA qPCR etc. tumor tissues up-regulated Taurine up-regulated gene 1 (TUG1) is a long non-coding RNA (lncRNA), has been reported that be dysregulated in various tumors, involved in proliferation and apoptosis in a variety of tumor cells. lncRNA TUG1 may be a useful prognostic biomarker in cancer patients. 29029461 2017 Prognostic value of long non-coding RNA TUG1 in various tumors. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 colorectal cancer C19.9 NA qPCR, Western blot etc. CRC tissues, cell lines (SW480, HCT116, HT29, SW620, LOVO etc.) up-regulated Our data showed that the levels of TUG1 were upregulated in both CRC cell lines and primary CRC clinical samples. TUG1 upregulation was closely correlated with the survival time of CRC patients. Overexpression of TUG1 in CRC cells increased their colony formation, migration, and invasion invitro and promoted their metastatic potential in vivo, whereas knockdown of TUG1 inhibited the colony formation, migration, and invasion of CRC cells invitro. It is also worth pointing out that TUG1 activated EMT-related gene expression 26856330 2016 The long non-coding RNA TUG1 indicates a poor prognosis for colorectal cancer and promotes metastasis by affecting epithelial-mesenchymal transition TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN53), gastric adenocarcinomas tissues up-regulated The expression pattern indicated that MALAT1 synchronize the expression level of KLF4 and miR-145 and MALAT1 had a strong impact than TUG1 in regulating KLF4 through sponging miR-145. 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 glioma NA M9380/3 qPCR, RNAi, Cell proliferation assay etc. glioma tissues, cell lines (U251 and SHG-44) down-regulated Taurine upregulated gene 1 expression was significantly inhibited in glioma and showed significant correlation with WHO Grade, tumor size and overall survival. Further experiments revealed that the dysregulation of taurine upregulated gene 1 affected the apoptosis and cell proliferation of glioma cells. Moreover, taurine upregulated gene 1 could induce the activation of caspase-3 and-9, with inhibited expression of Bcl-2, implying the mechanism in taurine upregulated gene 1-induced apoptosis. taurine upregulated gene 1 promoted cell apoptosis of glioma cells by activating caspase-3 and -9-mediated intrinsic pathways and inhibiting Bcl-2-mediated anti-apoptotic pathways, acting as a tumor suppressor in human glioma. 26748401 2016 LncRNA TUG1 acts as a tumor suppressor in human glioma by promoting cell apoptosis. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 bladder cancer C67 NA qPCR, Western blot etc. bladder cancer tissues, cell lines (SW780, HT1376, BIU87 and T24) up-regulated The levels of TUG1 and HMGB1 were remarkably increased in bladder cancer tissues and cell lines. TUG1 knockdown inhibited cell proliferation, promoted cell apoptosis and decreased colony survival in SW780 and BIU87 cells under radiation. 28376901 2017 Down-regulation of LncRNA TUG1 enhances radiosensitivity in bladder cancer via suppressing HMGB1 expression TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 bladder cancer C67 NA qPCR, RNAi, MTT assay etc. bladder cancer tissues, cell line (T24) up-regulated We observed significantly increased levels of TUG1 in tumor tissue in comparison to adjacent non-tumor bladder tissue. TUG1 levels were significantly increased in metastatic tumors and were associated with shorter overall survival of MIBC patients. TUG1 silencing in vitro led to 34 % decrease in cancer cell proliferation and 23 % reduction in migration capacity of cancer cells. 27460088 2016 Overexpression of long non-coding RNA TUG1 predicts poor prognosis and promotes cancer cell proliferation and migration in high-grade muscle-invasive bladder cancer. TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 colorectal cancer C19.9 NA qPCR, western blot, Luciferase reporter assay etc. colorectal cancer tissues, cell lines (HCT116, SW480, HT29, LOVO and SW620) up-regulated Our data showed that lncRNA TUG1 was upregulated in CRC cells, miR-600 was downregulated in CRC tissues, cell lines and CRC metastatic tissues, and low miR-600 expression predicted a poor clinical prognosis. 29776371 2018 LncRNA TUG1 promoted KIAA1199 expression via miR-600 to accelerate cell metastasis and epithelial-mesenchymal transition in colorectal cancer TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 osteosarcoma NA M9180/3 qPCR, etc. osteosarcoma cell lines (MG-63, U2OS, SAOS-2), hFOB cell line. osteosarcoma tissues, normal bone tissues. down-regulation In conclusion, our data support TUG1 as a potential prognostic predictor and gene therapy target with its high expression in tumor tissues and its association with carcinogenesis and progression in osteosarcoma.TUG1, which is induced by p53, can also bind to PRC2 and miRNAs and then play pivotal suppressor role in cancer cell growth. It was also reported that TUG1 promotes cell growth and apoptosis by epigenetically silencing of KLF2; Kaplan-Meier curve showed a decreased overall survival time of osteosarcoma patients with high TUG1 expression. 29970697 2018 Role of taurine upregulated gene 1 as a predictor of poor outcome in osteosarcoma. TUNAR TUNAR, HI-LNC78, LINC00617, TUNA 100507043 ENSG00000250366 NR_038861 GRCh38_14:95876392-95925571 neuroendocrine prostate cancer NA NA RNA-seq, Microarray, qPCR etc. neuroendocrine prostate cancer tissues up-regulated Top candidate lncRNAs FENDRR, H19, LINC00514, LINC00617, and SSTR5-AS4 identified in this study are implicated in the development of NEPC. 29757368 2018 The long noncoding RNA landscape of neuroendocrine prostate cancer and its clinical implications. TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR etc. PDAC tissues, cell lines (HPDE6-C7, PANC-1, BxPC-3, AsPC-1, and PL45) down-regulated Our data showed that the relative level of LOC285194 in PDAC cells was significantly lower than that in normal human pancreatic duct epithelial cell line. Also, the expression of LOC285194 in PDAC tissues was significantly lower than that in adjacent non-tumor tissues. By statistical analyses, low LOC285194 expression was observed to be closely correlated with clinical stage, lymphnode metastasis and liver metastasis. 25550852 2014 Expression of long non-coding RNA LOC285194 and its prognostic significance in human pancreatic ductal adenocarcinoma. TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 gastric cancer C16 NA microarray, qPCR, RNAi etc. gastric cancer tissues down-regulated The results indicated that TUSC7 was downregulated in GC samples and was an independent prognostic indicator of disease-free survival (DFS) and disease-specific survival (DSS) in GC patients.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC. 25765901 2015 Reciprocal repression between TUSC7 and miR-23b in gastric cancer. TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. HCC tissues, cell lines (HepG2, MHCC97L, Hep3B, SMMC-7721, MHCC97H, and Huh7) down-regulated In this study, we observed that the expression of TUSC7 was immensely decreased in HCC. Clinically, the lower expression of TUSC7 predicted poorer survival and may be an independent risk factor for HCC patients. Moreover, TUSC7 inhibited cell metastasis, invasion, and epithelial-to-mesenchymal transformation (EMT) through competitively binding miR-10a. Furthermore, we found that TUSC7 could decrease the expression of Eph tyrosine kinase receptor A4 (EphA4), a downstream target of miR-10a as well as an EMT suppressor, through TUSC7-miR-10a-EphA4 axis. 27002617 2016 Long non-coding RNA TUSC7 acts a molecular sponge for miR-10a and suppresses EMT in hepatocellular carcinoma. TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 glioma NA M9380/3 qPCR etc. glioma tissues down-regulated Previous studies13,14 indicated that FOXD2-AS1 expression was up-regulated in non-small cell lung cancer and gastric cancer. the low expression of TUSC7 was associated with poor clinicopathological characteristics of glioma, including WHO grade (p = 0.002) and KPS (p = 0.026). Then, the low TUSC7 level was correlated with shorter disease free survival (DFS) and overall survival (OS) than low level (both p = 0.05).TUSC7 may be a potential biomarker in the prognosis of glioma. 28925483 2017 Long non-coding RNA TUSC7 expression is independently predictive of outcome in glioma. TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues, cell lines (A549, H1299, H1650, H1975, H23, and H358) down-regulated The expression level of TUSC7 was lower in NSCLC tissues and lung cancer cells compared with their normal counterparts. Lower expression of TUSC7 in NSCLC tissues was associated with larger tumor size and higher TNM stage. Patients with lower TUSC7 expression had worse overall survival compared with the high expression cases. Univariate and multivariate analyses suggested that low expression of TUSC7 was an independent poor prognostic indicator for NSCLC patients. Moreover, upregulation of TUSC7 expression could inhibit proliferation of lung cancer cell in vitro 27158360 2016 Downregulation of the long non-coding RNA TUSC7 promotes NSCLC cell proliferation and correlates with poor prognosis TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 osteosarcoma NA M9180/3 qPCR, Cell transfection, Western blot, Flow cytometry assay etc. osteosarcoma tissues, cell lines (MG63 and HOS) down-regulated Here, we reported a novel lncRNA, tumor suppressor candidate 7 (TUSC7), was significantly downregulated in osteosarcoma tissues compared with paired non-tumor tissues and low expression of TUSC7 indicated poor survival of osteosarcoma patients. Further analysis revealed that loss copy number of TUSC7 was correlated with low expression of TUSC7, and additionally, loss of TUSC7 copy number also indicated poor prognosis of osteosarcoma patients. Cell counting kit 8 (CCK-8) assay revealed that after silence of TUSC7, cell proliferation ability increased and the colony formation ability also increased. 26781978 2016 Long non-coding RNA tumor suppressor candidate 7 functions as a tumor suppressor and inhibits proliferation in osteosarcoma. TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 osteosarcoma NA M9180/3 microarray, qPCR, FISH etc. osteosarcoma tissues, cell lines (U2OS, SAOS-2, HOS etc.) down-regulated Notably, these CNAs often involve the noncoding RNAs LOC285194 and BC040587 and, in some cases, a tumor suppressor gene that encodes the limbic system-associated membrane protein (LSAMP). Depleting either LSAMP or LOC285194 promoted proliferation of normal osteoblasts by regulation of apoptotic and cell-cycle transcripts and also VEGF receptor 1. Moreover, genetic deletions of LOC285194 or BC040587 were also associated with poor survival of osteosarcoma patients. 20048075 2010 Recurrent focal copy-number changes and loss of heterozygosity implicate two noncoding RNAs and one tumor suppressor gene at chromosome 3q13.31 in osteosarcoma. TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 colorectal cancer C19.9 NA qPCR, Cell transfection, Western blot, Luciferase reporter assay, CCK-8 assay etc. CRC tissues, cell lines (M5, DLD1, HCT116, SW480, SW620, and HT29) down-regulated TUSC7 was significantly downregulated in CRC tissues. Ectopic expression of TUSC7 in HCT116 and SW480 cells significantly inhibited cell proliferation rate. Flow cytometry analyses revealed cycles were arrested at G1 phase after TUSC7 overexpression. We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p. 28214867 2017 The Novel Long Noncoding RNA TUSC7 Inhibits Proliferation by Sponging MiR-211 in Colorectal Cancer. TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 colorectal cancer C19.9 NA qPCR etc. CRC tissues, cell lines (CaCO-2, HCT8, LoVo, CCC-HIE-2 etc.) down-regulated The relative expression levels of LOC285194 was significantly lower in tumor tissues and colorectal cancer cell lines compared with adjacent normal tissues and normal intestinal mucous cell line. In addition, low expression of LOC285194 was correlated with larger tumor size, higher tumor stage, and more distant metastasis. Our data indicate that LOC285194 might be a novel prognostic indicator in colorectal cancer and may be a potential target for diagnosis and gene therapy. 23680400 2013 Low expression of LOC285194 is associated with poor prognosis in colorectal cancer. u50535 NA NA NA NA NA colorectal cancer C19.9 NA qPCR, western blot, Luciferase reporter assay, RNA-seq, etc. Human CRC cell lines (HCT116, HCT8, DLD1, HCT15), CRC tissues. up-regulated Taken together, these findings suggest that u50535 can promote CRC growth and metastasis and may serve as a potential biomarker in CRC.Higher expression of u50535 obtained worse overall survival than lower expression (n?=?86). As for the luciferase assay of miR-200 interaction with ZEB1, the 3′-UTR regions of ZEB1 was cloned into psi-CHECK2 vector (Promega) and the miR200 mimic was purchased from Ribo company. LncRNA-u50535 expression is frequently increased and is associated with poor prognosis of CRC. 29970882 2018 The novel long noncoding RNA u50535 promotes colorectal cancer growth and metastasis by regulating CCL20. UBE2CP3 NA NA ENSG00000250384 NA GRCh38_4:57072683-57073132 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot etc. HCC tissues, cell line (HepG2 and SMMC-7721) up-regulated UBE2CP3 expression was higher in HCC tissues than in para-tumor tissues and was up-regulated in tissues with high EV density. Functionally, we found that in the co-culture systems, HCC cells overexpressing UBE2CP3 promoted HUVEC proliferation, migration and tube formation via the activation of ERK/HIF-1a/p70S6K/VEGFA signalling, increasing the level of VEGFA in HCC cell supernatant. In addition, the opposite results appeared when the expression of UBE2CP3 in HCC cells was knocked down. Consistent with these results, CAM angiogenesis assays and nude mouse tumorigenicity assays showed that UBE2CP3 expression up-regulated EV density in vivo. When grouped by both UBE2CP3 expression and EV density, HCC patients in the high category had poor OS. 29866133 2018 Long non-coding RNA UBE2CP3 enhances HCC cell secretion of VEGFA and promotes angiogenesis by activating ERK1/2/HIF-1α/VEGFA signalling in hepatocellular carcinoma. uc.338 NA NA NA NA NA non small cell lung cancer C34 M8046/3 qPCR etc. non small cell lung cancer tissues up-regulated We found that uc.338 expression levels were significantly upregulated in NSCLC compared with the matched noncancerous lung tissues. More importantly, Kaplan-Meier survival analysis demonstrated that higher uc.338 expression levels were associated with a shorter overall survival (P< 0.0016) and disease-free survival (p< 0.0001) in NSCLC patients. 29843223 2018 Up-regulation of long noncoding RNA uc.338 predicts poor survival in non-small cell lung cancer uc.38 NA NA NA NA NA breast cancer C50 NA qPCR, Western blot, RIP breast cancer tissues, cell lines (SUM1315, MCF-10A, MCF-7, ZR-75-1, BT-474, MDA-MB-231, SUM1315 and SK-BR-3) down-regulated The expression of uc.38, a T-UCR, was down-regulated in both breast cancer tissues and breast cancer cell lines. uc.38 was expressed at significantly lower levels in larger tumours and tumours of more advanced stages.up-regulation of uc.38 expression inhibited cell proliferation and induced cell apoptosis.uc.38 suppressed breast cancer. uc.38 negatively regulated the expression of the pre-B-cell leukaemia homeobox 1 (PBX1) protein and subsequently affected the expression of Bcl-2 family members,ultimately inducing breast cancer cell apoptosis.The level of expression and type of TUCR have been shown to be closely related to the survival rates of patients with cancer. 29312798 2017 uc.38 induces breast cancer cell apoptosis via PBX1. uc.388 NA NA NA NA NA colorectal cancer C19.9 NA qPCR etc. CRC tissues down-regulated Expression levels of uc.73 and uc.388 were significantly decreased in CRC tissue, and uc.73 indicated a positive correlation with overall survival. The lower expression of uc.388 was associated with the distal location of CRC. Our preliminary results suggest that uc.73 and uc.388 could be potential diagnostic and prognostic biomarkers in CRC patients. 22328099 2012 Expression levels of transcribed ultraconserved regions uc.73 and uc.388 are altered in colorectal cancer. uc.73 NA NA NA NA NA colorectal cancer C19.9 NA qPCR etc. CRC tissues down-regulated Expression levels of uc.73 and uc.388 were significantly decreased in CRC tissue, and uc.73 indicated a positive correlation with overall survival. The lower expression of uc.388 was associated with the distal location of CRC. Our preliminary results suggest that uc.73 and uc.388 could be potential diagnostic and prognostic biomarkers in CRC patients. 22328099 2012 Expression levels of transcribed ultraconserved regions uc.73 and uc.388 are altered in colorectal cancer. uc001gzl.3 NA NA NA NA NA lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. lung adenocarcinoma tissues up-regulated The remaining 10 lncRNAs, showed significantly different expression in the tumor samples. For 9 of these, expression was altered in the same direction as had been detected by microarray analysis. Differentially expressed lncRNAs in early stage lung adenocarcinoma and suggest that lncRNAs may be novel candidate biomarkers for the early detection of this disease. 25758555 2015 Identification of biomarkers for the detection of early stage lung adenocarcinoma by microarray profiling of long noncoding RNAs. UC001kfo ACTA2-AS1, ZXF1, uc001kfo.1 100132116 ENSG00000180139 NR_125373 GRCh38_10:88932390-88940820 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, MTT assay etc. HCC tissues, cell lines (GSG701, Hep3B, HepG2, Huh7, SMMC 7721 and HCC LM3) up-regulated The expression of UC001kfo was upregulated in HCC tissues and cell lines in comparison with tumour-adjacent tissues and normal hepatocytes, respectively. In addition, a high UC001kfo level was determined to be correlated with macro-vascular invasion and TNM stage of HCC. In addition, UC001kfo was verified to promote the proliferation, metastasis and epithelial-mesenchymal transition (EMT) in HCC cells in both in vitro and in vivo assays. Mechanistically, a-SMA was indicated as a potential target gene of UC001kfo in mediating HCC metastasis. 28088733 2017 Long non-coding RNA UC001kfo promotes hepatocellular carcinoma proliferation and metastasis by targeting a-SMA. UC001kfo ACTA2-AS1, ZXF1, uc001kfo.1 100132116 ENSG00000180139 NR_125373 GRCh38_10:88932390-88940820 lung adenocarcinoma C34 M8140/3 microarray, qPCR, RNAi etc. lung adenocarcinoma tissues, cell lines (A549) up-regulated Here we found that LncRNA ZXF1 levels were remarkably increased in lung adenocarcinoma tissues compared with adjacent non-cancerous lung tissues, and up-regulated LncRNA ZXF1 was correlated with lymph node metastasis, tumor pathological stage and the extent of lymph node metastasis. The 3-year overall survival rate of patients with higher LncRNA ZXF1 levels was remarkably reduced compared with patients with lower LncRNA ZXF1 levels, implying that patients with high levels of LncRNA ZXF1expression had a relatively poor prognosis. 24721325 2014 Enhanced expression of long non-coding RNA ZXF1 promoted the invasion and metastasis in lung adenocarcinoma. uc001lsz NA NA NA NA NA prostate cancer C61.9 NA qPCR etc. cell lines (Du-145, PC-3) up-regulated We found that comparing with respective normal cell line, uc001lsz was lowly expressed in gastric cancer (AGS, MGC-803 and SGC-7901), lung cancer (A549) and liver cancer (SMMC-7721 and HepG2) cell lines, while only highly expressed in prostate cancer (Du-145 and PC-3) cell lines. 24063685 2013 Long non-coding RNA expression profile in human gastric cancer and its clinical significances. uc001lsz NA NA NA NA NA lung cancer C34 NA qPCR etc. cell lines (A549) down-regulated We found that comparing with respective normal cell line, uc001lsz was lowly expressed in gastric cancer (AGS, MGC-803 and SGC-7901), lung cancer (A549) and liver cancer (SMMC-7721 and HepG2) cell lines, while only highly expressed in prostate cancer (Du-145 and PC-3) cell lines. 24063685 2013 Long non-coding RNA expression profile in human gastric cancer and its clinical significances. uc001lsz NA NA NA NA NA liver cancer C22.0 NA qPCR etc. cell lines (SMMC-7721, HepG2) down-regulated We found that comparing with respective normal cell line, uc001lsz was lowly expressed in gastric cancer (AGS, MGC-803 and SGC-7901), lung cancer (A549) and liver cancer (SMMC-7721 and HepG2) cell lines, while only highly expressed in prostate cancer cell lines (Du-145 and PC-3). 24063685 2013 Long non-coding RNA expression profile in human gastric cancer and its clinical significances. uc001lsz NA NA NA NA NA gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues, cell lines (GES-1, AGS, MGC-803, SGC-7901) down-regulated The most down-regulated lncRNAs in gastric cancer tissues were FER1L4, uc001lsz, BG491697, AF131784, uc009ycs, BG981369, AF147447, HMlincRNA1600, and AK054588; while the most up-regulated ones were H19, HMlincRNA717, BM709340, BQ213083, AK054978, and DB077273. 24063685 2013 Long non-coding RNA expression profile in human gastric cancer and its clinical significances. uc002pyc ZNF350-AS1, HCCAT3, uc002pyc NA NA NA NA colorectal cancer C19.9 NA microarray, qPCR, Luciferase reporter assay etc. CRC tissues, cell lines (HCT116, RKO, HT29, SW620 etc.) up-regulated Of the seletced lncRNAs, four lncRNAs named CCAT3, CCAT4, CCAT5, and CCAT6 (also named MYCLo-2) are upregulated in CRC cell lines, and two lncRNAs named CCAT7 and CCAT8 are downregulated in CRC cell lines. MYC-regulated lncRNAs, named MYCLos. The MYC-regulated MYCLos may function in cell proliferation and cell cycle by regulating MYC target genes such as CDKN1A (p21) and CDKN2B (p15), suggesting new regulatory mechanisms of MYC-repressed target genes through lncRNAs. 25663692 2015 Role of MYC-regulated long noncoding RNAs in cell cycle regulation and tumorigenesis. uc002pyc ZNF350-AS1, HCCAT3, uc002pyc 101669766 ENSG00000269235 NR_103847 GRCh38_19:51949134-51981367 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RIP, RNA pull-down assay etc. HCC tissues up-regulated AY129027, uc002pyc and DQ786243 were over-expressed in HCC, whereas the expression of AK055007 and AK123790 was decreased. 21769904 2011 Long noncoding RNA high expression in hepatocellular carcinoma facilitates tumor growth through enhancer of zeste homolog 2 in humans. uc002yug.2 LINC01426, lincRNA-uc002yug.2 NA NA NA NA esophageal squamous cell cancer NA NA qPCR, Western blot, Luciferase reporter assay etc. ESCC tissues up-regulated We found that lincRNA-uc002yug.2 was commonly overexpressed in ESCC. Moreover, lincRNA-uc002yug.2 promoted a combination of RUNX1 and alternative splicing (AS) factors in the nucleus to produce more RUNX1a, the short isoform and inhibitor of RUNX1, and reduce CEBPa (CCAAT/enhancer-binding protein-a) gene expression, thereby promoting ESCC progression. The expression levels of lincRNA-uc002yug.2 in ESCC might be a prognostic factor for survival. 25486427 2014 LincRNA-uc002yug.2 involves in alternative splicing of RUNX1 and serves as a predictor for esophageal cancer and prognosis. uc004bbl.1 NA NA NA NA NA lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. lung adenocarcinoma tissues down-regulated The remaining 10 lncRNAs, showed significantly different expression in the tumor samples. For 9 of these, expression was altered in the same direction as had been detected by microarray analysis. Differentially expressed lncRNAs in early stage lung adenocarcinoma and suggest that lncRNAs may be novel candidate biomarkers for the early detection of this disease. 25758555 2015 Identification of biomarkers for the detection of early stage lung adenocarcinoma by microarray profiling of long noncoding RNAs. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 bladder cancer C67 NA qPCR,Western blot Human bladder cancer cell lines (5637, UMUC2 and T24) down-regulated To explore the circulating exosomal lncRNA-UCA1, we isolated exosomes from the serum of bladder cancer patients and matched healthy donors.Hence, it is necessary to explore the precise mechanism that how cancer cells reshape their surrounding microenvironment under hypoxic conditions. Several studies have described that exosomal proteins and miRNAs derived from hypoxic tumor cells are transferred or delivered to modulate biological function and cell signaling of recipient cells [19, 31, 32]. 28841829 2017 Hypoxic exosomes facilitate bladder tumor growth and development through transferring long non-coding RNA-UCA1. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 glioblastoma NA M9440/3 qPCR etc. cell line (U251 and U87MG) up-regulated lncRNA UCA1/miR-182 axis has been regarded as a nodal driver of glioma invasion mediated by GB-associated stromal cells (GASCs) and GASC-secreted chemokine CXCL14.In clinical specimens, CXCL14 upregulation in GASCs also correlated with poor prognosis. Notably, CXCL14-high GASCs mediated lncRNA UCA1 upregulation and miR-182 downregulation in glioma cells. Moreover, miR-182 directly bound to the fructose-2,6-biphosphatase PFKFB2.UCA1/miR-182 axis thereby modulated GASC-induced glycolysis in glioma cells. Overall, UCA1/miR-182/PFKFB2 axis modulates chemokine CXCL14 secretion, glycolysis and invasion of glioma cells in GASCs. 29655792 2018 Long non-coding RNA UCA1/miR-182/PFKFB2 axis modulates glioblastoma-associated stromal cells-mediated glycolysis and invasion of glioma cells. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 gallbladder cancer C23.9 NA qPCR, Western blot etc. GBC tissues up-regulated UCA1 was significantly overexpressed in gallbladder cancer (GBC) and positively correlated with tumor size, lymph node metastasis,TNM stage and short survival time. UCA1 promoted GBC progression through recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p21 and E-cadherin, and epigenetically suppressing their transcript.The ‘sponge’ role of UCA1 in cytoplasm had been investigated more than once. Through binding to microRNAs (miRNAs) response elements that could directly suppress their target protein expression, UCA1 has an oncogenic function on various human cancers, such as bladder cancer, non-small cell lung cancer, hepatocellular carcinoma and etc. 28624787 2017 Long non-coding RNA UCA1 promotes gallbladder cancer progression by epigenetically repressing p21 and E-cadherin expression. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 multiple myeloma C42.1 M9732/3 qPCR cell line (BMPC) differential expression UCA1 levels correlated with albumin and monoclonal immunoglobulin serum levels, cytogenetic aberrations, and survival of MM patients.higher levels of UCA1 were significantly associated with worse OS of MM patients in the time period of 1-4 years. 28543758 2017 Deregulated expression of long non-coding RNA UCA1 in multiple myeloma UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown osteosarcoma cell lines (MG63, SAOS2, U2OS, HOS, SW1353), osteoblastic cell line (hFOB1.19) up-regulated HIF-1a induced cell growth through the UCA1/PTEN/AKT signaling pathway. To conclude, our integrated approach demonstrates that UCA1 confers a tumor promoter function by promoting cell proliferation and silencing of the PTEN/AKT signaling pathway in osteosarcoma. 29328452 2018 HIF-1a-induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 hypopharyngeal carcinoma C13 NA qPCR, RNAi, Cell cycle assay, Cell migration and invasion assay etc. HSCC tissues, cell line (FaDu) up-regulated We confirmed the upregulation of UCA1 in HSCC by assessing its expression levels in a cohort of 53 patient tumors and paired non-tumor samples. In addition, we found that high UCA1 expression was significantly associated with advanced T category, late clinical stage, greater lymphatic invasion, and worse prognosis. Furthermore, in vitro experiments demonstrated that UCA1 functioned as an oncogene by promoting the proliferation and invasion and preventing the apoptosis of HSCC cells. 28327194 2017 Upregulation of the long noncoding RNA UCA1 affects the proliferation, invasion, and survival of hypopharyngeal carcinoma. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 epithelial ovarian cancer C56.9 NA qPCR, RNAi, RIP, Luciferase reporter assay etc. ovarian cancer tissues, cell lines (OMC685, A2780, and SKOV3) up-regulated The results demonstrated that UCA1 expressions were markedly upregulated in cancer tissues than that in normal tissues. Findings of this study confirmed that not only UCA1 was aberrantly upregulated in EOC tissues and cells, but also correlated with status of lymph node metastasis and FIGO stage. Furthermore, univariate and multivariate analyses showed that UCA1 was a prognostic factor for overall survival in EOC patients. In vitro, knockdown of UCA1 reduced the invasion and migration ability of EOC cells. 26867765 2016 UCA1 functions as a competing endogenous RNA to suppress epithelial ovarian cancer metastasis. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR, Cell proliferation assay etc. PDAC tissues, cell lines (AsPC-1, BxPC-3, Capan-2, CFPAC-1, HPAC, MIA PaCa-2, PANC-1 and SW1990) up-regulated The qRT-PCR results showed that CRNDE, NR_036488, ENSG00000244649, AFAP1-AS and UCA1 expression was significantly increased and ENSG00000218510 expression was remarkably decreased in PDAC tissues compared with paired normal pancreatic tissues. Consistent with the findings in PDAC tissues, CRNDE, NR_036488, ENSG00000244649, AFAP1-AS1 and UCA1 expression was dramatically enhanced and ENSG00000218510 reduced in all or most of 8 PDAC cell lines in relative to the nonmalignant HPDE6-C7 cells or hTERT-HPNE cells at the RNA level. 27628540 2016 Analysis of long non-coding RNA expression profiles in pancreatic ductal adenocarcinoma. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 colon cancer C18 NA qPCR etc. colon cancer tissues up-regulated Compared with adjacent normal tissues, UCA1 was significantly upregulated in colon cancer tissues, especially in cases with LNM and advanced TNM stages. High UCA1 expression was associated with LMN, higher pT category, and advanced TNM stages. Patients with high UCA1 expression had worse survival time than those with low UCA1 expression. Furthermore, plasma levels of UCA1 in colon cancer patients were significantly higher than those of controls. 26885155 2015 Clinical significance of urothelial carcinoma associated 1 in colon cancer. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 ovarian cancer C56.9 NA qPCR etc. ovarian cancer tissues up-regulated UCA1 expression in ovarian cancer tissues was significantly upregulated compared with normal ovarian tissues. High UCA1 expression was related to lymph node metastasis, FIGO stage, and response to chemotherapy. 26851957 2016 UCA1 overexpression predicts clinical outcome of patients with ovarian cancer receiving adjuvant chemotherapy. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 cervical cancer C53 NA qPCR etc. cervical cancer tissues up-regulated HOTAIR and UCA1 both were significantly higher expressed in GC tumor tissues than adjacent non-tumor tissues.The results from the qRT-PCR validation in 82 newly diagnosed GC patients and the above bioinformatics results were 100% in agreement. To further analyze the association between the 2 key lncRNAs and clinicopathological characteristics of 82 GC patients, we found that HOTAIR was significantly associated with tumor size and lymphatic metastasis, and UCA1 was significantly associated with tumor size,TNM stage and lymphatic metastasis. HOTAIR and UCA1 were found to be significantly associated with overall survival.The miR-1 was downexpressed when lncRNA UCA1 was overexpressed in glioma cells.mRNA XIRP1 was found to interact with miRNA miR-133a-3p. Key miRNA miR-133a-3p was predicted to target key lncRNA HOTAIR. 29620291 2018 Integrated analysis of long non-coding RNA competing interactions revealed potential biomarkers in cervical cancer: Based on a public database. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 pancreatic cancer C25 NA qPCR, Western blot, Luciferase reporter assay, RNAi, RIP etc. cancer tissues, cell cells (BxPC-3, SW1990, PaTu8988, and PANC-1) up-regulated UCA1 promoted cell migration and invasion of pancreatic cancer cells.Importantly, we found that UCA1 overexpression inhibited YAP phosphorylation, and increased YAP expression.Mechanistically,UCA1 interacted with MOB1,Lats1,and YAP, forming shielding composites. Moreover,we demonstrated that UCA1 increased YAP nuclear localization and stabilization, and improved TEAD luciferase activity. The present study provides insights into the mechanistic regulation of UCA1 promoting pancreatic cancer progression through the Hippo signaling pathway.It remains to be investigated whether UCA1 can act as a ceRNA by competitively binding correlative miRNA to maintain stable expression of YAP in PC cells. 29510195 2018 LncRNA UCA1 promotes migration and invasion in pancreatic cancer cells via the Hippo pathway. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 prostate cancer C61.9 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. cell lines (DU145 and PC3) up-regulated UCA1 abundance was significantly higher in DU145-IRR cells compared to control cells. UCA1 siRNA-knockdown reversed the aggressive phenotype and significantly increased sensitivity to IR. UCA1 depletion inhibited growth, induced cell cycle arrest at the G2/M transition and decreased activation of the pro-survival Akt pathway. 27902466 2017 Long non-coding RNA urothelial carcinoma associated 1 (UCA1) mediates radiation response in prostate cancer. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 renal cell carcinoma C64.9 NA qPCR, Western blot, Luciferase reporter assay, RIP etc. renal cell carcinoma tissues, cell lines (769P, 786O, ACHN, A498, Caki2) up-regulated UCA1 expression was upregulated in RCC tissue and cells, and higher UCA1 expression was associated with advanced pathogenic status and poor prognosis of RCC patients. UCA1 knockdown suppressed proliferation and invasion and induced apoptosis in RCC cells. UCA1 inhibited miR129 expression by direct interaction in RCC cells. miR129 overexpression inhibited cell proliferation and invasion and promoted apoptosis. Moreover, miR129 downregulation abrogated UCA1 knockdown-mediated antiproliferation, anti-invasion, and proapoptosis effects in RCC cells. Furthermore, UCA1 acted as a ceRNA of miR129 to enhance target-gene SOX4 expression in RCC cells. UCA1 promoted cell proliferation and invasion and inhibited apoptosis by regulating SOX4 via miR129 in RCC, offering a promising therapeutic target and prognosis marker for RCC patients. 29760557 2018 UCA1 promotes cell proliferation and invasion and inhibits apoptosis through regulation of the miR129-SOX4 pathway in renal cell carcinoma. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 renal cell carcinoma C64.9 NA qPCR, Western blot, Luciferase reporter assay, RNAi renal cell carcinoma tissues, cell lines (786-O, ACHN, Caki-1, and Caki-2) up-regulated In this study, we found that urothelial carcinoma-associated 1 was overexpressed in renal cell carcinoma tissues compared with the adjacent normal tissues, and higher urothelial carcinoma-associated 1 expression levels were positively associated with advanced tumor stage and poor survival time in renal cell carcinoma patients. Moreover, urothelial carcinoma-associated 1 was found to be associated with enhancer of zeste homolog 2, which suppressed p21 expression through histone methylation (H3K27me3) on p21 promoter. These findings illuminated that urothelial carcinoma–associated 1 promoted renal cell carcinoma progression through enhancer of zeste homolog 2 and interacted with miR-495. 28466784 2017 LncRNA UCA1 promotes renal cell carcinoma proliferation through epigenetically repressing p21 expression and negatively regulating miR-495 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 esophageal squamous cell cancer NA NA qPCR, RNAi etc. ESCC tissues, cell lines (EC109, EC9706, KYSE150, KYSE510) up-regulated The relative level of UCA1 was significantly higher in ESCC tissues, and remarkably higher expression of UCA1 was found in esophageal cancer cell lines compared with the immortalized esophageal epithelial cell line NE1. The ESCC patients with higher UCA1 expression had an advanced clinical stage and a poorer prognosis than those with lower expression. In vitro assays, our data indicated that downregulation of UCA1 decrease cell proliferation, migration, and invasion ability. 25550835 2014 Overexpression of long non-coding RNA UCA1 predicts a poor prognosis in patients with esophageal squamous cell carcinoma. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. cell lines (Hl-60 and theU940) down-regulated Our outcomes revealed that SAM particularly when given at the starting phase downregulates ecCEBPA and UCA1 gene transcripts and ameliorate histopathological alterations in DEN-initiated HCC. Interestingly, SAM attenuates DEN-induced upregulation of PI3K/Akt protein expression. However, SAM upregulates the antioxidant enzymes mRNA transcripts and effectively diminishing DNA oxidation. The results of a DNA fragmentation assay further support the capacity of SAM to ameliorate DEN-induced hepatic malignancy. These results revealed the role of ecCEBPA and UCA1 in HCC and suggest that these lncRNAs may be helpful as prognostic and analytical biomarkers of HCC. 29748795 2018 Role of lncRNAs as prognostic markers of hepatic cancer and potential therapeutic targeting by S-adenosylmethionine via inhibiting PI3K/Akt signaling pathways. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated The expression of lncRNA-UCA1 and C-JUN was positive in 91.4%HCC patients with strong discriminating power between HCC and healthy subjects and CHC patients as well. The median follow up period was 29 months. The survival analysis showed that both lncRNA-UCA1 and C-JUN were independent prognostic factors. 27215316 2016 Association of long noncoding RNA and c-JUN expression in hepatocellular carcinoma. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 breast cancer C50 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. cell line (MDA-MB-231) differential expression Our study showed that SATB1 binds to the upstream region of UCA1 in vivo, and that its promoter activity increases with SATB1 depletion. Furthermore, simultaneous depletion of SATB1 and UCA1 potentiated suppression of tumor growth and cell survival. Thus, SATB1 repressed the expression of oncogenic UCA1, suppressing growth and survival of breast cancer cells. 27697109 2016 Epigenetic regulation of long noncoding RNA UCA1 by SATB1 in breast cancer. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 gastric cancer C16 NA qPCR, Western blot, RIP etc. cell lines (MGC-803 and BGC-823) up-regulated UCA1 was upregulated in HRGC cells, which promoted their migration.miR-7-5p could bind to specific sites of UCA1 to regulate the target EGFR through competitive endogenous RNA function.UCA1 directly interacted with miR-7-5p and decreased the binding of miR-7-5p to the EGFR 3'-untranslated region,which suppressed the degradation of EGFR mRNA by miR-7-5p.Therefore,long-term hypoxia induced UCA1 to promote cell migration by enhancing the expression of EGFR.This study thus reveals a new mechanism by which a hypoxic microenvironment promotes tumor metastasis, and highlights UCA1 as a potential biomarker for predicting the metastasis of gastric cancer to guide clinical treatment. 29723509 2018 Long non-coding RNA UCA1 upregulation promotes the migration of hypoxia-resistant gastric cancer cells through the miR-7-5p/EGFR axis. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 gastric cancer C16 NA qPCR etc. cell lines (HEK-293, HUVECs, SKBR3, A542, MCF7, NT2) up-regulated Our results showed ecCEBPA and UCA1 over-expression in GC tissues. Furthermore, lncRNAs associations with clinicopathological features were demonstrated both in the current and TCGA cohort. Kaplan-Meier analysis indicated that patients with higher UCA1 expression had a worse overall survival in the case of pancreatic and lung adenocarcinomas but not other solid cancer types including GC. These data demonstrate UCA1 and ecCEBPA involvement in GC and suggest that these lncRNAs might be useful as diagnostic/ prognostic biomarkers in cancer. 29147491 2017 Augmented expression levels of lncRNAs ecCEBPA and UCA1 in gastric cancer tissues and their clinical significance UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 gastric cancer C16 NA qPCR etc. gastric cancer tissues up-regulated qPCR results suggest that HOTAIR and UCA1 both were significantly higher expressed in GC tumor tissues than adjacent non-tumor tissues. The results from the qRT-PCR validation in 82 newly diagnosed GC patients and the above bioinformatics results. 26935047 2016 Integrated analysis of long non-coding RNA competing interactions reveals the potential role in progression of human gastric cancer. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RIP etc. HCC tissues, cell lines (MHCC97L, SMMC7721, MHCC97H, HepG2, SK-Hep1 etc.) up-regulated Herein, we found that UCA1 was aberrantly upregulated in HCC tissues and associated with TNM stage, metastasis and postoperative survival. UCA1 depletion inhibited the growth and metastasis of HCC cell lines in vitro and in vivo. the present study elucidates a novel lncRNA- miRNA-mRNA regulatory network that is UCA1-miR-216b-FGFR1-ERK signaling pathway in HCC, which may help to lead a better understanding the pathogenesis of HCC and probe the feasibility of lncRNA-directed diagnosis and therapy for this deadly disease. 25760077 2015 Upregulated lncRNA-UCA1 contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 bladder cancer C67 NA qPCR, Luciferase reporter assay, Western blot etc. cell lines (T24, 5637, J82, RT4, HT1376) up-regulated UCA1 negatively regulated miR-143 expression in a dose-dependent manner in bladder cancer cells. In addition,UCA1 and HMGB1 were upregulated and miR-143 was downregulated in bladder cancer specimens. Overall, the data suggested that UCA1 may promote the invasion and EMT of bladder cancer cells by regulating the miR-143/HMGB1 pathway, which exhibits an important regulatory role in the pathology of bladder cancer. 29113184 2017 LncRNA UCA1 promotes the invasion and EMT of bladder cancer cells by regulating the miR-143/HMGB1 pathway UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 bladder cancer C67 NA qPCR etc. bladder cancer tissues up-regulated 95.4% of RNA was isolated successfully from urinary sediments after the addition of RNasin UCA1 was highly specific (92.4%, 133/144) and quite sensitive (84.4%, 152/180) in the diagnosis of bladder cancer with a favorable AUC-ROC of 0.898 (95%CI: 0.851-0.945). It was especially valuable for superficial G(2)-G(3) patients (sensitivity: 86.4%, 92.3%) at a high risk for muscular invasion. 22490897 2012 Evaluation of novel gene UCA1 as a tumor biomarker for the detection of bladder cancer. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (AGS, MKN-28, SGC-7901, MKN-45, GES-1), GC tissues up-regulated UCA1 is significantly higher in GC tissues and cells compared with adjacent normal tissues and a gastric epithelium cell line,respectively. Higher UCA1 expression was associated with lymph node metastasis,TNM stage,and poor overall survival (OS) in GC patients.In vitro functional studies confirmed that UCA1 promotes cell proliferation,colony formation ability,and cell invasion in GC cells. We demonstrated that knockdown of UCA1 inhibits tumor growth in vivo. The double luciferase reporter,RNA-binding protein immunoprecipitation assay, and RNA pull down assay demonstrated that miR-590-3p serves as a target for UCA1. Moreover,we demonstrated that CREB1 is a downstream target of miR-590-3p and UCA1 activates CREB1 expression by sponging to miR-590-3p. 29516678 2018 UCA1 promotes cell proliferation and invasion of gastric cancer by targeting CREB1 sponging to miR-590-3p. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 gastric cancer C16 NA qPCR, Western blot etc. GC tissues, cell lines (MKN-28, SGC-7901, BGC-823, MGC-803, MKN-45 and GES-1) up-regulated UCA1 was aberrantly upregulated in gastric cancer tissues and gastric cancer cell lines, and was associated with TNM stage and metastasis. UCA1 regulates the PI3K-Akt-mTOR signaling proteins and their downstream mediators, to alter gastric cancer progression in vitro and in vivo. UCA1 in the tumorigenesis of gastric cancer. In addition, the study characterized a novel lncRNA-mRNA regulatory network, which may lead to a better understanding of the pathogenesis of gastric cancer and assist in lncRNA-directed diagnosis and therapy for this malignancy. high UCA1 expression correlated with tumor size, invasion depth, worsening differentiation, TNM stage, and the overall survival. 29212166 2017 Dysregulated lncRNA-UCA1 contributes to the progression of gastric cancer through regulation of the PI3K-Akt-mTOR signaling pathway. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 breast cancer C50 NA Microarray, qPCR, RIP, Luciferase reporter assay etc. breast cancer tissue, cell line MDA-MB-231-luc-D3H2LN up-regulated We observed that TGF-B induced genome-wide changes in lncRNA levels in breast cancer cells, among which AC026904.1 and UCA1 were highly expressed in metastatic breast cancer and closely associated with poor prognosis. UCA1 exerts a competitive endogenous RNA (ceRNA) activity in the cytoplasm. 29774079 2018 Long non-coding RNAs AC026904.1 and UCA1: a “one-two punch” for TGF-B-induced SNAI2 activation and epithelial-mesenchymal transition in breast cancer UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 esophageal squamous cell cancer NA NA qRT-PCR ect. The tumor tissues and para-carcinoma tissues up-regulated the up-regulation of UCA1 and MALAT1 lncRNAs in ESCC tissues can impact the degree of tumor progression and is predictive of postoperative survival. 30002691 2018 Expression of UCA1 and MALAT1 long-chain non-coding RNAs in esophageal squamous cell carcinoma tissues is predictive of patient prognosis. UCC NA NA NA NA NA colorectal cancer C19.9 NA qPCR, RNAi, RIP colorectal tumor tissues, cell lines (SW480, SW620, HCT116, Caco-2, DLD-1, and HT29) up-regulated A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines.UCC levels correlated with lymph node metastasis, Dukes’stage, and patient outcomes. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. 28492554 2017 The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143 UM9-5 NA 359822 ENSG00000280650 NR_002813 GRCh38_4:21843341-21853188 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues up-regulated Eight (lincRNA-VLDLR, MEG9, H19 antisense, ncR-uPAR, NEAT1 (family), LUST, UM9-5, and HOTAIR) were significantly down-regulated in HCC tumor compared to non-tumor tissues at a significance level. 26378581 2015 Exploration of Deregulated Long Non-Coding RNAs in Association with Hepatocarcinogenesis and Survival. UXT-AS1 NA 100133957 ENSG00000267064 NR_028119 GRCh38_X:47658833-47660377 colorectal cancer C19.9 NA qPCR, Western blot colorectal cancer tissues, cell lines (HT29, HCT116 and SW480) up-regulated UXT-AS1 was found to be significantly upregulated in colorectal cancer (CRC) and high expression levels of UXT-AS1 were significantly associated with poor prognosis in CRC patients. 28401004 2017 UXT-AS1-induced alternative splicing of UXT is associated with tumor progression in colorectal cancer VIM-AS1 NA 100507347 ENSG00000229124 NR_108061 GRCh38_10:17214239-17229985 colorectal cancer C19.9 NA qPCR, Western blot, in vitro knockdown etc. cell lines (SW1116, SW480, HT29, SW48), colorectal cancer tissue up-regulated VIM-AS1 transcript was significantly upregulated in high-grade, lymph node metastasis and vascular invasion tumors.The downregulation of VIM-AS1 could inhibit tumor cell proliferation by inducing apoptosis, cellular senescence and arresting the cell cycle.VIM-AS1 might play a crucial role in cell migration as well as the epithelial to mesenchymal transition (EMT) of CRC cells. VIM-AS1 promotes tumor growth and metastasis by inducing EMT in CRC cells and could be considered as a novel tumor marker with probable value in diagnosis and CRC treatment. 29656793 2018 Long noncoding RNA VIM-AS1 promotes colorectal cancer progression and metastasis by inducing EMT. VPS9D1-AS1 VPS9D1-AS1, MYU 100128881 ENSG00000261373 NR_036480 GRCh38_16:89711856-89718165 gastric cancer C16 NA qPCR gastric cancer tissues, cell line (GES1) down-regulated VPS9D1-AS1 expression level was markedly correlated with tumor size and TNM stage in gastric cancer.low expression of VPS9D1-AS1 were correlated with poor overall and disease free survival. 29036784 2017 Decreased expression of lncRNA VPS9D1-AS1 in gastric cancer and its clinical significance. VPS9D1-AS1 VPS9D1-AS1, MYU 100128881 ENSG00000261373 NR_036480 GRCh38_16:89711856-89718165 colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues, cell lines (HCT116, SW480, HT29 and SW620) up-regulated Notably, the overexpression of FAM83H-AS1 and VPS9D1-AS1 indicated shorter OS time than lower expression. The overexpression of FAM83H-AS1 and VPS9D1-AS1 was validated in cancerous tissues. Thus, FAM83H-AS1 and VPS9D1-AS1 may potentially enhance carcinogenesis or may be developed as prognostic biomarkers for CRC. 27895773 2016 Dysregulation of long non-coding RNA profiles in human colorectal cancer and its association with overall survival. XIAP-AS1 NA NA ENSG00000237331 NA NA gastric cancer C16 NA qPCR, RIP, Western blot gastric cell lines (Bgastric cancer823, Sgastric cancer7901, MKN28, AGS, Mgastric cancer803) up-regulated In conclusion, our results indicate that XIAP-AS1 is involved in XIAP transcription by interacting with Sp1. Additionally, XIAP-AS1 is a potential target for TRAIL-induced apoptosis in gastric cancer cells.However, there was no significant correlation between the levels of XIAP-AS1 and survival probability (P = 0.07). 28792527 2017 The long noncoding RNA XIAP-AS1 promotes XIAP transcription by XIAP-AS1 interacting with Sp1 in gastric cancer cells. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 glioblastoma NA M9440/3 qPCR, RIP, Luciferase reporter assay etc. glioblastoma tissues up-regulated Our results proved that XIST expression was up-regulated in glioma tissues and GSCs. Functionally, knockdown of XIST exerted tumor-suppressive functions by reducing cell proliferation, migration and invasion as well as inducing apoptosis. Mechanistic investigations defined the direct binding ability of the predicted miR-152 binding site on the XIST. In addition, XIST and miR-152 are probably in the same RNA induced silencing complex (RISC). 25578780 2015 Knockdown of long non-coding RNA XIST exerts tumor-suppressive functions in human glioblastoma stem cells by up-regulating miR-152. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 colon cancer C18 NA qPCR, Western blot, Luciferase reporter assay etc. colon cancer tissues, cell lines ( NCM460, Lovo, SW480, HCT116 and HT29) up-regulated XIST expression level was upregulated in colon cancer tissues and cell lines.In addition,the growth rate of cells transfected with si-XIST was significantly decreased compared to that with si-NC, which was reversed by miR-34a targeted with 3'-UTR. Moreover, miR-34a suppressed the expression of WNT1 by binding with the 3'-UTR, which interact with WNT1 to inhibit the proliferation of cells.Furthermore, miR-34a inhibitor rescued the dysregulation of WNT1, B-catenin,cyclinD1,c-Myc and MMP-7 by si-XIST.Besides, XIST knockdown inhibited tumor growth in vivo. In short, the current study suggests XIST plays as an important role in colon cancer progression targeted by miR-34a via Wnt/B-catenin signaling pathway,providing a novel insight for the pathogenesis and underlying therapeutic target for colon cancer. 29679755 2018 Long non-coding RNA XIST sponges miR-34a to promotes colon cancer progression via Wnt/B-catenin signaling pathway. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 esophageal squamous cancer C15 M8070/3 qPCR, Western blot, Luciferase reporter assay etc. esophageal squamous tissues, cell lines (KYSE30, KYSE510, KYSE410, KYSE520, KYSE140 and KYSE150) up-regulated XIST was significantly upregulated in esophageal squamous cancerous tissues and cancer cell lines,as compared with that in the corresponding non-cancerous tissues and immortalized normal squamous epithelial cells. High XIST expression predicted poor prognosis of esophageal squamous cancer patients. Lentivirus mediated knockdown of XIST inhibited proliferation, migration and invasion of esophageal squamous cancer cells in vitro and suppressed tumor growth in vivo. Knockdown of XIST resulted in elevated expression of miR-101 and decreased expression of EZH2. Further analysis showed that XIST functioned as the competitive endogenous RNA of miR-101 to regulate EZH2 expression. Our results showed that patients with high XIST level had a significantly shortened overall survival as well as disease-free survival than those with low XIST level. 29100288 2017 Long noncoding RNA XIST promotes malignancies of esophageal squamous cell carcinoma via regulation of miR-101/EZH2. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 pancreatic cancer C25 NA qPCR, Western blot, Luciferase reporter assay etc. cell lines (AsPC-1, BxPC3, SW1990,PANC-1, CAPAN-1, CAPAN-2) up-regulated XIST might be an oncogenic lncRNA that promoted proliferation of PC cell line through inhibiting miR- 140/miR-124 expression and promoting cell cycle-related factor expression, and could be regarded as a therapeutic target in human pancreatic carcinoma.XIST is highly expressed in PC tissues and cell line and related with clinicopathologic features. 29371940 2017 The lncRNA XIST interacts with miR-140/miR-124/iASPP axisto promote pancreatic carcinoma growth XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 nasopharyngeal cancer C11 NA qPCR, Luciferase reporter assay, Western blot etc. cell lines(CNE-1, CNE-2) up-regulated XIST was upregulated and miR-29c was downregulated in NPC cells.The expressions of XIST and miR-29c changed reversely in response to irradiation. Knockdown of XIST and miR-29c overexpression both resulted in a dramatic suppression of cell proliferation, a marked enhancement of radiosensitivity, and an obvious increase of g-H2AX foci formation in NPC cells. Luciferase reporter assay and qRT-PCR analysis demonstrated that XIST interacts with miR-29c and negatively regulates its expression. Moreover, miR-29c inhibition abrogated XIST knockdown-induced cell proliferation inhibition and radiosensitivity increase in NPC cells. 28985197 2017 Downregulation of lncRNA X Inactive Specifc Transcript (XIST) Suppresses Cell Proliferation and Enhances Radiosensitivity by Upregulating mir-29c in Nasopharyngeal Carcinoma Cells XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (MGC803, BGC823, SGC-7901, AGS, KATOIII) up-regulated A negative correlation was indicated between XIST and miR-185 in GC cells.In addition,TGF-B1 was predicted as a target gene of miR-185. miR-185 can modulate TGF-B1 expression negatively in vitro.Moreover, we found that sh-XIST inhibited GC development via decreasing TGF-B1 by upregulating miR-185 in vitro.Therefore,we speculated that XIST can act as a competing endogenous lncRNA (ceRNA) to regulate TGF-B1 by sponging miR-185 in GC.Taken these together,it was indicated that XIST/miR-185/TGF-B1 axis participated in the development of GC. XIST could act as a potential prognostic biomarker in GC development. 29053187 2018 XIST promotes gastric cancer (GC) progression through TGF-B1 via targeting miR-185. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 osteosarcoma NA M9180/3 qPCR, Western blotting, Luciferase reporter assay etc. cell lines (MG63, U2OS, Saos2, HOS, SOSP-9697, SV40) down-regulated XIST regulated PDCD4 expression by competitively binding to miR-21-5p. XIST inhibited cell proliferation and cell mobility by competitively binding to miR-21-5p and upregulating PDCD4 in OS. Our study demonstrated that lncRNA-XIST, which acts as a miRNA sponge, impedes miR-21-5p to maintain the expression of PDCD4, which contributes to the progression of OS. Our fndings suggest that the newly identifed XIST/miR-21-5p/PDCD4 axis could be a potential biomarker or therapeutic target for OS. 29048648 2017 Long non-coding RNA XIST regulates PDCD4 expression by interacting with miR-21-5p and inhibits osteosarcoma cell growth and metastasis XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 pancreatic cancer C25 NA qPCR, Luciferase reporter assay, Cell proliferation assay, MTT assay etc. prostate cancer tissues, cell lines (Patu8988, SW1990, BxPC-3, AsPC-1, CFPAC-1 and Panc-1) up-regulated lncRNA-XIST was specifically upregulated in PC tissues and cell lines, and high XIST expression in PC was related to poorer prognosis (larger tumor size, perineural invasion, lymph node micrometastases and shorter overall survival). XIST augmented PC cell proliferation. In the present study, XIST and miR-133a reciprocally inhibited each other in PC cells. Exogenous miR-133a expression significantly inhibited PC cell proliferation. Moreover, as exhibited by luciferase reporter gene assays, miR-133a bound to XIST and the 3'UTR of EGFR by direct targeting. In PC tissues, miR-133a expression was down-regulated and EGFR expression was up-regulated; miR-133a was inversely correlated with EGFR and XIST, respectively; XIST was positively correlated with EGFR. Taken together, these findings will shed light on the role and mechanism of XIST/miR-133a/EGFR in regulating PC cells proliferation. 28295543 2017 LncRNA XIST Promotes Pancreatic Cancer Proliferation through miR-133a/EGFR. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 nasopharyngeal cancer C11 NA qPCR, Western blot, Luciferase reporter assay etc. NPC tissues, cell lines (SUNE-1, CNE-1, HNE-1, CNE-2, C666-1 and HONE-1) up-regulated Here, we discovered that XIST was up-regulated in NPC tissues and higher expression of XIST contributed to a markedly poorer survival time. In addition, multivariate analysis demonstrated XIST was an independent risk factor for prognosis. XIST over-expression enhanced, while XIST silencing hampered the cell growth in NPC. Additionally, mechanistic analysis revealed that XIST up-regulated the expression of miR-34a-5p targeted gene E2F3 through acting as a competitive 'sponge' of miR-34a-5p. 27461945 2016 Long non-coding RNA XIST exerts oncogenic functions in human nasopharyngeal carcinoma by targeting miR-34a-5p. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 pancreatic cancer C25 NA qPCR, RNAi, in vitro knockdown, Luciferase reporter assay etc. cell lines (PANC-1, ASPC-1, MIA PaCa-2, HPAC, CFAPC-1, BxPC-3), PC tissues up-regulated Overexpression of XIST significantly promoted the proliferation,migration and invasion, and suppressed cell apoptosis of BxPC-3 cells; knockdown of XIST significantly inhibited the proliferation,migration and invasion,and accelerated cell apoptosis of PANC-1 cells. Subsequently, we found that microRNA-34a-5p (miR-34a-5p) was downregulated in PC tissues,and predicted a poor prognosis in PC patients. In addition, the results indicated that miR-34a-5p is a target gene of XIST and was significantly negatively correlated with XIST. More importantly, miR-34a-5p rescued the facilitation of malignant behavior mediated by XIST. These results indicated that XIST and miR-34a-5p may be potential effective therapeutic targets for PC. 29393501 2018 Long non-coding RNA XIST exerts oncogenic functions in pancreatic cancer via miR-34a-5p. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, MTT assay etc. gastric cancer tissues, cell lines (SGC-7901, BGC-823, HGC-27 and MKN-28) up-regulated XIST expression was significantly increased in GC tissues and cell lines. LncRNA XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to GC cell growth. LncRNA XIST also contributed to GC cell invasion both in vitro and in vivo. We revealed that XIST functioned as competing endogenous RNA to repress miR-497, which controlled its down-stream target MACC1. We proposed that XIST was responsible for GC cell proliferation and invasion and XIST exerted its function through the miR-497/MACC1 axis. 27911852 2017 Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 gastric cancer C16 NA qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. gastric cancer tissues, cell lines (SGC7901, HGC27, BGC823, MKN45, MKN28, and AGS) up-regulated lncRNA XIST was significantly up-regulated in gastric cancer tissues and cell lines. Overexpression of lncRNA XIST was markedly associated with larger tumor size, lymph node invasion, distant metastasis and TNM stage in gastric cancer patients. Functionally, knockdown of lncRNA XIST exerted tumor-suppressive effects by inhibiting cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo. Furthermore, an inverse relationship between lncRNA XIST and miR-101 was found. Polycomb group protein enhancer of zeste homolog 2 (EZH2), a direct target of miR-101, could mediated the biological effects that lncRNA XIST exerted. 27620004 2016 Long non-coding RNA XIST regulates gastric cancer progression by acting as a molecular sponge of miR-101 to modulate EZH2 expression. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay etc. hepatocellular carcinoma tumor tissues, cell lines (MHCC97L, MHCC97H, HepG2, SMMC7221, Huh7, Bel-7402) down-regulated XIST was significantly upregulated in HCC tissues and associated with tumor size and vascular invasion.Gain- and loss-of-function of XIST further presented that XIST promoted the progression of HCC cells, including proliferation, migration,and invasion. Moreover, silencing of XIST could inhibit tumor growth in vivo. XIST could target miR-194-5p and thus decrease miR-194-5p expression.Besides that,restoring XIST could reverse the inhibitory effect of miR-194-5p on the proliferation and invasion of HCC cells. We further elucidated such rescue role might through derepressing MAPK1 expression,the target of miR-194-5p.We pinpointed that LncRNA XIST can act as a ceRNA for MAPK1 mRNA through miR-194-5p. These results deepen our understanding of the role of XIST in HCC. 29227532 2018 LncRNA XIST functions as a molecular sponge of miR-194-5p to regulate MAPK1 expression in hepatocellular carcinoma cell. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP OS tissues, OS cell lines (MG-63, 143B, MHM and SJSA1) up-regulated XIST expression was significantly upregulated in OS tissues and cell lines and negatively correlated with clinical prognosis.XIST knockdown inhibited cancer cell proliferation and invasion in vitro, inhibited the EMT of OS cells in vitro, and suppressed subcutaneous tumor growth in vivo. Further analysis demonstrated that XIST regulated YAP expression by functioning as a competing endogenous RNA that sponged miR-195-5p in OS cells. XIST directly interacted with miR-195-5p and decreased the binding of miR-195-5p to the YAP 3'UTR, which suppressed the degradation of YAP mRNA by miR-195-5p. 29384226 2018 The expression of LncRNA RP11-87C12.5 is high in newly diagnosed ALL group and low in complete remission ALL group. In B-ALL, the expression of IncRNA RP11-87C12.5 significantly enhances in cCD79a low expression group. In newly diagnosed ALL group, compared with low expression group, lncRNA RP11-87C12.5 high expression group have higer remission rate and relapse rate, but the difference was not statistically significant.Long non-coding RNA XIST promotes osteosarcoma progression by targeting YAP via miR-195-5p. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 osteosarcoma NA M9180/3 qPCR osteosarcoma tissues, cell lines (HOS, SAOS-2,SOSP-9607, MG63, and U2-OS and hFOB 1.19) up-regulated The results showed that XIST was significantly up-regulated in osteosarcoma tissues and cell lines, and high XIST expression was significantly associated with advanced tumor size (p=0.009), advanced clinical stage (p=0.001) and present distant metastasis (p=0.009). Kaplan-Meier analysis showed that increased XIST expression was associated with poor overall survival of patients. 28682435 2017 High expression of long non-coding RNA XIST in osteosarcoma is associated with cell proliferation and poor prognosis XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 osteosarcoma NA M9180/3 qPCR, RIP, Western Blot etc. Human osteosarcoma cell lines (U2OS, Saos-2, 143B, MG-63, HOS), OS tissues up-regulated Taking all into account, Xist may function in promoting OS cell proliferation and may potentially serve as a novel biomarker and therapeutic target for OS.Due to recent advancements in multimodal treatments, the 5-year survival rate of OS patients has significantly improved over the past decades. 29254174 2017 Upregulation of long noncoding RNA Xist promotes proliferation of osteosarcoma by epigenetic silencing of P21. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 colorectal cancer C19.9 NA Microarray, qPCR etc. cell line(DLD2), CRC tissue down-regulated XIST was associated with POF1B,chorionic somatomammotropin hormone 1 (CSH1) and calmin (CLMN), leading to multiple signaling pathways or mechanisms. 29484395 2018 Identification of candidate genes and long non-coding RNAs associated with the effect of ATP5J in colorectal cancer. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 colorectal cancer C19.9 NA qPCR, Western blot colorectal cancer specimens tissues, Human colorectal cancer cell lines (HCT116, HT-29, SW620, SW480, DLD-1, RKO, LoVo) down-regulated Overall, our study demonstrated how lncRNA XIST regulates CRC progression and metastasis by competing for miR-200b-3p to modulate the expression of ZEB1. lncRNA XIST may be used as a biomarker to predict prognosis in CRC patients.survival in CRC patients. Knockdown of lncRNA XIST remarkably inhibited CRC cell proliferation, invasion, epithelial–mesenchymal transition (EMT) and CRC stem cell formation in vitro as well as tumor growth and metastasis in vivo. In this study, we used bioinformatics databases (Starbase v2.0, miRcode and RNAhybrid) and identified several miRNAs that might interact with lncRNA XIST. 28837144 2017 Long noncoding RNA XIST expedites metastasis and modulates epithelial-mesenchymal transition in colorectal cancer. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 non small cell lung cancer C34 M8046/3 qPCR, Western blot, RNA pull-down assay etc. NSCLC tissues, cell lines (A549, SK-MES-1, H1299, 95D, H460, H520, H1975, H157, SK-LU-1, and SPC-A-1) up-regulated We found that XIST is over-expressed in NSCLC, and its increased level is associated with shorter survival and poorer prognosis. Knockdown of XIST impaired NSCLC cells proliferation, migration and invasion in vitro, and repressed the tumorigenicity of NSCLC cells in vivo. Mechanistically, RNA immune-precipitation (RIP) and RNA pull-down experiment demonstrated that XIST could simultaneously interact with EZH2 to suppress transcription of its potential target KLF2. 27501756 2016 Long noncoding RNA XIST acts as an oncogene in non-small cell lung cancer by epigenetically repressing KLF2 expression. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 cervical cancer C53 NA qPCR, Western blot, Luciferase reporter assay, etc. cervical cancer tissues, cell lines (Hela, Caski, C4-1, Siha, GH329) up-regulated XIST upregulated Fus through competitively binding with miR-200a. patients with high expression of XIST had a lower survival rate than those with low expression of XIST 29909347 2018 LncRNA XIST accelerates cervical cancer progression via upregulating Fus through competitively binding with miR-200a. XLOC_000647 NA NA NA NA NA pancreatic cancer C25 NA Microarray, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown PC tissues, PC cell lines (MIA-PaCa-2, BxPC-3 and PANC-1) up-regulated Here, XLOC_000647 expression was down-regulated in PC tissues and cell lines. The expression level of XLOC_000647 was significantly correlated to tumor stage, lymph node metastasis, and overall survival. Overexpression of XLOC_000647 attenuated cell proliferation, invasion, and EMT in vitro and impaired tumor growth in vivo. Further, a significantly negative correlation was observed between XLOC_000647 levels and its genomic nearby gene NLRP3 in vitro and in vivo. Moreover, XLOC_000647 decreased NLRP3 by inhibiting its promoter activity. Knockdown of NLRP3 decreased proliferation of cancer cells, invasion, and EMT in vitro. Importantly, after XLOC_000647 was overexpressed, the corresponding phenotypes of cells invasion and EMT were reversed by overexpression of NLRP3. 29386037 2018 Long non-coding RNA XLOC_000647 suppresses progression of pancreatic cancer and decreases epithelial-mesenchymal transition-induced cell invasion by down-regulating NLRP3. XLOC_010235 lnc-NCOR2-1, XLOC_010235, linc-CCDC92-2 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western Blotting etc. cell lines (HepG2, Hep3B, SMMC-7721, Bel-7402 HCC) up-regulated XLOC was increased in HCC tissues and cell lines, and high level of XLOC was signifcantly correlated with poor prognosis. Additionally, silenced XLOC signifcantly inhibited cell proliferation, induced cell apoptosis and facilitated cell migration of HCC in vitro. The relationship between XLOC expression and clinicopathological features of HCC patients was analyzed. Then loss-of-function assays were conducted to determine the biological effect of XLOC in HCC cells. 29164575 2017 Long non-coding RNA XLOC_010235 correlates with poor prognosis and promotes tumorigenesis of hepatocellular carcinoma XLOC_010235 lnc-NCOR2-1, XLOC_010235, linc-CCDC92-2 NA NA NA NA gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues up-regulated The expression levels of six up-regulated lncRNAs (XLOC_010235, CACNAICAS3, INTS7, AC104699.1, TSNAX-DISC1, and PRSS21) and six down-regulated lncRNAs (RP11-789C1.1, RP11-528G1.2, MYLK-AS1, RP11-643M14.1, GS1-5L10.1, and AP001439.2) were determined by using qPCR. 26045391 2015 Identification of differentially expressed signatures of long non-coding RNAs associated with different metastatic potentials in gastric cancer. XLOC_010588 TUSC8, LINC01071, XLOC_010588 400128 ENSG00000237361 NR_104174 GRCh38_13:44400250-44405984 colorectal cancer C19.9 NA qPCR, Western blot, in vitro knockdown etc. cell lines (Caco-2, HT-29, SW480, SW620 and HCT116), CRC tissues up-regulated Expression of XLOC_010588 was significantly higher in CRC tissues when compared with that in adjacent normal tissues, and that XLOC_010588 was closely associated with metastasis and poor prognosis, thus indicating that XLOC_010588 may function as an oncogene. Additionally, downregulation of XLOC_010588 expression markedly inhibited the invasion and migration of CRC cells. Furthermore, it was demonstrated that XLOC_010588 may regulate the progression of CRC via the epithelial-mesenchymal transition (EMT) pathway. Notably, downregulation of XLOC_010588 inhibited the invasion and migration of CRC cells by regulating genes associated with EMT. 29436686 2018 Downregulation of the long non-coding RNA XLOC_010588 inhibits the invasion and migration of colorectal cancer. XLOC_010588 TUSC8, LINC01071, XLOC_010588 400128 ENSG00000237361 NR_104174 GRCh38_13:44400250-44405984 cervical cancer C53 NA qPCR, RNAi, Western blot etc. cervical cancer tissues, cell lines (HeLa, SiHa, HCC94) down-regulated The results showed that XLOC_010588 expression in cervical cancer was significantly downregulated. Decreased XLOC_010588 expression was correlated with FIGO stage, tumor size and SCC-Ag. Moreover, cervical cancer patients with XLOC_010588 lower expression have shown poorer prognosis. Western blot assays confirmed that XLOC_010588 physically associates with c-Myc, consequently decreasing the expression of c-Myc. The expression of XLOC_010588 and c-Myc is strongly correlated in cervical cancer tissues. 24667250 2014 Low expression of long noncoding XLOC_010588 indicates a poor prognosis and promotes proliferation through upregulation of c-Myc in cervical cancer. XLOC_010967 LINC00641, XLOC_010967 NA NA NA NA astrocytoma NA M9400/3 qPCR etc. astrocytoma tissues down-regulated Our analysis ultimately generated a list of 7 lncRNAs that were differentially expressed in astrocytomas in comparison to the NAT samples. Among these lncRNAs, ENST00000244906, ENST00000545440, NR_002809 and ENST00000436616 were shown to be upregulated by a factor greater than twofold, whereas 3 lncRNAs, XLOC_010967, BC002811 and ASO1937, were shown to be downregulated by a factor greater than twofold. 26252651 2016 The Use of Three Long Non-Coding RNAs as Potential Prognostic Indicators of Astrocytoma. XLOC_013014 LINC01233, XLOC_013014 100128139 ENSG00000269364 NR_110663 GRCh38_19:22532626-22533494 esophageal squamous cell cancer NA NA microarray, qPCR etc. OSCC tissues differential expression we identified a three-lncRNA signature (including the lncRNAs ENST00000435885.1, XLOC_013014 and ENST00000547963.1) which classified the patients into two groups with significantly different overall survival . The signature was applied to the test group and independent cohort and showed similar prognostic values in both. 24522499 2014 LncRNA profile study reveals a three-lncRNA signature associated with the survival of patients with oesophageal squamous cell carcinoma. XLOC_014515 APOA4 NA ENSG00000110244 NA GRCh38_11:116820700-116823306 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Cell proliferation assay, Cell migration assay etc. cell lines (HepG2, SMMC-7721 and HCCLM9) differential expression Knockdown of seven of the ten candidate lncRNAs significantly affected cell migration in at least one cell line; knockdown of three lncRNAs produced accordant alterations in cell migration in at least two cell lines by suppressing or promoting cell migration 28194035 2017 Recurrently deregulated lncRNAs in hepatocellular carcinoma. XLOC_015969 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Cell proliferation assay, Cell migration assay etc. cell lines (HepG2, SMMC-7721 and HCCLM9) differential expression Knockdown of seven of the ten candidate lncRNAs significantly affected cell migration in at least one cell line; knockdown of three lncRNAs produced accordant alterations in cell migration in at least two cell lines by suppressing or promoting cell migration 28194035 2017 Recurrently deregulated lncRNAs in hepatocellular carcinoma. XPLAID NA NA NA NA NA prostate cancer C61.9 NA RNA-seq, qPCR etc. prostate cancer tissues up-regulated The 43 differentially expressed (DE) lncRNAs between aggressive and indolent prostate cancers included 12 annotated and 31 novel lncRNAs. The top six DE lncRNAs were selected based on large, consistent fold-changes in the RNA-Seq results. Three of these candidates passed RT-qPCR validation, including AC009014.3 (P < .001 in tumor tissue) and a newly discovered X-linked lncRNA named XPLAID (P = .049 in tumor tissue and P = .048 in normal tissue). XPLAID and AC009014.3 show promise as prognostic biomarkers. SChLAP1 and XPLAID have elevated expression in both tumor and normal associated tissues of aggressive cancers, and AC009014.3 has elevated expression in tumors of indolent cancers. 29723810 2018 Long Noncoding RNAs AC009014.3 and Newly Discovered XPLAID Differentiate Aggressive and Indolent Prostate Cancers. Yiya LINC00538, PROX1UT, Yiya 100861504 ENSG00000281664 NR_046189 GRCh38_1:213924749-213926654 colorectal cancer C19.9 NA qPCR etc. CRC and liver tissues up-regulated The expression levels of four lncRNAs (GAS5, H19, MEG3 and Yiya) were significantly different between liver metastases and primary tumors of stage IV CRC patients. Furthermore, the high expression levels of GAS5 and Yiya were significantly associated with future occurrence of liver metastases in early stage CRC patients. 27391432 2016 Long non-coding RNAs: novel prognostic biomarkers for liver metastases in patients with early stage colorectal cancer Yiya LINC00538, PROX1UT, Yiya 100861504 ENSG00000281664 NR_046189 GRCh38_1:213924749-213926654 breast cancer C50 NA qPCR, etc. breast cancer tissues (Yixin-Bre-01, Duke-Bre-01), breast or lung cancer cell lines up-regulated Our results define a functional role for lncRNA in metabolic reprogramming in cancer, with potential clinical implications for its therapeutic targeting. In clinical specimens of breast cancer, YIYA was expressed in ~40% of cases where it correlated with CDK6 expression and unfavorable survival outcomes. 29967256 2018 Expression of long non-coding RNA YIYA promotes glycolysis in breast cancer. Z38 CLDND1, Z38, C3orf4, GENX-3745 56650 ENSG00000080822 NA GRCh38_3:98497912-98523066 breast cancer C50 NA microarray, qPCR etc. breast cancer tissues up-regulated Z38 was upregulated in breast cancer tissues. Furthermore, of 110 breast cancer patients, high Z38 expression was significantly associated with tumor-node-metastasis stage and lymph node metastasis. 28247935 2017 Prognostic significance of long noncoding RNA Z38 as a candidate biomarker in breast cancer. ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 prostate cancer C61.9 NA Western blot, Luciferase reporter, RIP cell lines (PC3, DU145, NCI-H1299, A549, T98G, U251, A375, A875, HUVEC, HBE, SK-MES-1, HeLa, 293, LO2). up-regulated Collectively, ZEB1-AS1 functions as an oncogene in prostate cancer via epigenetically activating ZEB1 and indirectly regulating downstream molecules of ZEB1. Also, BMI1 promotes cell survival and attenuated chemosensitivity to docetaxelin prostate cancer. Work in mammalian H3K4 methylation has primarily focused on MLL1, the function of which depends on the participation of the helper proteins WDR5, RBBP5 and ASH2L. The discrepancies above might be explained by different cell lines used in different studies or different splicing variants of ZEB1-AS1.A construct with site-directed mutation of the corresponding seed sequence GTCATAT was prepared by overlapping PCR and designated as pGL3-BMI1-MUT. Dual reporter gene assay was performed as described. 28830551 2017 Long noncoding RNA ZEB1-AS1 epigenetically regulates the expressions of ZEB1 and downstream molecules in prostate cancer. ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 esophageal squamous cell cancer NA NA qPCR etc. ESCC tissues up-regulated LNCRNA ZEB1-AS1 was found up-regulated in ESCC tissues compared to adjacent non-tumor tissues. Increased lncRNA ZEB1-AS1 expression was significantly associated with tumor grade, depth of invasion, and lymph node metastasis. Kaplan-Meier analysis revealed that ESCC patients with high ZEB1-AS1 expression had a poorer overall survival and disease-free survival. Furthermore, multivariate analysis suggested that ZEB1-AS1 expression was identified as an independent prognostic factor in patients with ESCC 26617942 2015 Expression of long non-coding RNA ZEB1-AS1 in esophageal squamous cell carcinoma and its correlation with tumor progression and patient survival ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 gastric cancer C16 NA qPCR, Western blot etc. cell lines (NCI-N87, SNU-1, AGS, MKN-45) up-regulated ZEB1-AS1 regulated gastric cancer cells migration, invasion and EMT process.ZEB1-AS1 positively regulated ZEB1 expression in gastric cancer cells, and had a strongly positive correlation with ZEB1 expression in gastric cancer tissues.Rescued-function studies showed ZEB1 was critical for ZEB1-AS1 induced gastric cancer cells migration, invasion and EMT process. 29113674 2017 LncRNA ZEB1-AS1 predicts unfavorable prognosis in gastric cancer ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 glioma NA M9380/3 qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. glioma tissues, cell lines (HS683, T98G, U87, and U251) up-regulated Here, we found that ZEB1-AS1 was highly expressed in glioma tissues, being closely related to clinical stage of glioma. Functionally, silencing of ZEB1-AS1 could significantly inhibit cell proliferation, migration, and invasion, as well as promote apoptosis. Knockdown of ZEB1-AS1 significantly induced the G0/G1 phase arrest and correspondingly decreased the percentage of S phase cells. Further analysis indicated that ZEB1-AS1 could regulate the cell cycle by inhibiting the expression of G1/S transition key regulators, such as Cyclin D1 and CDK2. Furthermore, ZEB1-AS1 functioned as an important regulator of migration and invasion via activating EMT through up-regulating the expression of ZEB1, MMP2, MMP9, N-cadherin, and Integrin-B1 as well as decreasing E-cadherin levels in the metastatic progression of glioma. 27589728 2016 A Long Noncoding RNA ZEB1-AS1 Promotes Tumorigenesis and Predicts Poor Prognosis in Glioma. ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 gastric cancer C16 NA qPCR, Luciferase reporter assay, RIP gastric cancer tissues, cell lines (SGC7901, HGC27, BGC823,MKN45, MKN28, and AGS, GES-1) up-regulated High ZEB1-AS1 expression was significantly correlated with advanced TNM stage, lymph node metastasis, and poor overall survival in GC patients. ZEB1-AS1 suppression reduced GC cell proliferation and invasion in vitro.ZEB1-AS1 inhibition suppressed GC cell growth. miR-335-5p expression was directly regulated by ZEB1-AS1. inhibition of miR-335-5p abrogated the suppression of proliferation and invasion of GC cells induced by ZEB1-AS1 depletion. Collectively, ZEB1-AS1 is critical for the proliferation and invasion of GC cells by regulating miR-335-5p. 29215918 2018 Downregulation of miR-335-5p by Long Noncoding RNA ZEB1-AS1 in Gastric Cancer Promotes Tumor Proliferation and Invasion. ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 colorectal cancer C19.9 NA qPCR, Western blot etc. colorectal cancer tissues, cell lines (SW480, DLD-1, HCT116, SW620) up-regulated It turns out that ZEB1-AS1 is upregulated in colorectal cancer tissues and its expression is significantly associated with overall survival rate and recurrence-free survival. 28618933 2017 High expression of long non-coding RNA ZEB1-AS1 promotes colorectal cancer cell proliferation partially by suppressing p15 expression ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 osteosarcoma NA M9180/3 qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. osteosarcoma tissues, cell lines (hFOB 1.19, HOS, U-2 OS, MG-63, and Saos-2) up-regulated The results showed that ZEB1-AS1 was upregulated in osteosarcoma tissues and cells. Increased expression of ZEB1-AS1 is correlated with larger tumor size, progressed Enneking stage, tumor metastasis, worse recurrence-free and overall survival of osteosarcoma patients. Functional experiments showed that enhanced expression of ZEB1-AS1 promotes osteosarcoma cells proliferation and migration. By contrast, ZEB1-AS1 knockdown inhibits osteosarcoma cells proliferation and migration. Mechanistically, ZEB1-AS1 directly binds and recruits p300 to the ZEB1 promoter region, induces an open chromatin structure, and activates ZEB1 transcription. 27829995 2016 Long noncoding RNA ZEB1-AS1 acts as an oncogene in osteosarcoma by epigenetically activating ZEB1. ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RNAi etc. HCC tissues, cell lines (Huh7, HepG2, etc.) up-regulated We found that ZEB1-AS1 is frequently upregulated in HCC samples, especially in metastatic tumor tissues. ZEB1-AS1 promotes tumor growth and metastasis, acts as an oncogene in HCC. The ZEB1-AS1 gene is located in physical contiguity with ZEB1 and positively regulates the ZEB1 expression. ZEB1 inhibition partially abrogates ZEB1-AS1-induced epithelial to mesenchymal transition (EMT) and cancer metastasis. 26073087 2015 Upregulation of long noncoding RNA ZEB1-AS1 promotes tumor metastasis and predicts poor prognosis in hepatocellular carcinoma. ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 gastric cancer C16 NA qPCR gastric cancer tissues, cell lines (MKN28, MKN45, BGC823, MGC803, KATOIII,and SGC7901) up-regulated qRT-PCR showed that compared with that in the normal gastric epithelial cell (GES-1), the expression level of lncRNA ZEB1-AS1 was up-regulated in gastric cancer cells (MKN28, MKN45, BGC823, MGC803, KATOIII, and SGC7901). 29771411 2018 Long non-coding RNA ZEB1-AS1 is associated with poor prognosis in gastric cancer and promotes cancer cell metastasis ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 glioma NA M9380/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. glioma tissues, cell line (HEB, A172, U87, T98G and SHG44) up-regulated Compared with normal brain tissues and cells, ZEB1-AS1 in glioma tissues and cell lines was shown to be expressed at high levels. Clinical association analysis indicated that ZEB1-AS1 expression was closely associated with tumor size (p = 0.014), KPS (p = 0.004) and WHO grade (p = 0.001). In addition, it was observed that high expression level of ZEB1-AS1 was remarkably associated with overall survival and could be an independent prognostic indicator of glioma using univariate and multivariate analysis. Functional experiments demonstrated that down-regulation of ZEB1-AS1 suppressed the proliferation, invasion, and migration of glioma cell in vitro. In the mechanism, we found that ZEB1-AS1 acted as a competing endogenous RNA to sponge miR-577. Moreover, miR-577 could reverse the tumor-promotive role of ZEB1-AS1 on glioma cells. 29863254 2018 Long non-coding RNA ZEB1-AS1 promotes glioma cell proliferation, migration and invasion through regulating miR-577. ZEB2-AS1 ZEB2-AS1, ZEB2-AS, ZEB2AS, ZEB2NAT 100303491 ENSG00000238057 NR_040248 GRCh38_2:144518097-144521477 pancreatic cancer C25 NA qPCR, Western blot, Luciferase reporter assay, RIP etc. pancreatic cancer tissues, cell lines up-regulated the expression level of ZEB2-AS1 was elevated in pancreatic cancer cell lines and tissues.ZEB2-AS1 inhibition decreased cell growth and invasion in pancreatic cancer. Mechanismly,ZEB2-AS1 exerted as a ceRNA and negatively regulated miR-204 expression. In addition, HMGB1 was identified as a down-stream target of miR-204. The miR-204/HMGB1 axis mediated ZEB2-AS1's effect on pancreatic cancer. lncRNA ZEB2-AS1 may be a candidate prognostic biomarker and a target for new therapies in pancreatic cancer patients. 29753015 2018 LncRNA ZEB2-AS1 promotes pancreatic cancer cell growth and invasion through regulating the miR-204/HMGB1 axis. ZEB2-AS1 ZEB2-AS1, ZEB2-AS, ZEB2AS, ZEB2NAT 100303491 ENSG00000238057 NR_040248 GRCh38_2:144518097-144521477 lung cancer C34 NA Western blot, in vitro knockdown etc. lung cancer cell lines (H-125, A549, 95D, NCI-H292, H1975), lung cancer tissues up-regulated ranscript level of ZEB2-AS1 in human lung cancer was markedly upregulated in vivo and in vitro. The knockdown of ZEB2-AS1 in A549 and NCI-H292 cells, and the overexpression of ZEB2-AS1 in H-125 and H1975 cells, altered colony formation and cell proliferative rate, as examined using colony formation and cell proliferation assays. Similarly, the overexpression of ZEB2-AS1 in H-125 and H1975 cells resulted in decreased expression of caspase-3, caspase-9, Bcl-2 and Bax. The results identified the effects of lncRNA ZEB2-AS1 on lung cancer progression through promoting its proliferation and inhibiting cell apoptosis, indicating that ZEB2-AS1 may serve as a novel prognostic factor for the diagnosis and treatment of human lung cancer in the clinic. 29552161 2018 Long non-coding RNA ZEB2-AS1 promotes proliferation and inhibits apoptosis in human lung cancer cells. ZEB2-AS1 ZEB2-AS1, ZEB2-AS, ZEB2AS, ZEB2NAT 100303491 ENSG00000238057 NR_040248 GRCh38_2:144518097-144521477 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. HCC tissues, cell lines (Hep3B, HepG2, Huh-7 and SMMC-7721) up-regulated The expression levels of ZEB2-AS1 were greater in HCC tissues when compared with the adjacent normal tissues. Furthermore, ZEB2-AS1 expression was significantly associated with the size of the primary tumor, intrahepatic metastasis and tumor-node-metastasis stage. Downregulation of ZEB2-AS1 was associated with decreased tumor growth and metastasis in HCC by the regulation of the expression levels of epithelial mesenchymal transition-induced markers. 27748842 2016 Downregulation of ZEB2-AS1 decreased tumor growth and metastasis in hepatocellular carcinoma. ZEB2-AS3 NA NA NA NA NA gastric cancer C16 NA qPCR, RNAi etc. cell lines (AGS1, MGC803, SGC7901, and MKN52), gastric adenocarcinomas tissues down-regulated Downregulation of LINCROR, POU3F3, HOTAIR, FALEC, NBAT1, and ZEB2-AS3 lncRNAs in TCGA gastric tumor datasets 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 acute myeloid leukemia NA M9861/3 qPCR etc. cell lines (HL-60, KG-1, ML-1 and SKNO-1) up-regulated ZFAS1 mRNA were significantly increased in all human four AML cell lines compared with the T lymphocytic leukemia cell line or Burkitt's lymphoma cell line. ZFAS1 promoted the proliferation and inhibited the apoptosis of AML cells.Li et al identified that ZFAS1 functions as an oncogene in hepatocellular carcinoma progression by binding miR-150 and abrogating its tumor-suppressive function.molecular abnormalities and outcome in older patients with cytogenetically normal AML and revealed that patients with an unfavorable lncRNA score had a shorter overall survival and disease-free survival rate than those with a favorable lncRNA score. 28672980 2017 Overexpression of long non-coding RNA zinc finger antisense 1 in acute myeloid leukemia cell lines influences cell growth and apoptosis. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated ZFAS1 was upregulated in NSCLC tissues and higher expression levels of ZFAS1 were found in more advanced tumor tissues. ZFAS1 expression levels were significantly associated with tumor differentiation grade, lymph node metastasis and TMN stage. Furthermore, we found that patients with higher ZFAS1 expression level are associated with a poorer overall survival. 28051258 2016 Overexpression of long-noncoding RNA ZFAS1 decreases survival in human NSCLC patients. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 glioma NA M9380/3 qPCR glioma tissues down-regulated Expression of lncRNAs MEG3, JPX, RNCR3, and ZFAS1 significantly differed between low and high malignancy grade. MEG3, JPX, RNCR3, and ZFAS1 showed significant decrease with tumour malignant progression. Expression of certain lncRNAs seems to be associated with patient's age at the time of diagnosis as correlation analysis showed moderate negative association for MEG3 (rs = 0.336, p = 0.009, R2 = 0.113), ZFAS1 (rs = 0.368, p = 0.004, R2 = 0.164), and RNCR3 (rs = 0.431, p = 0.001, R2 = 0.186). 29138748 2017 Identifying Novel Glioma-Associated Noncoding RNAs by Their Expression Profiles ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 breast cancer C50 NA qPCR, Western blot etc. cell lines (MCF10A, MDAMB-231, MCF7, T47D, and SKBR3) down-regulated The results revealed that ZFAS1 expression was significantly downregulated in breast cancer cell lines when compared with the levels in controls. In vitro experiments also demonstrated that ZFAS1 overexpression significantly suppressed cell proliferation by causing cell cycle arrest and inducing apoptosis in breast cancer cells. Further functional assays indicated that ZFAS1 overexpression inhibited cell migration and invasion by regulating epithelial mesenchymal transition. These findings indicated that the lncRNA ZFAS1 may be a tumor suppressor in breast cancer, and thus, may serve as a potential therapeutic target for patients with breast cancer. ZFAS1 overexpression in MCF-7 and MDA-MB-231 cells resulted in significantly decreased clonogenic survival. 29532866 2018 Downregulation of the long non-coding RNA ZFAS1 is associated with cell proliferation, migration and invasion in breast cancer. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 bladder cancer C67 NA qPCR, Luciferase reporter assay etc. bladder cancer tissues, cell lines (T24, RT4, 5637, SW780, SE780 and UM-UC-3) up-regulated ZFAS1 expression was significantly upregulated in bladder cancer tissues and cell lines.Furthermore, Kaplan-Meier analysis revealed that high ZFAS1 expression was significantly associated with unfavorable progression free survival (PFS) and overall survival(OS) of bladder cancer patients. Moreover, silencing of ZFAS1 expression could markedly suppress bladder cancer cells proliferation and colony formation, arrest cell cycle, promote cell apoptosis and inhibit cell migration in vitro. In addition, bioinformatics analysis, luciferase reporter assay,and pull down assay revealed that ZFAS1 straightly interacted with miR-329.Lastly, rescue experiments confirmed that miR-329 inhibitor reversed the tumor suppressing roles of ZFAS1 knockdown on bladder cancer cells.Collectively, our results illuminated that ZFAS1 could serve as an oncogene in the tumorigenesis of bladder cancer,and discovered the functional regulatory network of ZFAS1 sponging miR-329. 29653362 2018 The long noncoding RNA ZFAS1 facilitates bladder cancer tumorigenesis by sponging miR-329. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 osteosarcoma NA M9180/3 qPCR, Western blot, RIP etc. OS tissues, cell lines (KHOS, 143b, LM7, U2OS, MG-63, Nhost) up-regulated a functional role of ZFAS1 on OS growth and metastasis. The expression of ZFAS1 was signifiantly overex- pressed in OS samples and cell lines, and upregulation of ZFAS1 is signifiantly associated with unfavorable prognosis of OS patients. Functional assays also demonstrated that ZFAS1 enhanced the growth and metastatic ability of OS cells in vitro and in vivo.Mechanistically, we found that ZFAS1 positively regulated malignant phenotypes by competitively binding the miR-200b and miR-200c and upregulating BMI1.ZFAS1 also interacted with ZEB2 and regulated ZEB2 protein stability. Furthermore, we demonstrated that SP1 functions as an upstream activated factor of ZFAS1.ZFAS1 may be a potential therapeutic target for OS tumorigenesis and progression. 28744396 2017 LncRNA ZFAS1 promotes growth and metastasis by regulating BMI1 and ZEB2 in osteosarcoma. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 hepatocellular carcinoma C22.0 M8170/3 qPCR, RIP, Luciferase reporter assay etc. HCC tissues, cell lines (Huh7, HepG2, etc.) up-regulated ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14 and MMP16 expression, inhibiting these effects of miR-150. 26069248 2015 Amplification of long non-coding RNA ZFAS1 promotes metastasis in hepatocellular carcinoma. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 glioma NA M9380/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. glioma tissues, cell lines (U87 and U251) up-regulated We found that ZFAS1 was upregulated in glioma tissues and cell lines. High ZFAS1 expression in glioma tissues was significantly correlated with advanced tumor stage and poor overall survival. Furthermore, in vitro assays demonstrated that ZFAS1 inhibition significantly suppressed glioma cell proliferation, migration and invasion. Importantly, we further confirmed that epithelial-mesenchymal transition (EMT) and the Notch signaling pathway was inactivated in the glioma cells after ZFAS1 knockdown. 28081466 2017 Long non-coding RNA ZFAS1 is an unfavourable prognostic factor and promotes glioma cell progression by activation of the Notch signaling pathway. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 colorectal cancer C19.9 NA qPCR, Luciferase reporter assay colorectal cancer tissues, cell lines (HCT116, SW480, SW620, HT-29 and LOVO, HCoEpiC) up-regulated ZFAS1 expression was significantly upregulated in CRC tissues and cell lines. high ZFAS1 expression was significantly associated with Helicobacter pylori infection, lymph nodes metastasis, advanced TNM stage and poor overall survival of CRC patients. ZFAS1 inhibition could markedly suppress CRC cells proliferation and invasion both in vitro and in vivo.ZFAS1 directly interacted with miR-484. miR-484 inhibitor reversed the tumor suppressing roles of ZFAS1 knockdown on CRC cells. 29179614 2017 Long non-coding RNA ZFAS1 sponges miR-484 to promote cell proliferation and invasion in colorectal cancer. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 colorectal cancer C19.9 NA qPCR, RNAi, Cell migration and invasion assay etc. CRC tissues, cell lines (HCT8, HCT116, HT29, LoVo, SW480, SW620 and HEK-293T) up-regulated The ZFAS1 expression was significantly upregulated in 47.8% (76 of 159) of cancerous tissues compared with NCTs, and was higher in metastatic tumors than in corresponding primary CRC tumors. ZFAS1 expression in CRC was positively correlated with lymphatic invasion and TNM stage. Patients with increased ZFAS1 expression showed shorter relapse-free survival and overall survival. The knockdown of ZFAS1 decreased cell migration and invasive ability of LoVo and HCT116 cells in vitro. Moreover, silencing ZFAS1 expression inhibited the in vivo metastasis of CRC cells. 27461828 2016 Upregulation of long noncoding RNA ZFAS1 predicts poor prognosis and prompts invasion and metastasis in colorectal cancer. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 gastric cancer C16 NA microarray, qPCR, RNAi, RNA pull-down assay, Cell proliferation assay etc. gastric cancer tissues, cell lines (BGC823, SGC7901, MGC803, AGS, HGC27 etc.) up-regulated Here, we reported that ZFAS1 expression is also overexpressed in gastric cancer, and its increased level is associated with poor prognosis and shorter survival. Knockdown of ZFAS1 impaired gastric cancer cells proliferation and induced apoptosis in vitro, and inhibited tumorigenicity of gastric cancer cells in vivo. Mechanistically, RNA immunoprecipitation and RNA pull-down experiment showed that ZFAS1 could simultaneously interact with EZH2 and LSD1/CoREST to repress underlying targets KLF2 and NKD2 transcription. In addition, rescue experiments determined that ZFAS1 oncogenic function is partly dependent on repressing KLF2 and NKD2. 27246976 2016 Long noncoding RNA ZFAS1 promotes gastric cancer cells proliferation by epigenetically repressing KLF2 and NKD2 expression. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 nasopharyngeal cancer C11 NA qPCR, Western blot, etc. nasopharyngeal cancer tissues, cell lines (CNE-1, CNE-2, HNE-1, NP-69, HONE-1, SUNE-1) up-regulated ZFAS1 was overexpressed in NPC and was significantly related to tumor size, lymph node metastasis and poor prognosis of NPC. ZFAS1 could promote NPC by activating Wnt/B-catenin pathway. 29917194 2018 Long non-coding RAN ZFAS1 promotes nasopharyngeal carcinoma through activation of Wnt/β-catenin pathway. ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 441951 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Cell proliferation assay, Cell apoptosis assay etc. HCC tissues, cell lines (HepG2, Hep3B, SNU449, HuH-7) down-regulated Our results suggest that ZNFX1-AS1 was markedly downregulated in HCC samples and cell lines. Overexpression of ZNFX1-AS1 inhibited the cell proliferation and colony formation in HCC cell lines and also induced HCC cell apoptosis. Additionally, miR-9 was lowly expressed in HCC tissues and positively correlated with ZNFX1-AS1 expression. Meanwhile, significant upregulation of miR-9 and downregulation of the methylation of miR-9 promoter CpG island were observed when ZNFX1-AS1 was overexpressed. 27574442 2016 Long noncoding RNA ZNFX1-AS1 suppresses growth of hepatocellular carcinoma cells by regulating the methylation of miR-9. ZFPM2-AS1 SCAT3 102723356 ENSG00000251003 NR_125796 GRCh38_8:105780246-106060524 gastric cancer C16 NA qRT-PCR, Western blot assays, RNA pull-down assay, RIP the nontumorigenic human gastric cell line (GES-1); the gastric cancer cell lines (BGC-823, MKN-28, MKN-45, MGC-803, and SGC-7901), gastric cancer specimens and the corresponding noncancerous tissue specimens. up-regulated ZFPM2-AS1 expression was higher in gastric tumors than in normal gastric tissue. Also, increased ZFPM2-AS1 expression in gastric cancer specimens was associated with tumor size, depth of tumor invasion, differentiation grade, and TNM stage. Mechanistic experiments demonstrated that tumor-activated ZFPM2-AS1 could bind to and protect the degradation of macrophage migration inhibitory factor (MIF), a potent destabilizer of p53. Knockdown of MIF expression diminished ZFPM2-AS1's impact on p53 expression in gastric cancer cells. ZFPM2-AS1 expression was higher in gastric tumors than in normal gastric tissue. Also, increased ZFPM2-AS1 expression in gastric cancer specimens was associated with tumor size, depth of tumor invasion, differentiation grade, and TNM stage. Mechanistic experiments demonstrated that tumor-activated ZFPM2-AS1 could bind to and protect the degradation of macrophage migration inhibitory factor (MIF), a potent destabilizer of p53. Knockdown of MIF expression diminished ZFPM2-AS1's impact on p53 expression in gastric cancer cells. We treated AGS cells with the DNA methylation inhibitor 5-azacytidine but find no change of ZFPM2-AS1 expression in them 29985481 2018 ZFPM2-AS1, a novel lncRNA, attenuates the p53 pathway and promotes gastric carcinogenesis by stabilizing MIF. ZMAT1 ZMAT1 NA ENSG00000166432 NA GRCh38_X:101882288-101932031 gastric cancer C16 NA qPCR etc. gastric cancer tissues down-regulated We found for the first time that the lncRNA ZMAT1 transcript variant 2 is downregulated in gastric cancer tissues compared with adjacent normal tissues. The expression of ZMAT1 transcript variant 2 was inversely correlated with lymph node metastasis, depth of tumor invasion and tumor node metastasis stage. Univariate and multivariate analyses showed that ZMAT1 transcript variant 2 expression was an independent predictor for overall survival 26191264 2015 Downregulation of long noncoding RNA ZMAT1 transcript variant 2 predicts a poor prognosis in patients with gastric cancer ZNF667-AS1 NA 100128252 ENSG00000166770 NR_036522 GRCh38_19:56477250-56500666 cervical cancer C53 M8070/3 qPCR, microarray, western blot cell lines(SiHa) down-regulated the expression of LncRNA ZNF667-AS1 in cervical cancer was significantly lower than that in normal cervical tissues.the expression of LncRNA ZNF667-AS1 in cervical cancer tissues was lower than that in normal cervical tissues, which was consistent with that of TCGA.the expression of LncRNA ZNF667-AS1 was correlated with the total survival, tumor size and FIGO stage.Compared with the negative control group, the proliferation ability and cell cloning ability of cells with over-expressed LncRNA ZNF667-AS1 were significantly decreased, indicating that overexpression of ZNF667-AS1 inhibited the proliferation of SiHa cells. 29243775 2017 Independent prognostic Factor of low-expressed LncRNA ZNF667-AS1 for cervical cancer and inhibitory function on the proliferation of cervical canc ZNF674-AS1 ZNF674-AS1 401588 ENSG00000230844 NR_015378 GRCh38_X:46545493-46548408 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell lines (HepG2, HCCLM3, SK-Hep1, HuH7, Hep3B, and MHCC97H) down-regulated The expression of ZNF674-AS1 in the HCC cell lines was significantly downregulated compared with that in the normal liver cell line. The expression of ZNF674-AS1 was downregulated in 72% (99/137) of HCC tissues compared with that in paired adjacent normal tissues. The results showed that the ZNF674-AS1 expression level was significantly correlated with metastasis, clinical stage, and histopathologic grading. 27896271 2016 Expression and Clinical Significance of the Novel Long Noncoding RNA ZNF674-AS1 in Human Hepatocellular Carcinoma. ZNF750 ZNF750, ZFP750 NA ENSG00000141579 NA GRCh38_17:82829435-82840578 skin squamous cell carcinoma C44 M8070/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. cell line (SCC13) down-regulated In this study, we report that ZNF750 is exclusively deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor survival. Restoration of wildtype, but not mutant ZNF750 protein uniquely inhibited the malignant phenotypes of SCC cells both in vitro and in vivo. Notably, ZNF750 promoted the expression of a long non-coding RNA (TINCR), which mediated both cancer-inhibition and differentiation-induction effects of ZNF750. In addition, ZNF750 potently suppressed cell migration by directly inhibiting the transactivation of LAMC2. 27819679 2016 ZNF750 is a lineage-specific tumour suppressor in squamous cell carcinoma. ZNF750 ZNF750, ZFP750 NA ENSG00000141579 NA GRCh38_17:82829435-82840578 cervical squamous cell carcinoma C53 M8070/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. cell lines (C33A, CaSki, HT-3, ME180 and SiHa) down-regulated In this study, we report that ZNF750 is exclusively deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor survival. Restoration of wildtype, but not mutant ZNF750 protein uniquely inhibited the malignant phenotypes of SCC cells both in vitro and in vivo. Notably, ZNF750 promoted the expression of a long non-coding RNA (TINCR), which mediated both cancer-inhibition and differentiation-induction effects of ZNF750. In addition, ZNF750 potently suppressed cell migration by directly inhibiting the transactivation of LAMC2. 27819679 2016 ZNF750 is a lineage-specific tumour suppressor in squamous cell carcinoma. ZNF750 ZNF750, ZFP750 NA ENSG00000141579 NA GRCh38_17:82829435-82840578 lung squamous cell carcinoma C34 M8070/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. cell lines (Calu-1, ChagoK1, H2170 and H226) down-regulated In this study, we report that ZNF750 is exclusively deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor survival. Restoration of wildtype, but not mutant ZNF750 protein uniquely inhibited the malignant phenotypes of SCC cells both in vitro and in vivo. Notably, ZNF750 promoted the expression of a long non-coding RNA (TINCR), which mediated both cancer-inhibition and differentiation-induction effects of ZNF750. In addition, ZNF750 potently suppressed cell migration by directly inhibiting the transactivation of LAMC2. 27819679 2016 ZNF750 is a lineage-specific tumour suppressor in squamous cell carcinoma. ZNF750 ZNF750, ZFP750 NA ENSG00000141579 NA GRCh38_17:82829435-82840578 head and neck squamous cell carcinoma C76.0 M8070/3 qPCR, RNAi, Western blot, ChIP, Cell proliferation assay etc. cell lines (UMSCC1 and 93UV147) down-regulated In this study, we report that ZNF750 is exclusively deleted, mutated and underexpressed in human SCCs, and low ZNF750 expression is associated with poor survival. Restoration of wildtype, but not mutant ZNF750 protein uniquely inhibited the malignant phenotypes of SCC cells both in vitro and in vivo. Notably, ZNF750 promoted the expression of a long non-coding RNA (TINCR), which mediated both cancer-inhibition and differentiation-induction effects of ZNF750. In addition, ZNF750 potently suppressed cell migration by directly inhibiting the transactivation of LAMC2. 27819679 2016 ZNF750 is a lineage-specific tumour suppressor in squamous cell carcinoma. ZXF2 NA NA NA NA NA lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot, Cell apoptosis assay etc. lung adenocarcinoma tissues up-regulated The expression of ZXF2 was 2 fold or higher in 27 out of 40 (67.5%) cases of lung adenocarcinoma specimens than that in non-cancerous tissues. The relative expression level of ZXF2 was positively correlated with tumor lymph node metastasis and poor prognosis of the patients. In order to explore the molecular mechanisms of ZXF2 mediated tumor progression, ZXF2 expression was inhibited by siRNA in A549 cells, a highly aggressive and metastatic lung adenocarcinoma cell line. We found that siRNA-ZXF2 treatment inhibited cell proliferation leading to cell cycle arrest. The cell migration and invasion were suppressed by siRNA-ZXF2 treatment. Further biochemical studies revealed that the knockdown of ZXF2 led to down regulation of c-Myc signaling. 25896422 2015 Overexpression of Long Non-Coding RNA ZXF2 Promotes Lung Adenocarcinoma Progression Through c-Myc Pathway. UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot etc. lung adenocarcinoma tissues, cell lines (PC9, H1975, H460, H23, H1299) up-regulated In our study, UCA1 expression was significantly increased in lung cancer cells and patients with acquired resistance to EGFR-TKIs. Over-expression of UCA1 was significantly associated with a shorter progression-free survival (PFS), in tumors with respond to EGFR-TKIs. 26160838 2015 Long non-coding RNA UCA1 induces non-T790M acquired resistance to EGFR-TKIs by activating the AKT/mTOR pathway in EGFR-mutant non-small cell lung cancer