LncRNA name Synonyms Ensembl ID Refseq ID Position Cancer name ICD-0-3-T ICD-0-3-M Methods Sample (tissue/ cell line) Expression pattern Functional description PubMed ID Year Title 1 SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 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. 2 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 3 PRLB 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. 4 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 5 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 6 ROR LINC-ROR, ROR, lincRNA-RoR 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 7 ROR LINC-ROR, ROR, lincRNA-RoR 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 8 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 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. 9 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 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. 10 CRNDE-p CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 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. 11 FAL1 FALEC, FAL1, LINC00568, ncRNA-a1 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. 12 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 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. 13 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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-κB 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-κB/TS Signaling in Colorectal Cancer. 14 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 15 PTENP1-AS NA 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. 16 Sox2ot SOX2-OT, NCRNA00043, SOX2OT 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. 17 TINCR TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16 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. 18 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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. 19 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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. 20 ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 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 21 TP73-AS1 TP73-AS1, KIAA0495, PDAM 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. 22 CASC2 CASC2, C10orf5 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. 23 RP11-838N2.4 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 24 AGER AGER-1 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. 25 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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 26 FOXD2-AS1 FOXD3-AS1, pasFOXD3 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. 27 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 28 MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT 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. 29 ENSG00000240990 HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 ENSG00000240990 NA 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. 30 HOXA10 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. 31 ODRUL FOXC2-AS1, ODRUL 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 32 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 33 MIR100HG MIR100HG, AGD1, linc-NeD125, lncRNA-N2 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/β-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/β-catenin signaling 34 PAX8-AS1-N 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. 35 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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 1α, 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. 36 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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 37 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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 38 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 39 lncRNA-ATB LOC109207222 NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. cell lines (SMMC-7721, huh-7) down-regulated Expression of lncRNA-ATB reversed the effects of AS-IV on HCC cell migration, EMT, cell apoptosis, cell viability, and IL-11/STAT3 signaling. 29331759 2018 Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB. 40 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 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. 41 ENST01108 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. 42 GAPLINC GAPLINC, LINC01540 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. 43 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 44 LUCAT1 LUCAT1, SCAL1 ENSG00000248323 NR_103548 GRCh38_5:91303029-91314402 esophageal squamous cell cancer NA NA qPCR, Western blot, RIP, in vitro knockdown etc. cell lines (KYSE-30, TE-2, HCE-4, HCE-7), ESCC tissues up-regulated LUCAT1 knockdown reduced cell proliferation,induced apoptosis,and upregulated tumor-suppressor genes by reducing DNA methylation in KYSE-30?cells.Moreover,LUCAT1 siRNA reduced DNA methyltransferase 1 (DNMT1) protein levels without affecting transcription.LUCAT1 regulates the stability of DNMT1 and inhibits the expression of tumor suppressors through DNA methylation,leading to the formation and metastasis of ESCC. 29247823 2018 The long noncoding RNA LUCAT1 promotes tumorigenesis by controlling ubiquitination and stability of DNA methyltransferase 1 in esophageal squamous cell carcinoma. 45 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioblastoma NA M9440/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell line (U251) up-regulated MALAT1 was significantly upregulated in TMZ-resistant GBM cells.On the other hand,MALAT1 knockdown reduces TMZ resistance of GBM cells both in vitro and in vivo by inhibiting cell proliferation and promoting apoptosis.We also show that miR-101 overexpression reduced TMZ resistance of GBM cells and played an antagonistic role compared with MALAT1.Importantly,we demonstrate that MALAT1 promoted the chemoresistance through suppressing miR-101 signaling pathway via directly binding it in GBM cells.In conclusion,our study indicates that knockdown of MALAT1 reverses chemoresistance to TMZ via promoting miR-101 regulatory network in GBM and thus offers a novel prognostic marker and potential target. 29479863 2018 Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA-101 in glioblastoma. 46 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 prostate cancer C61.9 NA qPCR, Western blot, Luciferase reporter assay etc. cell lines (DU145 and PC3, HEK-293T), PCa tissues up-regulated MALAT1 expression levels were up-regulated in clinical DTX-resistant PCa samples.Overexpressed MALAT1 promoted cell proliferation,migration and invasion but decreased cell apoptosis rate of PCa cells in spite of DTX treatment.We identified miR-145-5p as a target of MALAT1.MiR-145-5p overexpression in PC3-DTX led to inhibited cell proliferation, migration and invasion as well as reduced chemoresistance to DTX,which was attenuated by MALAT1.Moreover,we determined that AKAP12 was a target of miR-145-5p,which significantly induced chemoresistance of PCa cells to DTX. Besides,it was proved that MALAT1 promoted tumour cell proliferation and enhanced DTX-chemoresistance in vivo. 29633510 2018 Long noncoding RNA MALAT1 enhances the docetaxel resistance of prostate cancer cells via miR-145-5p-mediated regulation of AKAP12. 47 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 breast cancer C50 NA qPCR, Western blot etc. BC tissues, cell lines (MDA-MB-231, MCF-7, SKBR3, MCF-10A) down-regulated MEG3 was significantly down-regulated in breast cancer tissues compared to adjacent normal tissues.MEG3/miR-421/E-cadherin regulatory axis may be a novel therapeutic target for breast cancer.endogenous miR-421 expression was negatively regulated by MEG3 in breast cancer cells and MEG3 regulated E-cadherin expression by sponging to miR-421 in breast cancer cells.Survival analysis showed that lower MEG3 predicted a poor DFS and OS for patients. Down-regulation of MEG3 enhances cisplatin resistance of lung cancer cells through activation of the WNT/b-catenin signaling pathway. 28463794 2017 LncRNA MEG3 inhibits cell epithelial-mesenchymal transition by sponging miR-421 targeting E-cadherin in breast cancer. 48 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 nasopharyngeal cancer C11 NA qPCR, Western blot etc. NPC tissues, cell lines (5-8F, CNE1, CNE2, S26, HNE1, SUNE1, HONE1, NP69) down-regulated NEAT1 is down-regulated in NPC tissues and is associated with poor prognosis. NEAT1 antagonized miR-101-3p through a competing endogenous RNA (ceRNA) mechanism and that the interaction between NEAT1 and EMP2 was miR-101-3p dependent. a novel connection of NEAT1, miR-101-3p and EMP2 in NPC migration and radiation resistance. NPC patients with high NEAT1 expression levels had longer overall survival than patients with low and negative NEAT1 expression levels. 29050268 2017 Long non-coding RNA NEAT1 regulates epithelial membrane protein 2 expression to repress nasopharyngeal carcinoma migration and irradiation-resistance through miR-101-3p as a competing endogenous RNA mechanism. 49 NR2F1-AS1 NA ENSG00000237187 NR_021490 GRCh38_5:93409359-93585648 hepatocellular carcinoma C22.0 M8170/3 qPCR, Microarray, Western blot etc. cell lines (Huh7, HepG2, Lo-2), HCC tissues up-regulated miR-363 targeted the 3'-UTR of NR2F1-AS1 and ABCC1 mRNA,presenting that NR2F1-AS1 promoted ABCC1 expression through endogenous sponging miR-363.NR2F1-AS1 regulates HCC OXA resistance through targeting miR-363-ABCC1 pathway,providing a vital theoretic mechanism and therapeutic target for HCC chemoresistance. 29602203 2018 LncRNA NR2F1-AS1 regulates hepatocellular carcinoma oxaliplatin resistance by targeting ABCC1 via miR-363. 50 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 glioma NA M9380/3 qPCR, Luciferase reporter assay etc. gliomas tissues, cell lines (U87, U251 and HEK-293T) up-regulated PVT1 was up-regulated in glioma specimens and cell lines.Knockdown of PVT1 impaired the malignant behaviors of glioma cells via the suppression of proliferation,migration and invasion,as well as through promotion of apoptosis. Furthermore,PVT1 was identified to affect the glioma cells via binding to miR-190a-5p and miR-488-3p, which were down-regulated and played tumor suppressor roles in glioma cells. Over-expression of MEF2C up-regulated JAGGED1 by increasing the promoter activity of JAGGED1.Over-expression of PVT1 promotes multiple drug-resistance in gastric cancer. 29501773 2018 PVT1 regulates the malignant behaviors of human glioma cells by targeting miR-190a-5p and miR-488-3p. 51 SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 ENSG00000203875 NR_003038 GRCh38_6:85660950-85678736 lung adenocarcinoma C34 M8140/3 Western blot, in vitro knockdown, Luciferase reporter assay, RNAi etc. cell line (PC9, A549, HEK-293T), lung adenocarcinoma tissues down-regulated Overexpression of SNHG5 suppressed the expression of miR-377, while the knockdown of SNHG5 increased the miR-377 expression. MiR-377 expression was significantly upregulated in LAD specimens with acquired gefitinib resistance and was negatively correlated with SNHG5 expression. In addition, CASP1 was predicted as a downstream target of miR-377.Knockdown of CASP1 in SNHG5-overexpression PC9GR cells abolished their gefitinib resistance. 29592872 2018 The long non-coding RNA SNHG5 regulates gefitinib resistance in lung adenocarcinoma cells by targeting miR-377/CASP1 axis. 52 TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 glioblastoma multiforme NA M9440/3 qPCR, Western blot, in vitro knockdown etc. cell line (U87), GBM tissues down-regulated Low expression of TUSC7 in GBM cells and tissues resistant to TMZ.Upregulation of TUSC7 suppressed both TMZ resistance and expression of multidrug resistance protein 1 (MDR1) in U87TR cells.TUSC7 acted by directly targeting and silencing expression of miR-10a gene,and miR-10a mediated TUSC7-induced inhibition on TMZ resistance in U87TR cells. 29397407 2018 Long non-coding RNA TUSC7 inhibits temozolomide resistance by targeting miR-10a in glioblastoma. 53 TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 esophageal squamous cell cancer NA NA qPCR, Western blot, RIP, luciferase reporter assays ESCC cell lines (TE-13, KYSE140, EC9706, KYSE30, Het-1A), ESCC tissues down-regulated TUSC7 was downregulated in ESCC tissues and cells,and low TUSC7 indicated worse overall survival.TUSC7 specifically bound to miR-224, and we proved miR-224 was upregulated in ESCC and negatively correlated with TUSC7 expression.Overexpression of TUSC7/inhibition of miR-224 suppressed cell proliferation,colony formation and chemotherapy resistance of ESCC cells,and promoted cell apoptosis.TUSC7 suppressed the proliferation and chemotherapy resistance of ESCC cells by increasing DESC1 expression via inhibiting miR-224.TUSC7 suppressed chemotherapy resistance of ESCC by downregulating miR-224 to modulate DESC1/EGFR/AKT pathway. 29530057 2018 LncRNA-TUSC7/miR-224 affected chemotherapy resistance of esophageal squamous cell carcinoma by competitively regulating DESC1. 54 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 colorectal cancer C19.9 NA qPCR, Western blot, RIP, Luciferase reporter assay etc. primary CRC tissues, cell lines (HEK-293T, HCT8, HCT116, HT29, LoVo) up-regulated We found that UCA1 was up-regulated in CRCs and negatively correlated with survival time in two CRC cohorts. Functional assays revealed the in vitro and in vivo growth-promoting function of UCA1 and revealed that UCA1 can decrease the sensitivity of CRC cells to 5-FU by attenuating apoptosis. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression. 27046651 2016 LncRNA—UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p 55 ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 epithelial ovarian cancer C56.9 NA qPCR, Cell transfection, Western blot, Luciferase reporter assay, MTT assay etc. EOC tissues, cell lines (OVCAR3, Caov3, OVCA429, SKOV3, A2780, and COV644) up-regulated ZFAS1 was upregulated in epithelial ovarian cancer tissues, and was negatively correlated to the overall survival rate of patients.While depletion of ZFAS1 inhibited proliferation, migration, and development of chemoresistance, overexpression of ZFAS1 exhibited an even higher proliferation rate, migration activity, and chemoresistance in EOC cell lines. We further found miR-150-5p was a potential target of ZFAS1, which was downregulated in epithelial ovarian cancer tissue.MiR-150-5p subsequently inhibited expression of transcription factor Sp1,as evidence by luciferase assays. Inhibition of miR-150-5p rescued the suppressed proliferation and migration induced by depletion of ZFAS1 in epithelial ovarian cancer cells,at least in part. 28099946 2017 Long non-coding RNA ZFAS1 interacts with miR-150-5p to regulate Sp1 expression and ovarian cancer cell malignancy. 56 AC026166.2-001 MTCO1P5 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. 57 ADAMTS9-AS2 ADAMTS9-AS2 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. 58 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 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. 59 ATB LOC109207222 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. 60 ATB LOC109207222 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 61 ATB LOC109207222 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-β2. 27267902 2016 Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a. 62 ATB LOC109207222 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?217 and then inducing EMT. 29657927 2018 Gene Expression Analysis of Two Epithelial-mesenchymal Transition-related Genes: Long Noncoding RNA-ATB and SETD8 in Gastric Cancer Tissues. 63 lncRNA-ATB LOC109207222 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-β is an Independent Prognostic Marker of Gastric Cancer. 64 BANCR BANCR, LINC00586 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-κB signaling by directly inhibiting NCF2 expression, while miR-532-5p silencing in GC enhanced NF-κB 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-κB pathway activation.Interestingly, NCF2 could in turn increase the promoter activity and expression of LINC01410 via NF-κB, 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. 65 BC032469 CTD-3080P12.3 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. 66 CASC15 CASC15, LINC00340, lnc-SOX4-1 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. 67 CASC2 CASC2, C10orf5 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. 68 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 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. 69 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 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. 70 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 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. 71 CCAT2 CCAT2, LINC00873, NCCP1 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. 72 CCAT2 CCAT2, LINC00873, NCCP1 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. 73 CCAT2 CCAT2, LINC00873, NCCP1 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. 74 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 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. 75 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 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 β-catenin, c-myc and cyclinD1. 28469804 2017 Long noncoding RNA CRNDE activates Wnt/β-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer 76 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 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. 77 DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 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. 78 DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 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. 79 DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 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. 80 DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 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 81 DGCR5 DGCR5, LINC00037, NCRNA00037 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. 82 Dleu2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 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. 83 EWSAT1 EWSAT1, LINC00277, NCRNA00277, TMEM84 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. 84 FABP5P3 NA 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. 85 FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 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. 86 FEZF1-AS1 NA 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. 87 FEZF1-AS1 NA 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. 88 FLVCR1-AS1 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. 89 FTH1P3 FTH1P3, FTHL3, FTHL3P 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. 90 FTX FTX, LINC00182, MIR374AHG, NCRNA00182 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/β-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 91 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 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. 92 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 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. 93 GIHCG 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. 94 GUARDIN 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. 95 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 96 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 97 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 98 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 99 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 100 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 101 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 102 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 103 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 104 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 105 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 106 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 107 HAGLROS NA 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. 108 HCAL 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. 109 HCP5 NA 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. 110 HEIH HEIH, HCCAT2, LINC-HEIH, LINC00848, lncRNA-HEIH 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. 111 HERG LOC644794 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 112 HIF1A-AS2 HIF1A-AS2, 3'aHIF-1A, aHIF 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. 113 HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 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. 114 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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 115 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 116 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 117 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 118 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 119 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 120 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 121 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 122 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 123 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 124 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 125 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 126 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 127 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 128 HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 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 129 HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 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. 130 HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 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. 131 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 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. 132 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 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. 133 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 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. 134 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 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 135 HOXD-AS1 HAGLR, HOXD-AS1, Mdgt ENSG00000224189 NA 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 136 HOXD-AS1 HAGLR, HOXD-AS1, Mdgt ENSG00000224189 NA 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. 137 HOXD-AS1 HAGLR, HOXD-AS1, Mdgt ENSG00000224189 NA 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. 138 HOXD-AS1 HAGLR, HOXD-AS1, Mdgt ENSG00000224189 NA 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. 139 HULC HULC, HCCAT1, LINC00078, NCRNA00078 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. 140 HULC HULC, HCCAT1, LINC00078, NCRNA00078 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. 141 HULC HULC, HCCAT1, LINC00078, NCRNA00078 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. 142 HULC HULC, HCCAT1, LINC00078, NCRNA00078 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. 143 ILF3-AS1 XLOC_013222 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 144 KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 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. 145 KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 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 3β (GSK3β)/β?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. 146 lncRNA-LET NPTN-IT1, lncRNA-LET 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 TGFβ1 expression level did not show significant difference in clinical outcome. 28839463 2017 TGFβ1 Promotes Gemcitabine Resistance through Regulating the LncRNA-LET/NF90/miR-145 Signaling Axis in Bladder Cancer 147 LeXis 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. 148 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA 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. 149 Linc00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA 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. 150 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA 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. 151 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA 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. 152 LINC00174 NA 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. 153 Linc00176 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. 154 LINC00319 NA 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. 155 LINC00319 NA 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. 156 LINC00339 LINC00339 ENSG00000218510 NA 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. 157 LINC00460 NA 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. 158 LINC00473 LINC00473, C6orf176, bA142J11.1 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, IKKα 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 IKKα. 159 linc00511 LINC00511, LCAL5, onco-lncRNA-12 ENSG00000227036 NA 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. 160 LINC00657 NORAD, LINC00657 NA NA 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 161 LINC00668 NA 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. 162 linc00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 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. 163 Linc00675 NORAD, LINC00657 ENSG00000260032 NA 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/β-catenin signaling. 164 LINC01088 NA 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. 165 LINC01234 NA 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 β (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. 166 LINC01296 DUXAP9, LINC01296, FLJ39632, lncRNA-CTD903 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. 167 LINC01296 DUXAP9, LINC01296, FLJ39632, lncRNA-CTD903 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. 168 LOC100129148 LOC100129148 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. 169 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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). 170 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 171 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 172 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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 β 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. 173 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 174 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 175 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 176 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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 β4 (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. 177 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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 178 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 179 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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 180 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 181 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 182 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 183 MAP3K20 MLK7, MLTK, MLTKalpha, MLTKbeta, MRK, ZAK 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. 184 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 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. 185 MINCR MINCR, LINC01604 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. 186 MIR100HG MIR100HG, AGD1, linc-NeD125, lncRNA-N2 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-β also induces LIN28B inhibiting its maturation.Notably, we demonstrate that inactivation of miR-125b or miR-100 affects the TGF-β-mediated response indicating that these miRNAs are important TGF-β 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-β induces an lncRNA, whose encoded miRNAs, miR-100, let-7a and miR-125b play opposing roles in controlling PDAC tumourigenesis. 29748571 2018 TGF-β induces miR-100 and miR-125b but blocks let-7a through LIN28B controlling PDAC progression. 187 miR210HG NA 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. 188 MT1JP MT1JP, MT1, MT1J, MT1NP, MTB 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. 189 MT1JP MT1JP, MT1, MT1J, MT1NP, MTB 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. 190 n340790 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 191 NBAT1 NBAT1, CASC14, NBAT-1 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-21 192 NCK1-AS1 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. 193 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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 β-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. 194 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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 195 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 196 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 197 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 198 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 199 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 200 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 201 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, RNAi etc. cell lines (MCF-7, MDA-MB-231) down-regulated we demonstrated that downregulating the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in breast cancer cells inhibited cell growth and induced cell apoptosis. In addition, the RNA-binding protein fused in sarcoma/translocated in liposarcoma (FUS/TLS) physically interacted with NEAT1, and reducing the expression of FUS/TLS also induced cell apoptosis. Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis 27147820 2016 NEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548 202 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 203 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 204 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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/PPARα 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. 205 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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. 206 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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-IκB. 207 NNT-AS1 NA 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. 208 NNT-AS1 NA 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 209 NORAD NA 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. 210 NR_024015 TDRG1, LINC00532 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. 211 BLACAT1 BLACAT1, LINC00912, UBC1, onco-lncRNA-30 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-144 212 OIP5-AS1 OIP5-AS1, cyrano, linc-OIP5 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. 213 OIP5-AS1 OIP5-AS1, cyrano, linc-OIP5 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. 214 PART-1 NA ENSG00000152931 NA 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. 215 PCAT14 NA 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-372 216 PCAT7 NA 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. 217 PCAT7 NA 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. 218 PDIA3P 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. 219 PFKFB2 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. 220 PlncRNA-1 CBR3-AS1, PlncRNA-1, PlncRNA1 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/β-catenin pathway through the miR-204 in CRC cells.the PlncRNA-1/miR-204/ Wnt/β-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. 221 PTENP1 PTENP1, PTEN-rs, PTEN2, PTENpg1, PTH2, psiPTEN 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 222 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 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. 223 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 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. 224 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 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. 225 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 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. 226 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 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-195 227 ROR LINC-ROR, ROR, lincRNA-RoR 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 228 ROR LINC-ROR, ROR, lincRNA-RoR 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. 229 ROR LINC-ROR, ROR, lincRNA-RoR 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 230 ROR LINC-ROR, ROR, lincRNA-RoR 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. 231 ROR LINC-ROR, ROR, lincRNA-RoR 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. 232 ROR LINC-ROR, ROR, lincRNA-RoR 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. 233 RP11-396F22.1 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. 234 RP11-436H11.5 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 235 RP11-909B2.1 NA 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. 236 SMARCC2 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. 237 SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 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. 238 SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 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 239 SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 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. 240 SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 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. 241 SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 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. 242 SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 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. 243 SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 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. 244 SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 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. 245 SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 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-153 246 SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 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. 247 SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 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. 248 SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 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. 249 SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 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. 250 SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN 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. 251 SNHG20 SNHG20, C17orf86, LINC00338, NCRNA00338, SCARNA16HG 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. 252 SNHG3 SNHG3, NCRNA00014, RNU17C, RNU17D, U17HG, U17HG-A, U17HG-AB 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. 253 SNHG6 SNHG6, HBII-276HG, NCRNA00058, U87HG 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 254 SNHG7 SNHG7, NCRNA00061 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. 255 SNHG7 SNHG7, NCRNA00061 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/β-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/β-catenin signaling pathway. 29360452 2018 Long noncoding RNA SNHG7 promotes the progression and growth of glioblastoma via inhibition of miR-5095. 256 SNHG8 SNHG8, LINC00060, NCRNA00060 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-152 257 SOX21-AS1 NA 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. 258 SOX2OT SOX2-OT, NCRNA00043, SOX2OT 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-122 259 SPRY4-IT1 SPRY4-IT1, SPRIGHTLY 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. 260 TINCR TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16 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. 261 TINCR TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16 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. 262 TP73-AS1 TP73-AS1, KIAA0495, PDAM 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 263 TP73-AS1 TP73-AS1, KIAA0495, PDAM 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 264 TTN-AS1 NA 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. 265 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 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, α-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 266 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 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. 267 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 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. 268 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 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-382 269 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 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 270 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 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. 271 TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 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. 272 TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 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. 273 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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. 274 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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. 275 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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. 276 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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-495 277 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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. 278 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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. 279 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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 280 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 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. 281 UCC 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-143 282 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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, β-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/β-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/β-catenin signaling pathway. 283 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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. 284 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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 285 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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 286 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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-β1 was predicted as a target gene of miR-185. miR-185 can modulate TGF-β1 expression negatively in vitro.Moreover, we found that sh-XIST inhibited GC development via decreasing TGF-β1 by upregulating miR-185 in vitro.Therefore,we speculated that XIST can act as a competing endogenous lncRNA (ceRNA) to regulate TGF-β1 by sponging miR-185 in GC.Taken these together,it was indicated that XIST/miR-185/TGF-β1 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-β1 via targeting miR-185. 287 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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 288 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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. 289 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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. 290 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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. 291 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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. 292 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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. 293 ZEB2-AS1 ZEB2-AS1, ZEB2-AS, ZEB2AS, ZEB2NAT 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. 294 ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 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. 295 ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 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. 296 ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 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. 297 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 chronic myeloid leukemia NA M9863/3 qPCR, Cell transfection, Western blot, Luciferase reporter assay, Cell proliferation assay etc. blood, cell line (K562) down-regulated MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells.Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells. 28190319 2017 LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21. 298 SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT ENSG00000232956 NR_003697 GRCh38_7:44983023-44986961 renal cell carcinoma C64.9 NA qPCR, Western blot etc. cell lines (ACHN, OSRC2, 786O, 769P, CAKI1 and HK2) up-regulated In the present study, the expression levels of small nucleolar RNA host gene 15 (SNHG15) were significantly upregulated in renal cell carcinoma (RCC) tissues and cell lines compared with in adjacent tissues and a proximal tubule epithelial cell line, as determined by reverse transcription?quantitative polymerase chain reaction. Subsequently, knockdown of SNHG15 expression with small interfering RNA inhibited RCC proliferation, invasion and migration, was determined by western blotting and Transwell assays. Furthermore, the present study suggested that SNHG15 may be involved in the nuclear factor-κB signaling pathway, induce the epithelial?mesenchymal transition process, and promote RCC invasion and migration. SNHG16 exerts its effects by acting as a ceRNA, competitively binding miR-98 with E2F transcription factor 5 protein. 29750422 2018 Knockdown of SNHG15 suppresses renal cell carcinoma proliferation and EMT by regulating the NF-κB signaling pathway. 299 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 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 300 DLEU1 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 ENSG00000176124 NR_002605 GRCh38_13:50082171-50723236 chronic lymphocytic leukemia NA M9823/3 qPCR etc. blood differential expression Here, we propose a model of a multigenic pathomechanism in 13q14.3, where several tumor suppressor genes, including the miRNA genes miR-16-1 and miR-15a, are co-regulated by the two long non-coding RNA genes DLEU1 and DLEU2 that span the critical region. 19347735 2009 Chronic lymphocytic leukemia and 13q14: miRs and more. 301 DLEU2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 ENSG00000231607 NR_002612 GRCh38_13:49982552-50125720 chronic lymphocytic leukemia NA M9823/3 qPCR etc. blood differential expression Here, we propose a model of a multigenic pathomechanism in 13q14.3, where several tumor suppressor genes, including the miRNA genes miR-16-1 and miR-15a, are co-regulated by the two long non-coding RNA genes DLEU1 and DLEU2 that span the critical region. 19347735 2009 Chronic lymphocytic leukemia and 13q14: miRs and more. 302 DLEU2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 ENSG00000231607 NR_002612 GRCh38_13:49982552-50125720 chronic lymphocytic leukemia NA M9823/3 qPCR, Western blot, Northern blot, Luciferase reporter assay etc. blood, cell lines (HEK293, U2OS etc.) down-regulated The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way. 19591824 2009 DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1. 303 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, Luciferase reporter assay, Western blot pancreatic ductal adenocarcinoma tissues up-regulated the suppressed cell proliferation caused by H19 knockdown could be rescued by inhibiting miR-675 expression.As a transcript of the first exon of H19,the level of miR-675 was negatively correlated with H19 expression in microdissected PDAC tissues.And the decrease of E2F-1 protein expression caused by siH19 could be partially reversed by miR-675 knockdown.there might be a H19/miR-675/E2F-1 regulatory loop in cell cycle modulation. 29344285 2018 Long noncoding RNA H19 derived miR-675 regulates cell proliferation by down-regulating E2F-1 in human pancreatic ductal adenocarcinoma. 304 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR etc. blood up-regulated Plasma long non-coding HOTAIR as anon-invasive biomarker in GC.Plasma HOTAIR was significantly up-regulated in GC patients compared with controls.HOTAIR may also serve as a competitive endogenous RNA (ceRNA). In GC, it prevents transcriptional suppression of HER2 mRNA through competition for miR-331-3p. 29683069 2018 Plasma long non-coding RNA HOTAIR as a potential biomarker for gastric cancer. 305 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 laryngeal squamous cell cancer C32.3 NA qPCR, Western blot etc. blood (serum) up-regulated The expression of exosomal miR-21 and HOTAIR was significantly higher in patients with LSCC than those with vocal cord polyps. There were significant differences of serum exosomal miR-21 and HOTAIR expressions between the advanced T classifications (T3/T4) or clinical stages (III/IV) and the early stages. The patients with lymph node metastasis had higher serum exosomal miR-21 and HOTAIR expressions than those without. 25099764 2014 Combined detection of serum exosomal miR-21 and HOTAIR as diagnostic and prognostic biomarkers for laryngeal squamous cell carcinoma. 306 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, Luciferase reporter assay etc. Tumor tissues, blood, cell lines (MDA-MB-231 and BT549) up-regulated we found that HOTAIR was increased in the peripheral blood mononuclear cells and cancer tissues from breast cancer patients, and was especially higher in patients with metastatic breast cancer. In addition, we found that estrogen promoted HOTAIR through its receptor GPER and estrogen-induced breast cancer cell migration was reversed by deleting HOTAIR in TN breast cancer cells MDA-MB-231and BT549. Furthermore, we identified that E2-GPER induces the level of HOTAIR through the suppression of miR-148a. miR-148a level was negatively correlated with HOTAIR level in breast cancer patients. 25928008 2016 Estradiol induces HOTAIR levels via GPER-mediated miR-148a inhibition in breast cancer 307 LINC0086 SMIM10L2A, LED, LINC00086, LINC0086, NCRNA00086 NA 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. 308 MIR155HG MIR155HG, BIC, MIRHG2, NCRNA00172 ENSG00000234883 NR_001458 GRCh38_21:25561909-25575168 diffuse large B-cell lymphoma NA M9680/3 qPCR, Northern blot etc. Blood, cell lines (Ramos, JY25, CB33, U266, Jurkat, K562, HL60 etc.) up-regulated Relative to the control B cells, BIC RNA levels were elevated from 2- to 10-fold in DLBCL cells, with one sample showing an increase of >20-fold. 15738415 2005 Accumulation of miR-155 and BIC RNA in human B cell lymphomas. 309 PVT1-5 NA NA NA NA lung cancer C34 NA qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown lung cancer tissues, lung cancer cell lines (A549, H226, H1299 and H446) up-regulated PVT1-5 expression was significantly increased in lung cancer tissues and cell lines.miR-126 was associated with lncRNA-PVT1-5. Furthermore, knockdown of lncRNA-PVT1-5 in cells could down-regulate the expression of SLC7A5, the target of oncogenic miR-126, resulting in the cell proliferation. Conversely, inhibiting the expression of miR-126 markedly increased the expression of SLC7A5 and alleviated cell proliferation inhibition. 29277611 2017 Long non-coding RNA PVT1-5 promotes cell proliferation by regulating miR-126/SLC7A5 axis in lung cancer. 310 RMRP RMRP, CHH, NME1, RMRPR, RRP2 ENSG00000269900 NR_003051 GRCh38_9:35657751-35658018 gastric cancer C16 NA qPCR, RNAi, Flow cytometry assay etc. blood up-regulated RMRP levels in tissue, plasma and gastric juices from patients with gastric cancer were significantly different from those from controls. Its levels were significantly associated with Borrmann type and metastasis. Plasma and gastric juice RMRP had higher sensitivity and specificity than commonly used markers (such as carcinoembryonic antigen and carbohydrate antigen 19-9). Knockdown of RMRP significantly inhibited cell proliferation in vitro and in vivo, whereas overexpression of RMRP promoted cell growth. Acting as a miR-206 sponge, RMRP modulated cell cycle by regulating Cyclin D2 expression. 27192121 2016 LncRNA-RMRP promotes carcinogenesis by acting as a miR-206 sponge and is used as a novel biomarker for gastric cancer. 311 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 breast cancer C50 NA qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown breast cancer cell line (SKBR-3) up-regulated A luciferase reporter assay confirmed the association of miR-18a with wild-type UCA1 but not with UCA1 mutated at the predicted miR-18a-binding site. The direct targeting of YAP1 by miR-18a was verified by the observation that miR-18a mimic suppressed luciferase expression from a construct containing the YAP1 3' untranslated region. Meanwhile,reciprocal repression of UCA1 and miR-18a were found to be Argonaute 2-dependent. Knockdown of YAP1 recapitulated the effect of UCA1 silencing by reducing the viability of trastuzumab-treated breast cancer cells, whereas inhibition of miR-18a abrogated UCA1 knockdown-induced improvement of trastuzumab sensitivity in breast cancer cells. 29408336 2018 Long non-coding RNA UCA1 desensitizes breast cancer cells to trastuzumab by impeding miR-18a repression of Yes-associated protein 1. 312 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 glioma NA M9380/3 qPCR, Western blot etc. glioma tissues, cell lines (U-251, M059J) up-regulated MEG3 was then overexpressed by ligating to a lentiviral vector.Overexpressed MEG3 inhibited the proliferation of U-251 cells, and restrained the expression of proliferation marker proteins Ki67 and proliferating cell nuclear antigen (PCNA). However, cell apoptosis rate of U-251 cells and the expression of apoptosis marker proteins were elevated by MEG3. Furthermore, miR-93 was predicted a direct target of lncRNA-MEG3 by bioinformatics analysis. Overexpressed MEG3 counteracted the role of miR-93 in facilitating proliferation and inhibiting apoptosis in U-251 cells. Moreover, MEG3 restained the activation of phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT) pathway by reducing cytomembrane translocation of AKT. 28791407 2017 Long non-coding RNA MEG3 inhibits cell growth of gliomas by targeting miR-93 and inactivating PI3K/AKT pathway 313 LINC00894-002 NA NA NA NA breast cancer C50 NA qPCR, Western blot etc. cell lines (MCF-7/WT and MCF-7/TamR) down-regulated LINC00894-002 exhibits the most sophisticated network pattern and is the most downregulated lncRNA in MCF-7/TamR cells. Moreover,LINC00894-002 is directly upregulated by ERα.Knocking down LINC00894-002 downregulates expression of miR-200a-3p and miR-200b-3p, upregulates the expression of TGF-β2 and ZEB1,and finally contributes to TamR.Herein, we report the first case of an inhibitory lncRNA against TamR through the miR-200-TGF-β2-ZEB1 signaling pathway. 29738694 2018 Downregulation of LINC00894-002 Contributes to Tamoxifen Resistance by Enhancing the TGF-β Signaling Pathway. 314 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 medulloblastoma NA M9470/3 qPCR, Luciferase reporter assay, Western blot. cell lines (MB DAOY) up-regulated ANRIL was up-regulated in MB and its silence significantly lowered cell viability and migration but promoted cell apoptosis.ANRIL acted as a sponge of miR-323 and its silence functioned through up-regulating miR-323. BRI3 and CDK6 were target genes of miR-323 and the effect of BRI3 on DAOY cells was the same as ANRIL.ANRIL suppression could reduce phosphorylated levels of p38 MAPK, ERK and AKT, and inhibit Wnt signaling pathway through positively regulating BRI3. ANRIL inhibition repressed cell proliferation and migration but promoted cell apoptosis through miR-323-mediated regulation of BRI3, which could activate p38 MAPK, ERK, and AKT as well as Wnt signaling pathway. 28513871 2017 Potential Role of Long Non-Coding RNA ANRIL in Pediatric Medulloblastoma Through Promotion on Proliferation and Migration by Targeting miR-323. 315 CTA NA ENSG00000253603 NR_149110 GRCh38_8:56074592-56075274 osteosarcoma NA M9180/3 qPCR, Western blot, MIT, Luciferase reporter assays osteosarcoma tissues, cell lines (Saos-2, U-2OS and MG-63) down-regulated Our data showed that lncRNA CTA was markedly downregulated in OS tissues compared to their matched non-tumor tissues. In addition, OS patients with low lncRNA CTA levels showed a worse prognosis when compared with those with high expression of lncRNA CTA. LncRNA CTA could be activated by doxorubicin (DOX), and could promote OS cell apoptosis by competitively binding miR-210, while inhibit cell autophagy. 28415557 2017 Long non-coding RNA CTA sensitizes osteosarcoma cells to doxorubicin through inhibition of autophagy 316 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (MG63 and U2OS) up-regulated MALAT1 was increased in human OS tissues and cell lines.MALAT1 knockdown suppressed OS cell growth and metastasis,induced OS cell apoptosis and delayed tumor growth in an OS xenograft model.We also detected downregulation of microRNA-509 (miR-509), a suppressor of OS growth,in OS tissues and cell lines.Then,we identified that miR-509 is a direct target of MALAT1 and Ras-related C3 botulinum toxin substrate 1 (Rac1) is a direct target of miR-509.MALAT1 may promote OS cell growth through inhibition of miR-509, leading to the activation of Rac1/JNK pathway.Our results suggest a MALAT1/miR-509/Rac1 axis that mediates OS cell proliferation and tumor progression. 28560950 2018 MALAT1 Promotes the Proliferation and Metastasis of Osteosarcoma Cells By Activating the Rac1/JNK Pathway Via Targeting MiR-509. 317 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 prostate cancer C61.9 NA qPCR, Luciferase reporter assay, in vitro knockdown PC tissues, PC cell lines (LNCap, PC3, DU145 and C4-2) down-regulated CASC2 and SPRY2 expression was down-regulated in PC tissues and cell lines,the overexpression of CASC2 and SPRY2 could suppress PC cell proliferation, promote PC cell apoptosis, and enhance the sensitivity of PC cells to docetaxel. CASC2 positively regulated SPRY2 expression and inhibited downstream extracellular regulated protein kinases (ERK) signaling activation through SPRY2. miR-183 inhibition enhanced the cytotoxicity of docetaxel on PC cells, which could be partially attenuated by SPRY2 knockdown. 29373811 2018 Long non-coding RNA CASC2 regulates Sprouty2 via functioning as a competing endogenous RNA for miR-183 to modulate the sensitivity of prostate cancer cells to docetaxel. 318 ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, RIP etc. cell lines (SPC-A1 and H1299) up-regulated Long intergenic non-protein coding RNA, regulator of reprogramming (linc-ROR), was first discovered in induced pluripotent stem cells (iPSCs) and was upregulated in docetaxel-resistant LAD cells. The function of linc-ROR exerted in LAD cells depended on the sponging of miR-145, therefore, releasing the miR-145 target FSCN1, and thus contributing to the acquisition of chemoresistance and EMT phenotypes of docetaxel-resistant LAD cells. 28388536 2017 Long noncoding RNA ROR regulates chemoresistance in docetaxel-resistant lung adenocarcinoma cells via epithelial mesenchymal transition pathway 319 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 oral squamous cell carcinoma C06.9 M8070/3 qPCR, Luciferase reporter assay, Western blot oral squamous cell carcinoma tissues, cell lines (Tca8113, TSCCA, CAL-27, SCC-9, NHOK) up-regulated UCA1 expression was upregulated in OSCC tissues, cell lines, and CDDP resistant OSCC cells. UCA1 facilitated proliferation, enhanced CDDP chemoresistance, and suppressed apoptosis in OSCC cells.UCA1 could interact with miR-184 to repress its expression. downregulation of miR-184 partly reversed the tumor suppression effect and CDDP chemosensitivity of UCA1 knockdown in CDDP-resistant OSCC cells.UCA1 could perform as a miR-184 sponge to modulate SF1 expression.depletion of UCA1 further boosted CDDP-mediated repression effect on tumor growth. UCA1 accelerated proliferation, increased CDDP chemoresistance and restrained apoptosis partly through modulating SF1 via sponging miR-184 in OSCC cells. 29125238 2017 LncRNA UCA1 promotes proliferation and cisplatin resistance of oral squamous cell carcinoma by sunppressing miR-184 expression. 320 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, RNAi, Luciferase reporter assays etc. lung adenocarcinoma tissues, cell lines (A549, A549/DDP ) up-regulated LncRNA XIST expression was markedly increased in cisplatin-resistant A549/DDP cells compared with parental A549 cells as shown by qRT-PCR. LncRNA XIST overexpression in A549 cells increased their chemosensitivity to cisplatin both in vitro and in vivo by protecting cells from apoptosis and promoting cell proliferation. We revealed that XIST functioned as competing endogenous RNA to repress let-7i, which controlled its down-stream target BAG-1. We proposed that XIST was responsible for cisplatin resistance of LAD cells and XIST exerted its function through the let-7i/BAG-1 axis. 28961027 2017 LncRNA XIST promotes human lung adenocarcinoma cells to cisplatin resistance via let-7i/BAG-1 axis 321 TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 endometrial cancer NA M8380/3 qPCR endometrial carcinoma tissues down-regulated In this study, the low expression of TUSC7 was confirmed in endometrial carcinoma tissues and was associated with high pathological stages of endometrial carcinoma, which revealed that TUSC7 might be involved in tumorigenesis and progression of endometrial carcinoma. Moreover, the expression of TUSC7 in endometrial carcinoma tissues and cell lines resistant to CDDP and Taxol was lower than that in sensitive endometrial carcinoma tissues and cell lines, which indicated that the TUSC7 expression level was positively correlated with the response of endometrial carcinoma patients to chemotherapy with CDDP and Taxol. MiR-23b upregulation mostly reversed the TUSC7-induced regulatory effects on HEC1A/CR cell line. 28653877 2017 Long non-coding RNA tumor suppressor candidate 7 advances chemotherapy sensitivity of endometrial carcinoma through targeted silencing of miR-23b 322 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 acute myeloid leukemia NA M9861/3 qPCR, Western blot, Luciferase reporter assay, RIP etc. acute myeloid leukemia tissues, cell lines (HL60 and HS-5) up-regulated UCA1 expression was upregulated following ADR-based chemotherapy.Knockdown of UCA1 increased the cytotoxic effect of ADR and inhibited HIF-1α-dependent glycolysis in ADR-resistant AML cells.Additionally, UCA1 functioned as a ceRNA of miR-125a by directly binding to miR-125a. HK2,a target of miR-125a,was positively regulated by UCA1 in HL60 and HL60/ADR cells.More notably, UCA1 overexpression overturned miR-125-mediated inhibition on HIF-1α-dependent glycolysis in HL60 and HL60/ADR cells.Furthermore, 2-deoxy-glucose (2-DG) exposure inhibited HIF-1α-dependent glycolysis,and attenuated UCA1-induced increase of chemoresistance in HL60 and HL60/ADR cells. 29663500 2018 Knockdown of LncRNA-UCA1 suppresses chemoresistance of pediatric AML by inhibiting glycolysis through the microRNA-125a/hexokinase 2 pathway. 323 AC023115.3 NA ENSG00000236605 NA GRCh38_2:67324627-67325304 glioblastoma NA M9440/3 qPCR, westen blot, microarray etc. cell lines (U87MG and U251MG) down-regulated AC023115.3 was preferentially enriched in the Ago2-containing microRNA ribonucleoprotein complexes (miRNPs) compared with the immunoprecipitates with control IgG,indicating that AC023115.3 is present in the Ago2-containing miRNPs likely through an association with microRNAs. AC023115.3 was induced by cisplatin and suppressed glioma chemoresistance.AC023115.3 inhibited cisplatin-induced autophagy. AC023115.3 promoted cisplatin-induced apoptosis via decreasing autophagy. AC023115.3 acted as a miR-26a sponge and inhibited its activity.AC023115.3 sensitized glioma cell to cisplatin-induced apoptosis through regulation of the miR-26a-GSK3β-Mcl1 signalling. 28499919 2017 Long non-coding RNA AC023115.3 suppresses chemoresistance of glioblastoma by reducing autophagy 324 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 nasopharyngeal cancer C11 NA qPCR, RNAi, Luciferase reporter assay, MTT assay etc. NPC tissues, cell lines (CNE1, CNE2, S18, HONE1, and 5-8F) up-regulated ANRIL was highly expressed and let-7a was downregulated in NPC tissues and cells. Luciferase assay revealed that ANRIL could negatively regulate miR-let-7a expression. ANRIL knockdown inhibited NPC cell proliferation and induced apoptosis, while anti-let-7a reversed these effects. Combination treatment of si-ANRIL and DDP led to a lower viability, a more DNA strand breaks damage and a higher comet tail length compared with any single treatment, whereas let-7a inhibitor abolished these effects. Furthermore, depletion of ANRIL exacerbated DDP-induced cytotoxicity in NPC cells in vivo. 28117929 2017 Downregulation of lncRNA ANRIL represses tumorigenicity and enhances cisplatin-induced cytotoxicity via regulating microRNA let-7a in nasopharyngeal carcinoma. 325 lncRNA-ATB LOC109207222 NA NA NA breast cancer C50 NA microarray, qPCR, Western blot, Luciferase reporter assay, MTT assay etc. cell line (SKBR-3) up-regulated We identified long noncoding RNA activated by TGF-β (lnc-ATB) was the most remarkably upregulated lncRNA in TR SKBR-3 cells and the tissues of TR breast cancer patients. We found that lnc-ATB could promote trastuzumab resistance and invasion-metastasis cascade in breast cancer by competitively biding miR-200c, up-regulating ZEB1 and ZNF-217, and then inducing EMT. In addition, we also found that the high level of lnc-ATB was correlated with trastuzumab resistance of breast cancer patients. 25871474 2015 LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer. 326 BLACAT1 BLACAT1, LINC00912, UBC1, onco-lncRNA-30 ENSG00000281406 NR_103783 GRCh38_1:205434886-205437879 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (BGC-823, SGC-7901, MGC-803,GES-1),gastric cancer tissue up-regulated In vitro, BLACAT1 knockdown decreased the expression levels of drug resistance related genes and ABCB1 protein. BLACAT1 knockdown significantly promoted apoptosis and down-regulated the invasion and the IC50 value of oxaliplatin.In vivo, BLACAT1 knockdown suppressed the tumor growth of gastric cancer cells. Bioinformatics tools and luciferase assay indicated that miR-361 both targeted 3'-UTR of BLACAT1 and ABCB1mRNA, suggesting the BLACAT1/miR-361/ABCB1 regulatory pathway. 29710482 2018 Long noncoding RNA BLACAT1 modulates ABCB1 to promote oxaliplatin resistance of gastric cancer via sponging miR-361. 327 CASC2 CASC2, C10orf5 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. 328 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 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/β-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/β-catenin signaling. 329 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 ENSG00000245694 NA GRCh38_16:54845189-54929189 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell migration and invasion assay etc. CRC tissues, cell lines (SW480, HCT116 and HT-29) up-regulated We confirmed the upregulation of CRNDE in both primary specimens from colorectal cancer patients and colorectal cancer cell lines. Overexpression of CRNDE promoted the migration and invasion potency of colorectal cancer cells. Knockdown of CRNDE with OXA treatment decreased cell viability and promoted DNA damage and cell apoptosis. Further in-depth mechanistic studies revealed that CRNDE functioned as a competing endogenous RNA for miR-136, led to the de-repression of its endogenous target, E2F transcription factor 1 (E2F1). 28115855 2017 Long noncoding RNA CRNDE functions as a competing endogenous RNA to promote metastasis and oxaliplatin resistance by sponging miR-136 in colorectal cancer. 330 DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 malignant glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assays, in vitro knockdown etc. cell lines (U87MG, U251MG, LN18,U138MG) up-regulated Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. DNACR also attenuated cisplatin-induced cell apoptosis in vitro and in vivo. DANCR upregulated AXL via competitively binding miR-33a-5p, miR-33b-5p, miR-1-3p, miR-206, and miR-613. Through upregulating AXL, DANCR activated PI3K/Akt/NF-κB signaling pathway in glioma cells. Inhibiting AXL/PI3K/Akt/NF-κB signaling pathway reversed the effects of DANCR on cisplatin resistance.DANCR promotes cisplatin resistance via activating AXL/PI3K/Akt/NF-κB signaling pathway in glioma.DANCR would be a potential biomarker for predicting cisplatin sensitivity and a therapeutic target for enhancing cisplatin efficacy in glioma. 29572052 2018 Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. 331 DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR ENSG00000226950 NR_024031 GRCh38_4:52712404-52720351 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RNAi, RIP etc. cell line (A549, H1299,H358,HBE), lung ADC tissue up-regulated Differentiation antagonizing non-protein coding RNA (DANCR) was up-regulated in lung adenocarcinoma (ADC) and that the knockdown of DANCR inhibited tumour cell proliferation, migration and invasion and restored cell apoptosis rescued; cotransfection with a miR-496 inhibitor reversed these effects. 29266795 2017 LncRNA-DANCR contributes to lung adenocarcinoma progression by sponging miR-496 to modulate mTOR expression. 332 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 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 333 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colon cancer C18 NA qPCR, Cell transfection, Western blot, ChIP, Luciferase reporter assay, MTT assay etc. colon cancer tissues, cell lines (HT-29 and DLD-1) up-regulated VDR signaling was able to inhibit the expression of H19 through regulating C-Myc/Mad-1 network.H19, on the other hand, was able to inhibit the expression of VDR through micro RNA 675-5p (miR-675-5p). Furthermore, H19 overexpression induced resistance to the treatment with 1,25(OH)2D3 both in vitro and in vivo. 28189050 2017 H19 Overexpression Induces Resistance to 1,25(OH)2D3 by Targeting VDR Through miR-675-5p in Colon Cancer Cells. 334 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc. LAD tissues, cell line (A549/CDDP) up-regulated Our results showed that HOTAIR was significantly upregulated in A549/CDDP cells compared with parental A549 cells. The results showed that si-HOTAIR increased miR-326 expression (Fig. 6b) and synergistically reduced SP1 expression (Fig. 6c), ultimately enhanced sensitivity to cisplatin in A549/CDDP cells. In contrast to si-HOTAIR, pcDNA/HOTAIR vector inhibited miR-326 expression and synergistically enhanced SP1 expression in A549 cells 27460077 2016 miR-326 reverses chemoresistance in human lung adenocarcinoma cells by targeting specificity protein 1. 335 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay etc. gastric cancer tissues, cell lines (SGC-7901 and BGC-823) up-regulated HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway. 27900563 2016 LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes. 336 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA GRCh38_2:87454781-87636740 colon cancer C18 NA qPCR, Western blot, Luciferase reporter assay, Cell proliferation assay etc. colon cancer tissues, cell lines (SW480, Caco2, SW620 and HT29) up-regulated Elevated expression of Linc00152 was observed by using qRT-PCR in colon cancer tissues when compared with adjacent normal mucosa. Linc00152 as a candidate prognostic indicator of outcome and drug responsiveness in colon cancer patients, and the involvement of competing endogenous RNAs mechanism in Linc00152/miR-193a-3p/ERBB4/AKT signaling axis may provide a novel choice in the investigation of drug resistance. 27633443 2016 Linc00152 Functions as a Competing Endogenous RNA to Confer Oxaliplatin Resistance and Holds Prognostic Values in Colon Cancer. 337 LINC00161 LINC00161, C21orf100, NCRNA00161 ENSG00000226935 NR_026552 GRCh38_21:28539318-28540355 osteosarcoma NA M9180/3 microarray, qPCR, RNAi, RIP, Dual-luciferase reporter assay etc. cell lines (MG-63 and U2OS) up-regulated Here, we found that lncRNA LINC00161 was induced by cisplatin in osteosarcoma cells. Elevated LINC00161 increased cisplatin-induced apoptosis and reversed the cisplatin-resistant phenotype of osteosarcoma cells by upregulating IFIT2. Further mechanistic studies revealed that LINC00161 could sponge endogenous miR-645 and inhibit its activity leading to IFIT2 increase. In addition, we identified that LINC00161 enhanced cisplatin-induced apoptosis through regulation of the miR-645-IFIT2 pathway. 27609068 2016 Long non-coding RNA LINC00161 sensitises osteosarcoma cells to cisplatin-induced apoptosis by regulating the miR-645-IFIT2 axis. 338 lncARSR NA NA NA NA renal cell carcinoma C64.9 NA qPCR, RNAi, Western blot, Northern blot, ChIP, Luciferase reporter assay, ISH etc. RCC tissues, cell lines (786-O and ACHN) up-regulated Compared with matched pre-therapy tumors, lncARSR was abundant in sunitinib-resistant RCC. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response. 27117758 2016 Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA. 339 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioblastoma multiforme NA M9440/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. GBM tissues, serum, cell lines (U87 and U251) down-regulated Four lncRNAs (MALAT1, LOC100506474, MEG3 and PRNCR1) were found significantly dysregulated in responding tissues compared with non-responding tissues. Only MALAT1 was significantly desregulated in serum. LncRNA MALAT1 inhibition re-sensitized TMZ resistant cells through up-regulating miR-203 and down-regulating TS expression. On the other hand, MALAT1 overexpression promoted resistance by suppressing miR-203 and promoting TS expression. 28187000 2017 MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression. 340 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 nasopharyngeal cancer C11 NA qPCR, Western blot, RIP, Luciferase reporter assay etc. NPC cell lines (5-8F, CNE-2, HONE-1, SUNE-1), NPE cell line (NP-69) up-regulated We found that MALAT1 regulated radioresistance by modulating cancer stem cell (CSC) activity. Furthermore, we found that there was reciprocal repression between MALAT1 and miR-1, and slug was identified as a downstream target of miR-1. Taking these observations into consideration, we proposed that MALAT1 regulated CSC activity and radioresistance by modulating miR-1/slug axis, which indicated that MALAT1 could act as a therapeutic target for NPC patients 26482776 2015 The role of MALAT1/miR-1/slug axis on radioresistance in nasopharyngeal carcinoma. 341 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc. cell lines (BEL-7402, BEL-7402/5-FU) up-regulated The results showed that MALAT1 was over two times higher in BEL-7402/5-FU cells than in BEL-7402 cells. It was HIF-2α, but not HIF-1α induced MALAT1 upregulation in HCC cells. Dual luciferase assay demonstrated that there were at least two binding sites of miR-26b in MALAT1. Therefore, we infer that there is a HIF-2α-MALAT1-miR-216b axis in HCC cells. Cell viability assay showed that both MALAT1 siRNA and miR-216b mimics reduced IC50 of 5-FU, ADR and MMC in BEL-7402/5-FU cells. MALAT1 siRNA and miR-216b mimics showed similar effect as 3-MA on reducing LC3-II levels, inhibiting p62 degradation and suppressing GFP-LC3 puncta formation in BEL-7402/5-FU cells. 27524242 2016 The HIF-2α-MALAT1-miR-216b axis regulates multi-drug resistance of hepatocellular carcinoma cells via modulating autophagy. 342 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 ovarian cancer C56.9 NA qPCR, Western blot, Luciferase reporter assay, Flow cytometry assay, CCK-8 assay etc. cell lines (EVs, A2780, A2780cp, OVCAR-3 and SKOV3) up-regulated Curcumin weakened the EVs-N's capability to induce drug resistance and induced significant changes of lncRNAs in the EVs. MEG3 is one of the most upregulated lncRNAs. Curcumin led to demethylation in the promoter region of MEG3 and 5-AZA-dC treatment restored MEG3 expression in a dose dependent manner. MEG3 restoration by curcumin significantly reduced miR-214 in cells and in EVs. Functionally, miR-214 inhibition weakened the EVs-N's capability to enhance chemoresistance, while miR-214 overexpression increased the capability of EVs-CU in inducing chemoresistance. 28175963 2017 Curcumin suppresses cisplatin resistance development partly via modulating extracellular vesicle-mediated transfer of MEG3 and miR-214 in ovarian cancer. 343 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 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 344 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Dual-luciferase reporter assay etc. cell lines (A549, H460, H1299) up-regulated In this study, we found that EGCG upregulated CTR1 and increased platinum accumulation in NSCLC (A549, H460 and H1299) cells, cDDP-resistant A549 cells and a nude mouse xenograft model. Cisplatin-induced inhibition of cell growth was enhanced by EGCG treatment in vitro and in vivo. MicroRNA hsa-mir-98-5p appears to suppress CTR1 gene expression, while long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) appears to enhance it. 27270317 2016 NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells. 345 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 nasopharyngeal cancer C11 NA qPCR, Western blot etc. nasopharyngeal carcinoma tissues, cell lines (HK-1, CNE-1, CNE-2 subclone S18 and SUNE1) down-regulated NEAT1 was upregulated and let-7a-5p was downregulated in NPC tissues,as well as NPC cell lines.Inhibition of NEAT1 markedly repressed the cisplatin resistance of NPC cells. NEAT1 was demonstrated to interact with let-7a-5p. Besides, a negative correlation between NEAT1 and let-7a-5p expression was observed in NPC tissues.Rsf-1 was confirmed as a target of let-7a-5p.NEAT1 remarkably reversed the inhibitory effect of let-7q-5p on the cisplatin resistance of NPC cells in vitro. Additionally, NEAT1 knockdown inhibited the Ras-MAPK pathway in NPC cells.NEAT1 knockdown suppressed tumor growth in the presence of cisplatin in vivo.Overall,these findings suggest that NEAT1/let-7a-5p axis regulates the cisplatin resistance in NPC by targeting Rsf-1 and modulating the Ras-MAPK signaling pathway. 29565706 2018 LncRNA NEAT1/let-7a-5p axis regulates the cisplatin resistance in nasopharyngeal carcinoma by targeting Rsf-1 and modulating the Ras-MAPK pathway. 346 lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 NA NA NA glioma NA M9380/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. glioma tissues down-regulated we found that lincRNA-p21 negatively regulated the expression and activity of β-catenin in GSCs. Downregulation of lincRNA-p21 in GSCs was resulted from upregulation of Hu antigen R (HuR) expression caused by miR-146b-5p downregulation. MiR-146b-5p overexpression increased apoptosis and radiosensitivity, decreased cell viability, neurosphere formation capacity and stem cell marker expression, and induced differentiation in GSCs. Moreover, knock-down lincRNA-p21 or HuR and β-catenin overexpression could rescue the phenotypic changes resulted from miR-146b-5p overexpression in GSCs 27166258 2016 MiR-146b-5p overexpression attenuates stemness and radioresistance of glioma stem cells by targeting HuR/lincRNA-p21/β-catenin pathway 347 PRINS PRINS, NCRNA00074 NA NA NA colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay, FISH etc. cell line (HT-29) differential expression RNA interference-based gain- and loss-of-function experiments examined miR-491-PRINS axis to exert the TFF3-mediated phenotype. Chemical inhibition of selected pathways showed that phosphatidylinositol 3-kinase/AKT accounts for TFF3-mediated downregulation of miR-491-5p and accumulation of PRINS. Moreover, we showed that PRINS colocalises with PMAIP1 (NOXA) in nuclei of HT-29/B6 possessing inhibitory effects. 28149533 2017 TFF3-dependent resistance of human colorectal adenocarcinoma cells HT-29/B6 to apoptosis is mediated by miR-491-5p regulation of lncRNA PRINS. 348 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 cervical cancer C53 NA qPCR, RNAi, Western blot, RIP, ChIP, Dual-luciferase reporter assay, RNA pull-down assay, Cell proliferation assay etc. cell lines (HPV-16- positive CaSki and SiHa) up-regulated PVT1 directly interacts with EZH2 and the complex anchors in the promoter region of miR-195. PVT1 overexpression resulted in increased H3K27me3 levels in the miR-195 promoter region, while PVT1 knockdown decreased H3K27me3 levels in the promoter region. In addition, PVT1 could competitively bind with miR-195. MiR-195 overexpression suppressed PVT1 expression in the cancer cells. Both PVT1 and miR-195 could inhibit paclitaxel (PTX) induced epithelial-to-mesenchymal transition (EMT) and also sensitize CaSki cells to PTX. 28296507 2017 LncRNA PVT1 epigenetically silences miR-195 and modulates EMT and chemoresistance in cervical cancer cells. 349 linc-ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. CRC tissues, cell lines (SW480, SW1116, LS174T, HCT116 and LoVo) up-regulated lincRNA-ROR was upregulated in CRC cell lines and tissue samples. We further showed that knockdown of lincRNA-ROR enhanced the sensitivity to radiotherapy for CRC by inhibiting cell viability and promoting apoptosis. Activity of the p53/miR-145 pathway may help explain the role of lincRNA-ROR for stress-induced regulation in CRC therapy.Combined specific knockdown of lincRNA-ROR and radiotherapy treatment in xenograft model resulted in a significant reduction in the tumor growth. 27696511 2017 The long noncoding RNA-ROR promotes the resistance of radiotherapy for human colorectal cancer cells by targeting the p53/miR-145 pathway. 350 SNHG6 SNHG6, HBII-276HG, NCRNA00058, U87HG 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-β-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. 351 TP53TG NA NA NA NA non small cell lung cancer C34 M8046/3 qPCR, Western blot, luciferase reporter assay, RIP, in vitro knockdown etc. cell line (HBE, A549), NSCLC tissue down-regulated TP53TG1 level was downregulated in NSCLC tissues and cell lines.Upregulated TP53TG1 enhanced cisplatin sensitivity and apoptosis of A549/DDP cells,while TP53TG1 depletion inhibited cisplatin sensitivity and apoptosis of A549 cells.TP53TG1 suppressed miR-18a expression in A549 cells.Moreover,TP53TG1-mediated enhancement effect on cisplatin sensitivity was abated following the restoration of miR-18a expression in A549/DDP cells, while si-TP53TG1-induced decrease of cisplatin sensitivity and apoptosis was counteracted by miR-18a inhibitor in A549 cells. Furthermore, TP53TG1 promoted PTEN expression via inhibiting miR-18a.Finally,TP53TG1 sensitized NSCLC cells to cisplatin in vivo. 29588850 2018 TP53TG1 enhances cisplatin sensitivity of non-small cell lung cancer cells through regulating miR-18a/PTEN axis. 352 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 bladder cancer C67 NA qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. bladder cancer tissues up-regulated We confirmed that TUG1 was overexpressed in bladder cancer tissues and established cell lines. Knockdown of TUG1 inhibited bladder cancer cell metastasis both in vitro and in vivo. Furthermore, we found that TUG1 promoted cancer cell invasion and radioresistance through inducing epithelial-to-mesenchymal transition (EMT). Interestingly, TUG1 decreased the expression of miR-145 and there was a reciprocal repression between TUG1 and miR-145 in an Argonaute2-dependent manner. ZEB2 was identified as a down-stream target of miR-145 and TUG1 exerted its function through the miR-145/ZEB2 axis. 26318860 2015 Double-negative feedback loop between long non-coding RNA TUG1 and miR-145 promotes epithelial to mesenchymal transition and radioresistance in human bladder cancer cells. 353 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 chronic myeloid leukemia NA M9863/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. cell line (K562) up-regulated UCA1 was significantly upregulated in K562/IM and K562/IM-R cells compared with K562 cells, and UCA1 in K562/IM cells was higher than that in K562/IM-R cells. Overexpression of UCA1 increased MDR1 expression to promote IM resistance of CML cells. Furthermore, for the first time, we demonstrated that UCA1 functions as a competitive endogenous (ceRNA) of MDR1 through completely binding the common miR-16. 27854515 2017 lnclncRNA UCA1 Contributes to Imatinib Resistance by Acting as a ceRNA Against miR-16 in Chronic Myeloid Leukemia Cells.RNA UCA1 Contributes to Imatinib Resistance by Acting as a ceRNA Against miR-16 in Chronic Myeloid Leukemia Cells. 354 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 acute myeloid leukemia NA M9861/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell line (K562, HL60, MG63, hhFOB1.19HEK293) up-regulated lncRNA UCA1 was upregulated in ML cell lines.Knockdown of lncRNA UCA1 inhibited cell viability, migration, invasion,and prompted apoptosis of ML cells in vitro. LncRNA UCA1 could bind with miR-126 and downregulate miR-126 expression. Simultaneously, the anti-growth and anti-metastasis actions of lncRNA UCA1 knockdown on ML cells were reversed by miR-126 suppression. RAC1 was a target gene of miR-126,and the anti-ML actions of miR-126 were abolished by RAC1 overexpression.Moreover, PI3K/AKT and JAK/STAT signaling pathways were blocked by miR-126 overexpression while were activated by RAC1 overexpression. 29762824 2018 Long noncoding RNA UCA1 promotes cell proliferation, migration and invasion of human leukemia cells via sponging miR-126 355 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 lung cancer C34 NA luciferase reporter assay, qPCR, western blot etc. cell lines (WI-38, HEL-1) up-regulated This result indicated that the up-regulated expression of lncRNA UCA1 was involved in the canceration of normal lung cells. These findings will be helpful for understanding the critical roles of lncRNA UCA1 and miRNA-144 in lung cancer cells, and provide new therapeutic strategy for lung cancer therapy.The experimental study from Cheng et al. demonstrated that lncRNA UCA1 promoted non-T790M cells acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) by activating the AKT/mammalian target of rapamycin (mTOR) pathway in EGFR-mutant NSCLC. 28762326 2017 Long Noncoding RNA Urothelial Carcinoma Associated 1 Promotes the Proliferation and Metastasis of Human Lung Tumor Cells by Regulating MicroRNA-144 356 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 breast cancer C50 NA qPCR, Western blot, Dual-luciferase reporter assay, Flow cytometry assay etc. cell lines (MCF-7, BT474, LCC2, and LCC9) up-regulated Our findings reveal that tamoxifen induces UCA1 upregulation in ER-positive breast cancer cells in a HIF1α-dependent manner. UCA1 upregulation results in significantly enhanced tamoxifen resistance. The upregulated UCA1 sponges miR-18a, which is a negative regulator of HIF1α. Therefore, UCA1 upregulation is further enhanced through a miR-18a-HIF1α feedback loop. 27629141 2016 Long non-coding RNA UCA1 enhances tamoxifen resistance in breast cancer cells through a miR-18a-HIF1α feedback regulatory loop. 357 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 gastric cancer C16 NA qPCR, Western blot, Flow cytometry assay etc. gastric cancer tissues, cell line (SGC-7901) up-regulated UCA1 was significantly upregulated in the cancerous tissues and its expression was negatively correlated with miR-27b expression level. Inhibition of UCA1 significantly restored miR-27b expression in MDR gastric cancer cells. UCA1 knockdown and miR-27b overexpression reduced IC50 of ADR, DDP, and 5-FU in SGC-7901/ADR cells and increased ADR induced cell apoptosis. 27694794 2016 Long Non-Coding RNA (LncRNA) Urothelial Carcinoma Associated 1 (UCA1) Increases Multi-Drug Resistance of Gastric Cancer via Downregulating miR-27b. 358 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 bladder cancer C67 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. bladder cancer tissues, cell lines (5637 and UMUC-2) differential expression In the present study, knockdown of UCA1 decreased chemosensitivity to cisplatin/gemcitabine by suppressing cell proliferation and inducing apoptosis, while overexpression of UCA1 increased chemosensitivity in bladder cancer cells. Moreover, UCA1 activated transcription factor CREB which led to miR-196a-5p expression by binding with its promoter. miR-196a-5p induction is involved in UCA1 inhibition of apoptosis induced by cisplatin/gemcitabine via targeting p27Kip1. 27591936 2016 Long non-coding RNA UCA1 promotes cisplatin/gemcitabine resistance through CREB modulating miR-196a-5p in bladder cancer cells. 359 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 bladder cancer C67 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (5637, T24) up-regulated lncRNA XIST possesses the reverse function in bladder cancer cells.miR-200c overexpression and XIST knockdown could inhibit cell clone formation,self-renewal ability and EMT in BCSC-like cells. miR-200c knockdown could restore the tumour growth inhibition caused by XIST knockdown. 29559853 2018 LncRNA XIST/miR-200c regulates the stemness properties and tumourigenicity of human bladder cancer stem cell-like cells. 360 AC130710 GACAT3, LINC01458, lncRNA-AC130710 ENSG00000236289 NR_126559 GRCh38_2:16050427-16085801 gastric cancer C16 NA qPCR etc. gastric cancer tissues, cell lines (AGS, BGC-823, MGC-803, SGC-7901 etc.) up-regulated AC130710 in gastric cancer was significantly higher. Its expression level was significantly associated with tumor size, tumor-node-metastasis (TNM) stages, and distal metastasis. miR-129-5p may play an important role in the downregulation of AC130710 in gastric cancer cells. These results indicated that lncRNA-AC130710 may be a potential tumor marker for gastric cancer prognosis. 24969565 2014 lncRNA-AC130710 targeting by miR-129-5p is upregulated in gastric cancer and associates with poor prognosis. 361 ADAMTS9-AS2 ADAMTS9-AS2 ENSG00000241684 NR_038264 GRCh38_3:64684909-65011468 rectal adenocarcinoma NA M8140/0 qPCR etc. rectal adenocarcinoma tissues down-regulated HULC, CRNDE and PVT1 expression levels were increased, and the expression level of ADAMTS9 AS5 was decreased in READ tumor tissues compared to adjacent non tumor tissues. 29512732 2018 Construction of a ceRNA network reveals potential lncRNA biomarkers in rectal adenocarcinoma. 362 ADPGK-AS1 NA ENSG00000260898 NR_040107 GRCh38_15:72782835-72798199 pancreatic cancer C25 NA Microarray, qPCR, Western blot etc. cell lines (HEK-293T, PANC-1 and SW-1990) up-regulated MiR-205-5p was low-expressed while ZEB1 and ADPGK-AS1 were high-expressed in PC tissues and cells compared with the normal.Dual-luciferase reporter gene assay proved that ADPGK-AS1 could directly target miR-205-5p and miR-205-5p could directly target ZEB1 3'UTR. The expression of MiR-205-5p was negatively correlated with proliferation,migration and invasion, and positively correlated with apoptosis rate of PC cells, while ZEB1 and ADPGK-AS1 had an inversed effect. Further in vitro and in vivo investigation indicated that epithelial-mesenchymal transition (EMT) could be restrained by miR-205-5p through targeting ZEB1. ADPGK-AS1 strongly promoted the tumorigenesis via downregulating miR-205-5p expression and induced the EMT process in vivo. ADPGK-AS1 inhibited miR-205-5p and therefore promoted PC progression through activating ZEB1-induced EMT. 29667486 2018 LncRNA ADPGK-AS1 promotes pancreatic cancer progression through activating ZEB1-mediated epithelial-mesenchymal transition. 363 AF113014 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. liver cancer tissues, cell lines (SMMC7721, HepG2, SK-Hep1 and Huh7) differential expression AF113014 is differentially expressed between HCC cell lines and normal hepatocytes.Furthermore,we discovered that AF113014 up-regulated Egr2 expression through interacting with miR-20a. 28542387 2017 LncRNA-AF113014 promotes the expression of Egr2 by interaction with miR-20a to inhibit proliferation of hepatocellular carcinoma cells 364 AF119895 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 Microarray, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown HCC tissues, HCC cell lines (SMMC7721, Huh7, HepG2 and SK-Hep1) up-regulated AF119895 promoted migration and invasion of HCC cells both in vitro and in vivo.Furthermore,we identified that NXF3 was a downstream target of AF119895.NXF3 depletion could decrease HCC cells migration and invasion.In addition,AF119895 could act as an endogenous sponge by binding to miR-6508-3p and reduce miR-6508-3p expression. And miR-6508-3p could regulate NXF3 by interacting with its 3'UTR. 29274323 2017 AF119895 regulates NXF3 expression to promote migration and invasion of hepatocellular carcinoma through an interaction with miR-6508-3p. 365 AF147447 AC009084.3 ENSG00000280416 NA GRCh38_16:66944660-66945096 gastric cancer C16 NA microarray, qPCR, Western blot, Luciferase reporter assay etc. gastric cancer tissues, cell lines (7901 and MKN45) down-regulated We identified an lncRNA-AF147447 decreased expressed by H. pylori infection, which can inhibit GC proliferation and invasion in vitro and in vivo, act as a tumor suppressor in the development of H. pylori induced GC. LncRNA AF147447 could repress MUC2 expression by direct binding or increasing miR-34c expression. We also found that transcription factor E2F1 could be recruited to lncRNA AF147447 promoter by RNA immunoprecipatation and RNA pull down assays. 27835575 2016 Helicobacter pylori infection related long noncoding RNA (lncRNA) AF147447 inhibits gastric cancer proliferation and invasion by targeting MUC2 and up-regulating miR-34c. 366 AGAP2-AS1 AGAP2-AS1, PUNISHER 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. 367 AKR7L AKR7L, AFAR3, AFB1-AR 3, AFB1-AR3, AKR7A4 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. 368 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines(U251) up-regulated ANRIL was upregulated in glioma cells and its suppression inhibited cell proliferation, migration and invasion but promoted cell apoptosis. ANRIL acted as a sponge of miR-34a, and Sirt1 is a target of miR-34a. Then, Sirt1 was proved to function through activation of the PI3K/AKT and mTOR signaling pathways. In conclusion, ANRIL was upregulated in glioma, and its inhibition could repress cell proliferation, migration and invasion but inhibit cell apoptosis through miR-34a-mediated downregulation of Sirt1, involving the inactivation of the PI3K/AKT and mTOR pathways. 29057547 2017 Knockdown of long non-coding RNA ANRIL inhibits proliferation, migration, and invasion but promotes apoptosis of human glioma cells by upregulation of miR-34a. 369 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 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. 370 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 nasopharyngeal cancer C11 NA qPCR, Luciferase reporter assays NPC tissues, cell lines (5-8F, CNE1, CNE2 and HONE1) up-regulated The expression of lncRNA ANRIL was upregulated in NPC tissues and cells. Moreover, knockdown of ANRIL repressed proliferation, promoted apoptosis, and improved radiosensitivity in NPC via functioning as a miR-125a sponge. 28402230 2017 Downregulation of lncRNA ANRIL inhibits proliferation, induces apoptosis, and enhances radiosensitivity in nasopharyngeal carcinoma cells through regulating miR-125a 371 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 cervical cancer C53 NA qPCR, Luciferase Reporter Assay primary cervical cancer tissues, cell lines (HeLa, CaSki, SiHa, HT-3, and C33A) up-regulated RT-PCR showed that ANRIL expression was significantly upregulated in cervical cancer tumors and cell lines. The bioinformatics prediction program and luciferase assay predicted and validated that miR-186 directly targeted ANRIL. The expression level of miR-186 was downregulated in cervical cancer tumors and cell lines and was negatively correlated to that of ANRIL. 28550682 2017 Long Noncoding RNA ANRIL Promotes Cervical Cancer Development by Acting as a Sponge of miR-186 372 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 hepatocellular carcinoma C22.0 M8170/3 qRT-PCR, Luciferase reporter assay, in vitro knockdown, RIP HCC tissue, HCC cell lines (SMMC772, HUH7, Hep3B, and HepG2) up-regulated ANRIL was upregulated and miR-122-5p was downregulated in HCC tissues and cells. ANRIL was negatively correlated with miR-122-5p expression in HCC tissues. Knockdown of ANRIL or miR-122-5p overexpression suppressed HCC cell viability, colony formation ability, metastasis, and invasion. ANRIL was demonstrated to directly bind to miR-122-5p and inhibit its expression.Forced expression of ANRIL abolished the inhibitory effect of miR-122-5p overexpression on HCC progression. In vivo experiment demonstrated that ANRIL knockdown impeded tumor growth in vivo and increased miR-122-5p expression. 29127494 2017 Knockdown of LncRNA ANRIL suppresses cell proliferation, metastasis, and invasion via regulating miR-122-5p expression in hepatocellular carcinoma. 373 AP5M1 NA ENSG00000053770 NA GRCh38_14:57268909-57298742 gastric cancer C16 NA qPCR,RNAi etc. cell lines (AGS1, MGC803, SGC7901 and MKN55), gastric adenocarcinomas tissues up-regulated Further, we performed bioinformatic screening of miRNAs that share common miRNA response elements (MREs) with lncRNAs and their downstream mRNA targets. The prediction identified three microRNAs (miR-21, miR-145 and miR-148a) and five gastric cancer-specific target genes (EGFR, KLF4, DNMT1 and AGO4) which also showed strong correlation with lncRNAs in regression analysis. Finally, we constructed an integrated lncRNA-miRNA-mRNA interaction network of the candidate genes to understand the post-transcriptional gene regulation. The ceRNA network analysis revealed that the differentially regulated miR-21 and miR-148a were playing as central candidates coordinating sponging activity of the lncRNAs analyzed (H19, TUG1 and MALAT1) in this study and the overexpression of H19 and miR-21 could be a signature event of gastric tumorigenesis that could serve as prognostic indicators and therapeutic targets. 29719612 2018 Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA network in gastric cancer. 374 ASLNC02525 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 Luciferase reporter experiment,qPCR etc. cell lines (HepG2, QGY-7701, SMMC-7721, L-02) up-regulated ASLNC02525, as an RNA sponge, broke the negative regulation of twist1 by hsa-miRNA-489-3p, and once ASLNC02525 was silenced, the highly expressed hsa-miRNA?489-3p regained its regulation on twist1 and inhibited the proliferation and invasion. 28713968 2017 Inhibition of proliferation and invasion of hepatocellular carcinoma cells by lncRNA-ASLNC02525 silencing and the mechanism. 375 ATB LOC109207222 NA NA NA lung cancer C34 NA qPCR, Western blot etc. cell line (A549) up-regulated ATB overexpression promoted proliferation, migration, and invasion of A549 cells. Meanwhile, EMT of A549 cells was also enhanced. ATB silence showed the opposite influence. Expression of miR-494 was negatively regulated by ATB. Following experiments showed ATB-induced alterations of proliferation, migration, invasion, and EMT were all reversed by miR-494 overexpression. Finally, we proved that ATB increased phosphorylated levels of AKT, JAK1, and STAT3, and those increases were all reversed by miR-494 overexpression. We interestingly figured out that ATB promoted proliferation, migration, invasion, and EMT through down-regulating miR-494 in A549 cells. Moreover, ATB might activate AKT and the JAK/STAT3 pathway via down-regulating miR-494. 29693289 2018 LncRNA ATB promotes proliferation and metastasis in A549 cells by down-regulation of microRNA-494. 376 ATB LOC109207222 NA NA NA bladder cancer C67 NA qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown bladder cancer cell line T24 up-regulated lncRNA-ATB was a molecular sponge of miR-126,and exerted tumor promoting effects by down-regulation of miR-126. Moreover, KRAS was a direct target of miR-126, and negatively regulated by miR-126.Finally, overexpression of KRAS increased cell viability, migration and invasion, as well as activated PI3K/AKT and mTOR signal pathways in T24 cells. 29321082 2018 Long noncoding RNA ATB promotes proliferation, migration and invasion in bladder cancer by suppressing microRNA-126. 377 ATB LOC109207222 NA NA NA thyroid cancer C73.9 NA qPCR etc. PTC tissues, cell lines (IHH-4, TPC-1, K1, HTH83, Nthy-ori 3-1) up-regulated ATB is upregulated in PTC tissues compared with noncancerous tissues. ATB is upregulated and functions as an oncogene in PTC. Furthermore, lncRNA-ATB may serve as a diagnostic biomarker and therapeutic target for PTC. High-expression of lncRNA-ATB is associated with large tumor size and lymph node metastasis.LncRNA-ATB has been reported to promote cancer metastasis via binding and negatively regulating miR-200 family,and then inducing epithelial-mesenchymal transition22. 28770959 2017 The expression and function of long noncoding RNA lncRNA-ATB in papillary thyroid cancer. 378 lncRNA-ATB LOC109207222 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-β actives lnc-ATB and TGF-β2 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/TGFβ2 feedback loop. 379 lncRNA-ATB LOC109207222 NA NA NA hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues, cell lines (SMMC-7721) up-regulated In this study, we observed that the lncRNA-activated by TGFβ1 (lncRNA-ATB) was upregulated in hepatocellular carcinoma (HCC) metastases and associated with poor prognosis. lncRNA-ATB upregulated ZEB1 and ZEB2 by competitively binding the miR-200 family and then induced EMT and invasion. In addition, lncRNA-ATB promoted organ colonization of disseminated tumor cells by binding IL-11 mRNA, autocrine induction of IL-11, and triggering STAT3 signaling. 24768205 2014 A long noncoding RNA activated by TGFβ1-promotes the invasion-metastasis cascade in hepatocellular carcinoma. 380 BANCR BANCR, LINC00586 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. 381 BANCR BANCR, LINC00586 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 melanoma NA M8720/3 qPCR, Luciferase reporter assay, Western blot melanoma tissues, cells lines (A375, A875 and M14, and human epidermal melanocytes) up-regulated the expression of the BANCR was low in melanocytic nevus and human melanocytes but high in melanoma tissues and cell lines. Knockdown of BANCR inhibited melanoma cell proliferation and invasion, and induced cell apoptosis.the inhibitory effect of BANCR siRNA in cell growth and migration.miR?204 was a direct target of BANCR and neurogenic locus notch homolog protein 2 (Notch2) was a direct target of miR?204. BANCR may promote melanoma cell growth through inhibition of miR-204, leading to the activation of Notch2 pathway. BANCR knockdown inhibited tumor growth in vivo. 29075789 2017 BANCR contributes to the growth and invasion of melanoma by functioning as a competing endogenous RNA to upregulate Notch2 expression by sponging miR?204. 382 BC040587 LINC00901, LSAMP-AS4, TCONS_00005428 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. 383 BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 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 384 BCYRN1 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 cervical cancer C53 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (SiHa, HeLa, CaSki, Ect1/E6E7), cervical cancer tissues up-regulated MicroRNA (miR)-138 was predicted as a direct target of BCYRN1 and the expression of miR-138 was elevated in HeLa cells transfected with BCYRN1 siRNA. Subsequently, elevated levels of miR-138 were suppressed by transfection with miR-138 inhibitor in HeLa cells pretreated with BCYRN1 siRNA.BCYRN1 siRNA partially counteracted the effect of miR-138 inhibitor on promoting cell viability and mobility in HeLa cells. BCYRN1 siRNA was able to prevent tumor growth, and reduced the expression of migration marker proteins metalloproteinase 2 and vascular endothelial cell growth factor, with enhanced expression levels of miR-138. These results suggest that lncRNA BCYRN1 promotes the proliferation and invasion of cervical cancer via targeting miR-138. 29552212 2018 Long non-coding RNA BCYRN1 promotes the proliferation and metastasis of cervical cancer via targeting microRNA-138 in vitro and in vivo. 385 C2DAT1 NA NA NA NA osteosarcoma NA M9180/3 Luciferase Reporter Assay ,qPCR,Western blot etc. cell lines (MG63, OS-732, hFOB1.19) differential expression C2dat1 suppression reduced cell viability,invasion and migration,while increased cell apoptosis in OS-732 cells. MiR-34a-5p was a target of C2dat1. 28810936 2017 LncRNA C2dat1 Promotes Cell Proliferation, Migration, and Invasion by Targeting MiR-34a-5p in Osteosarcoma Cells. 386 CAMTA1 NA ENSG00000171735 NA GRCh38_1:6785324-7769706 breast cancer C50 NA qPCR, Western blot, Luciferase Reporter Assays cell line (MDA-MB-231) differential expression Our findings suggested that LncCAMTA1 might promote proliferation and mobility of human breast cancer cell via binding with miR-20b. And VEGF was directly target of miR-20b and regulated activation of MAPK/ERK and JAK/STAT3 signal pathways. 28550685 2017 Long Noncoding RNA CAMTA1 Promotes Proliferation and Mobility of Human Breast Cancer Cell Line MDA- MB-231 Via Targeting miR-20b 387 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 breast cancer C50 NA qPCR, Western blot, in vitro knockdown etc. cell line (HCC1937, LCC9, MDA-MB-231, MCF-7), breast cancer tissues down-regulated Overexpression of lncRNA CASC2 significantly repressed proliferation and metastasis while caused cell cycle arrest and much more early apoptosis of breast cancer.The inactivation of TGF-signal pathway was involved in the function of lncRNA CASC2.lncRNA CASC2 was a key factor in the tumorigenesis and malignancy of breast cancer, thereby possibly was a potential therapy target for the treatment of breast cancer. 29523222 2018 Up-regulation of lncRNA CASC2 suppresses cell proliferation and metastasis of breast cancer via inactivating of the TGF-? signaling pathway. 388 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 melanoma NA M8720/3 Microarray, qPCR,Western blot, Luciferase reporter assay cell line (293T, A375, C8161, HMCB, G361, WM115, MM96L, M14, HaCaT), melanoma tissues down-regulated CASC2 could efficiently sponge miR-181a,thereby facilitating the expression of PLXNC1. Up-regulation of CASC2 suppressed the cell proliferation and invasion,but induced the apoptosis of melanoma cells. LncRNA CASC2 can promote PLXNC1 expression by sponging miR-181a,thereby inhibiting the proliferation and invasion of melanoma cells,indicating that lncRNA CASC2 functions via the miR-181a/PLXNC1 axis in melanoma. 29514220 2018 Long non-coding RNA CASC2 inhibits tumorigenesis via the miR-181a/PLXNC1 axis in melanoma. 389 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 malignant melanoma NA M8720/3 qPCR, Western blot, Luciferase reporter assay MM tissues, malignant melanoma cell lines (A375, A2058 and HTB63) down-regulated CASC2 acted as a molecular sponge for miR-18a-5p and RUNX1 was a target gene of miR-18a-5p. Moreover, CASC2 overexpression promoted the expression of RUNX1, while upregulated miR-18a-5p significantly reversed the effect of CASC2 on RUNX1 level.Upregulated CASC2 may inhibit cell proliferation, migration and invasion through regulating miR-18a-5p and its target gene RUNX1 in MM. 29422114 2018 Upregulated lncRNA CASC2 may inhibit malignant melanoma development through regulating miR-18a-5p/RUNX1. 390 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 renal cell carcinoma C64.9 NA qPCR, Cell transfection, Dual-luciferase reporter assay, Cell proliferation assay etc. RCC tissues, cell lines (786-O and A498) down-regulated The present study confirmed that CASC2 was downregulated in human RCC tissues and human RCC cell lines (786-O and A498). Restoration of CASC2 expression via transfection with a pcDNA3.1(+)-CASC2 vector was able to inhibit cell proliferation and migration in 786-O and A498 cells. Bioinformatics analysis and dual-luciferase reporter assays confirmed that CASC2 was a direct target gene of miR-21. miR-21 was able to decrease the expression of CASC2 in 786-O and A498 cells. Furthermore, overexpression of miR-21 partly abrogated CASC2-mediated inhibition of 786-O and A498 cell proliferation and migration. 27222255 2016 Downregulation of lncRNA CASC2 by microRNA-21 increases the proliferation and migration of renal cell carcinoma cells. 391 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 osteosarcoma NA M9180/3 qPCR, Western blot osteosarcoma tissues, osteosarcoma cell lines (MG- 63, SW1353, Saos- 2, SOSP-9607 and U2OS) down-regulated CASC2 expression was downregulated in osteosarcoma samples and cell lines. Moreover, we showed that downregulated expression of CASC2 was correlated with advanced TNM stage. Furthermore, overexpression of CASC2 inhibited osteosarcoma cell proliferation, colony formation, and invasion. In addition, we indicated that ectopic expression of CASC2 suppressed miR-181a expression and enhanced the expression of Ras association domain family member 6 (RASSF6), PTEN and ATM in osteosarcoma cell, which were the direct target gene of miR-181a. Moreover, we indicated that RASSF6 expression was downregulated in osteosarcoma samples and cell lines and downregulated expression of RASSF6 was correlated with advanced TNM stage. We found that the expression of RASSF6 was positively correlated with the expression of CASC2 in osteosarcoma tissues. 29194827 2017 Downregulation of lncRNA CASC2 facilitates osteosarcoma growth and invasion through miR-181a. 392 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 colorectal cancer C19.9 NA qPCR, Flow cytometry assay, Cell proliferation assay etc. CRC tissues, cell lines (CACO2, SW480, SW620, HCT-116, HT-29 etc.) down-regulated In this study, CASC2 expression was significantly decreased in CRC tissues and CRC cell lines, and decreased expression was significantly more frequent in patients with advanced tumor-node-metastasis stage disease (TNM III and IV). Further functional experiments indicate that CASC2 could directly upregulate PIAS3 expression by functioning as a competing endogenous RNA (ceRNA) for miR-18a. This interactions leads to the de-repression of genes downstream of STAT3 and consequentially inhibition of CRC cell proliferation and tumor growth in vitro and in vivo by extending the G0/G1-S phase transition. 27198161 2016 The long noncoding RNA CASC2 functions as a competing endogenous RNA by sponging miR-18a in colorectal cancer. 393 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 glioma NA M9380/3 qPCR, Luciferase reporter assay etc. glioma tissues, cell lines (U251, U87) down-regulated In this study, we confirmed that CASC2 was lowly expressed in glioma tissues as well as in U251 and U87 glioma cell lines. Overexpression of CASC2 inhibited the malignancy of glioma cells, including proliferation, migration, and invasion, and promoted cell apoptosis. We found that up-regulated CASC2 decreased the expression of miR-21 significantly and there is a reciprocal repression between CASC2 and miR-21 in an Argonaute2-dependent manner. 25446261 2014 Long non-coding RNA CASC2 suppresses malignancy in human gliomas by miR-21. 394 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. HCC tissues, cell lines (HepG2, HuH7) down-regulated lncRNA CASC2, acting as an onco-suppressor, was involved in the pathogenesis and progression of HCC, and its possible mechanism was induced the growth inhibition on HCC through miR-24-3p/SOX7 axis. Our results revealed a possible regulatory mechanism in HCC pathogenesis and warranted that lncRNA CASC2 was an important regulator in HCC. 29091305 2017 LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR-24-3p 395 CASC2 CASC2, C10orf5 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. HCC tissues, cell lines (MHCC-97L, Hep-3B, HepG2, Huh7, SMMC-7721, MHCC-97H and LO2) down-regulated CASC2 expression was markedly downregulated in aggressive HCC tissues compared with non-aggressive HCCs (P < 0.01, Fig. 1b). The CASC2/miR-367/FBXW7 axis may be a ponderable and promising therapeutic target for HCC. CASC2 low-expressing and miR-367 high-expressing HCC patients showed the poorest clinical outcome. CASC2 was recognized as a competing endogenous RNA (ceRNA) for miR-367 and could exert its anti-metastatic effects on cell migration, invasion and EMT progression through CASC2/miR-367/FBXW7 axis, which might inject some new vitalities into the development therapeutic targets for HCC. 28716020 2017 Long non-coding RNA CASC2 suppresses epithelial-mesenchymal transition of hepatocellular carcinoma cells through CASC2/miR-367/FBXW7 axis. 396 CASC2c CASC2, C10orf5 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. 397 CASC7 NA NA NA NA colon cancer C18 NA qPCR, Luciferase reporter assay, Western blot etc. cell lines (SW480, HCT-116) down-regulated CASC7 overexpression could inhibit cell viability, migration and invasion, and promote apoptosis in CRC cells. CASC7 and ING3 were both a target of miR-21 in CRC cells, and CASC7 could control ING3 expression by regulating miR-21. Moreover, we have found that CASC7 inhibited colon cancer cell proliferation and migration via miR- 21/ING3 axis. These observations suggested that CASC7 played an important role in CRC pathogenesis and may be considered as a novel diagnostic marker of CRC. 28954383 2017 Long non-coding RNA CASC7 inhibits the proliferation and migration of colon cancer cells via inhibiting microRNA-21 398 CAT104 NA NA NA NA gastric cancer C16 NA qRT-PCR, Western blot, Luciferase reporter assay gastric carcinoma cell line (NCI-N87, SGC7901, BGC823, BGC803 and AGS) up-regulated CAT104 was highly expressed in human GC NCI-N87, SGC7901, BGC823, BGC803 and AGS cells. Suppression of CAT104 decreased NCI-N87 cell viability, migration and invasion, but promoted apoptosis. CAT104 knockdown enhanced the expression of microRNA-381 (miR-381) expression in NCI-N87 cells. miR-381 participated in the regulation effects of CAT104 on NCI-N87 cell viability, migration, invasion and apoptosis. Zinc finger E-box binding homeobox 1 (ZEB1) was identified as a direct target of miR-381. Overexpression of ZEB1 revealed the miR-381 mimicinduced cell viability, migration and invasion inhibition.Suppression of ZEB1 revealed the miR-381 inhibitor-induced activation of c-Jun N-terminal kinase pathway (JNK) and Wnt/? signaling pathways in NCI-N87 cells. 29295724 2018 Long non-coding RNA CAT104 promotes cell viability, migration and invasion in gastric carcinoma cells through activation of microRNA-381 inhibiting zinc finger E-box binding homeobox 1 (ZEB1) expression. 399 CAT104 NA NA NA NA osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (MG63 and OS-732, hFOB1.19, HEK293) up-regulated CAT104 was highly expressed in osteosarcoma MG-63 and OS-732 cells. Knockdown of CAT104 significantly inhibited OS-732 cell proliferation, migration and invasion, but promoted cell apoptosis. CAT104 regulated the expression of miR-381 and miR-381 participated in the effects of CAT104 on OS-732 cells. Zinc finger E box binding homeobox 1 (ZEB1) was a direct target gene of miR-381, which was involved in the regulatory roles of miR381 in OS-732 cell proliferation, migration, invasion and apoptosis, as well as c-Jun Nterminal kinase (JNK) and Wnt/?-catenin pathways. Suppression of CAT104 exerted significant inhibitory effects on osteosarcoma cell proliferation, migration and invasion by regulating the expression of miR-381 and downstream ZEB1, as well as JNK and Wnt-catenin pathways. 29523223 2018 Knockdown of long non-coding RNA CAT104 inhibits the proliferation, migration and invasion of human osteosarcoma cells by regulating microRNA-381. 400 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 gallbladder cancer C23.9 NA qPCR, Western blot, Luciferase reporter assay etc. gallbladder cancer tissues up-regulated In this study, we demonstrated that CCAT1 was upregulated in gallbladder cancer (GBC) tissues. CCAT1 silencing downregulated, whereas CCAT1 overexpression enhanced the expression of miRNA-218-5p target gene Bmi1 through competitively 'spongeing' miRNA-218-5p. Our data revealed that CCAT1 knockdown impaired the proliferation and invasiveness of GBC cells, at least in part through affetcing miRNA-218-5p-mediated regulation of Bmi1. Moreover, CCAT1 transcript level was correlated with Bmi1 mRNA level in GBC tissues. 25569100 2015 Long non-coding RNA CCAT1 promotes gallbladder cancer development via negative modulation of miRNA-218-5p. 401 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 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. 402 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 retinoblastoma C69.2 M9510/3 qPCR, RNAi, Western blot, Cell migration and invasion assay etc. RB tissues, cell lines (SO-RB50, Y79 and WERI-RB1) up-regulated The expression of lncRNA CCAT1 in RB tissues was significantly increased compared with normal tissues. It was also shown that lncRNA CCAT1 in RB SORB50, Y79 and WERI-RB1 cells was significantly higher than that in normal podiatric retina. LncRNA CCAT1 promotes the proliferation migration and invasion, and reduces cell apoptosis of SO-RB50 and Y79 cells, probably through negative modulation of miR-218-5p. 28088735 2017 Long non-coding RNA CCAT1 promotes human retinoblastoma SO-RB50 and Y79 cells through negative regulation of miR-218-5p. 403 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 osteosarcoma NA M9180/3 qPCR, RNAi etc. osteosarcoma tissues, cell lines (143b, KHOS, MG-63, and U2OS) up-regulated Our findings revealed that CCAT1 was upregulated in osteosarcoma tissues and cells, and was involved in the proliferation and migration of osteosarcoma via regulating miR-148a/phosphatidyl inositol 3-kinase interacting protein 1 (PIK3IP1) signal pathway. 28549102 2017 Long non-coding RNA CCAT1/miR-148a axis promotes osteosarcoma proliferation and migration through regulating PIK3IP1 404 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 laryngeal squamous cell cancer C32.3 NA qPCR, Western blot laryngeal squamous cell carcinoma tissues up-regulated CCAT1 expression was upregulated in LSCC tissues compared with the normal adjacent tissues. We also demonstrated that CCAT1 overexpression suppressed the expression of let-7 and enhanced the expression of HMGA2 and Myc, the direct target genes of let-7. 27830017 2016 CCAT1 promotes laryngeal squamous cell carcinoma cell proliferation and invasion 405 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 glioma NA M9380/3 qPCR, Luciferase reporter assay, Western blot, RIP glioma tissues, cell lines (U87,LN229,HEK293T) up-regulated CCAT1 expression was significantly increased, while miR-181b decreased,in glioma tissues. Interestingly, miR-181b expression was negatively correlated with the CCAT1 level in glioma samples. Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process, and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b.CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRα. 28475287 2017 lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR-181b. 406 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 laryngeal squamous cell cancer C32.3 NA qPCR, western blot, Luciferase reporter assays etc. laryngeal squamous cell cancer tissues, cell lines (AMC-HN-8 and TU212) up-regulated The results showed that expressions of colon cancer-associated transcript-1 and zinc finger protein, X-linked were significantly higher while microRNA-218 expression was significantly lower in the laryngeal squamous cell cancer tissues than those in the adjacent normal tissues. Moreover, a novel CCAT1-miR-218-ZFX regulatory axis was demonstrated in the proliferation and invasion of LSCC cells in vitro and in vivo. 28631575 2017 Long non-coding RNA CCAT1/miR-218/ZFX axis modulates the progression of laryngeal squamous cell cancer 407 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 colon cancer C18 NA qPCR, Western blot, Luciferase reporter assay etc. GC tissues, cell lines (MGC-803, SGC-7901, AGS etc.) up-regulated we provide the first evidence that CCAT1 regulates miR-490 in gastric cancer (GC) cells. Interestingly, miR-490 can also repress CCAT1 expression. CCAT1 expression was significantly upregulated, and miR-490 expression was downregulated in GC. The negative correlation between miR-490 and CCAT1 expression was observed in GC tissues. Importantly, CCAT1 contains a putative miR-490-binding site, and deletion of this binding site abolishes their miR-490 responsiveness. Post-transcriptional CCAT1 silencing by miR-490 significantly suppressed GC cell migration. Furthermore, miR-490 directly bound to the hnRNPA1 mRNA 3'-UTR to repress its translation. Inhibition of miR-490 rescued CCAT1 siRNA-mediated suppression of cell migration. hnRNPA1 expression was significantly upregulated in GC specimens, and there was a negative correlation between miR-490 and hnRNPA1 expression and also a positive correlation between hnRNAP1 expression level and CCAT1 level 26825578 2016 The long noncoding RNA colon cancer-associated transcript-1/miR-490 axis regulates gastric cancer cell migration by targeting hnRNPA1 408 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 glioma NA M9380/3 qPCR, RNAi, Luciferase reporter assay, Flow cytometry assay etc. glioma tissues, cell lines (U87 and U251) up-regulated lncRNA-CCAT1 expression was significantly upregulated in glioma cancer tissues and cell lines compared with controls. After inhibiting CCAT1 expression in glioma cell line U251 with siRNA-CCAT1 (si-CCAT1), the cell viability and cell colony formation were decreased, the cell cycle was arrested in G1 phase, and the cell apoptosis was increased. After up-regulating CCAT1 expression in U251 cells, miR-410 level was decreased. Luciferase reporter assay confirmed that CCAT1 targeted miR-410. Correlation analysis showed that CCAT1 expression was negatively related to miR-410 expression in glioma cancer tissues. 27765628 2016 Long non-coding RNA CCAT1 promotes glioma cell proliferation via inhibiting microRNA-410. 409 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RNAi, Luciferase reporter assay hepatocellular carcinoma tissues, cell lines (MHCC97H, MHCC97L, Hep3B, and SMCC-7721) up-regulated In this study, we found that the long non-coding RNA colon cancer–associated transcript 1 was upregulated in hepatocellular carcinoma tissues (p? 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. 433 ENST00000515084 CASC22, LINC01373, LincRNA-ENST00000515084, TCONS_00024290 ENSG00000260887 NA GRCh38_16:52258564-52280638 breast cancer C50 NA qPCR, Luciferase reporter assay, Cell viability assay, Transient transfection etc. cell lines (MCF-7 and Bcap-37) up-regulated We found that the C allele of the rs12325489C>T polymorphism in the exonic regions of lincRNA-ENST00000515084 was associated with a significantly increased risk of breast cancer, compared with the rs12325489TT genotype. Biochemical analysis demonstrated that the C to T base change at rs12325489C>T disrupts the binding site for miRNA-370, thereby influencing the transcriptional activity of lincRNA-ENST00000515084 in vitro and in vivo, and affecting cell proliferation and tumor growth. 24879036 2014 A polymorphism rs12325489C>T in the lincRNA-ENST00000515084 exon was found to modulate breast cancer risk via GWAS-based association analyses. 434 ENST00000518554 DCAF13, GM83, HSPC064, Sof1, WDSOF1 ENSG00000164934 NA GRCh38_8:103414714-103443453 glioblastoma NA M9440/3 microarray, qPCR etc. glioblastoma tissues down-regulated In our expression profling analysis, the lncRNA ENST00000520186, ENST00000559981, ENST00000547415 and ENST00000518554 were separately considered as the ceRNA of miR-15a, miR-21, miR-29b and miR-29c in GBM. So far, these ceRNAs have not been reported implicated in GBM. Four mRNAs may be regulated by these miRNAs and lncRNAs, the PPP3CA have been reported to be aberrantly expressed in other tumors, but have not been studied in GBM. 27600337 2016 Identification and functional characterization of lncRNAs acting as ceRNA involved in the malignant progression of glioblastoma multiforme. 435 ENST00000520186 FBXO41, FBX41 ENSG00000163013 NA GRCh38_2:73254682-73284431 glioblastoma NA M9440/3 microarray, qPCR etc. glioblastoma tissues up-regulated In our expression profling analysis, the lncRNA ENST00000520186, ENST00000559981, ENST00000547415 and ENST00000518554 were separately considered as the ceRNA of miR-15a, miR-21, miR-29b and miR-29c in GBM. So far, these ceRNAs have not been reported implicated in GBM. Four mRNAs may be regulated by these miRNAs and lncRNAs, the PPP3CA have been reported to be aberrantly expressed in other tumors, but have not been studied in GBM. 27600337 2016 Identification and functional characterization of lncRNAs acting as ceRNA involved in the malignant progression of glioblastoma multiforme. 436 ENST00000535511 RP11-768F21.1, LOC105370027 NA NA GRCh38_12:119387991-119594240 colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues up-regulated qRT-PCR was performed to assess their expression levels in 14 pairs of matched colorectal tumor/non-tumor sample. This analysis revealed that miR-133b was significantly downregulated in CRC tumor samples, while UBD and lncRNA ENST00000535511 were significantly upregulated in CRC tumor samples. A significantly positive correlation between UBD and lncRNA ENST00000535511 was also observed. 28177879 2017 Comprehensive analysis of differentially expressed profiles of lncRNAs and construction of miR-133b mediated ceRNA network in colorectal cancer. 437 ENST00000547415 NOVA1, Nova-1 ENSG00000139910 NA GRCh38_14:26443093-26597754 glioblastoma NA M9440/3 microarray, qPCR etc. glioblastoma tissues down-regulated In our expression profling analysis, the lncRNA ENST00000520186, ENST00000559981, ENST00000547415 and ENST00000518554 were separately considered as the ceRNA of miR-15a, miR-21, miR-29b and miR-29c in GBM. So far, these ceRNAs have not been reported implicated in GBM. Four mRNAs may be regulated by these miRNAs and lncRNAs, the PPP3CA have been reported to be aberrantly expressed in other tumors, but have not been studied in GBM. 27600337 2016 Identification and functional characterization of lncRNAs acting as ceRNA involved in the malignant progression of glioblastoma multiforme. 438 ENST00000548900.1 RP11-1143G9.4 NA NA GRCh38_12:69353493-69354225 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. 439 ENST00000559981 PLEKHH1 ENSG00000054690 NA GRCh38_14:67533301-67589612 glioblastoma NA M9440/3 microarray, qPCR etc. glioblastoma tissues up-regulated In our expression profling analysis, the lncRNA ENST00000520186, ENST00000559981, ENST00000547415 and ENST00000518554 were separately considered as the ceRNA of miR-15a, miR-21, miR-29b and miR-29c in GBM. So far, these ceRNAs have not been reported implicated in GBM. Four mRNAs may be regulated by these miRNAs and lncRNAs, the PPP3CA have been reported to be aberrantly expressed in other tumors, but have not been studied in GBM. 27600337 2016 Identification and functional characterization of lncRNAs acting as ceRNA involved in the malignant progression of glioblastoma multiforme. 440 FBXL19-AS1 NA ENSG00000260852 NR_024348 GRCh38_16:30919319-30923269 colorectal cancer C19.9 NA microarray, qPCR, Luciferase reporter assay etc. cell lines (LoVo, HT29, HCT116, SW620) up-regulated FBXL19-AS1 was the most significantly upregulated lncRNA in metastatic tumors. Our results reveal the cancer-promoting effect of FBXL19-AS1, acting as a molecular sponge in negatively modulating miR-203, which might provide a new insight for understanding of CRC development. 28479250 2017 Long non-coding RNA FBXL19-AS1 plays oncogenic role in colorectal cancer by sponging miR-203 441 FER1L4 FER1L4, C20orf124 ENSG00000088340 NA GRCh38_20:35558737-35607562 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. HCC tissues, cell lines (HepG2, Huh7, Hep3B, and HCCM3) down-regulated FER1L4 was lowly expressed in HCC tissue specimens as well as in malignant HCC cell lines, while the situation is opposite in miR-106a-5p. FER1L4 could exert a tumor suppressive impact on HCC, which at least, in part, through suppressing miR-106a-5p expression. FER1L4, as well as miR-106a-5p, can predict the clinical prognosis of HCC alone or combined, which may be a novel therapeutic target for treating HCC. lncRNA FER1L4 and miR-106a-5p functioned as competing endogenous RNA (ceRNA) that miR-106a-5p could regulate the expression of FER1L4 by targeting PTEN in human gastric cancer. 28759956 2017 Long non-coding RNA Fer-1-like protein 4 acts as a tumor suppressor via miR-106a-5p and predicts good prognosis in hepatocellular carcinoma. 442 FER1L4 FER1L4, C20orf124 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. 443 FER1L4 FER1L4, C20orf124 ENSG00000088340 NA GRCh38_20:35558737-35607562 gastric cancer C16 NA qPCR, RNAi, Western blot etc. gastric cancer tissues, cell lines (AGS, MGC-803, SGC-7901) down-regulated We observed that FER1L4 was downregulated in gastric cancer and that its level corresponded with that of PTEN mRNA. Both FER1L4 and PTEN mRNA were targets of miR-106a-5p. Further experiments demonstrated that FER1L4 downregulation liberates miR-106a-5p and decreases the abundances of PTEN mRNA and protein. More importantly, FER1L4 downregulation accelerated cell proliferation by promoting the G0/G1 to S phase transition. 26306906 2015 Long noncoding RNA FER1L4 suppresses cancer cell growth by acting as a competing endogenous RNA and regulating PTEN expression. 444 FER1L4 FER1L4, C20orf124 ENSG00000088340 NA GRCh38_20:35558737-35607562 gastric cancer C16 NA microarray, qPCR, RNAi etc. gastric cancer tissues, cell lines (GES-1, AGS, MGC-803, SGC-7901 etc.) differential expression RB1 is one of miR-106a-5p's targets, and has been validated by dual luciferase reporter assay25. In this study, the interaction between FER1L4 and miR-106a-5p was first predicted by miRcode. Then dual luciferase reporter assay showed that the luciferase activity of the mutant FER1L4 plasmid was about 56% higher than that of the wild-type plasmid. This indicated that the mutations introduced in the seed matches impair the ability of miR-106a-5p to bind to FER1L4. qRT-PCR analysis revealed that transfection of small interfering RNA (siRNA) against FER1L4 not only reduced FER1L4 levels in GES-1, AGS, MGC-803 and SGC-7901, but also reduced RB1 levels in all cells tested. 25124853 2014 Long noncoding RNA associated-competing endogenous RNAs in gastric cancer. 445 FGFR3-AS NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 RT-qPCR, Western blot, in vitro knockdown human liver cancer cell lines (SMMC-7721, BEL-7404 (7404), Huh7, Hep3B and HepG2 ) up-regulated FGFR3-AS1 knockdown significantly inhibited cell proliferation but induced apoptosis.Moreover,FGFR3-AS1 knockdown led to more HCC cells arrested in G0 stage. Besides, FGFR3-AS1 knockdown significantly inhibited cell migration and invasion. Additionally,we found that FGFR3-AS1 silence dramatically delayed tumor growth in vivo.In mechanism, we found FGFR3-AS1 silence decreased the activation of PI3K/AKT signaling pathway.LncRNAs could regulate cell proliferation,apoptosis, migration and invasion by sponging miRNAs or interacting with specific proteins.Furthermore, western blot (WB) results indicated that FGFR3-AS1 knockdown promoted the expression of P21 but inhibited CYCLIN D1 expression. 29463348 2018 Long non-coding RNA FGFR3-AS1 promotes hepatocellular carcinoma carcinogenesis via modulating PI3K/AKT pathway. 446 FTH1P3 FTH1P3, FTHL3, FTHL3P ENSG00000213453 NA GRCh38_2:27392784-27393367 uveal melanoma C69.9 M8720/3 qPCR, Western blot etc. cell lines (OCM-1A, MUM-2C, C918, MUM-2B) up-regulated lncRNA FTH1P3 was commonly up-regulated in uveal melanoma cell lines and tissues and acted as an oncogene in uveal melanoma progression by inhibiting miR-224-5p expression. These results suggest that lncRNA FTH1P3 plays a crucial role in uveal melanoma and investigation of the underlying mechanism may be a target for the treatment of uveal melanoma. 29095823 2017 Long non-coding RNA FTH1P3 facilitates uveal melanoma cell growth and invasion through miR-224-5p 447 FTX FTX, LINC00182, MIR374AHG, NCRNA00182 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. 448 FTX FTX, LINC00182, MIR374AHG, NCRNA00182 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. 449 GACAT3 GACAT3, LINC01458, lncRNA-AC130710 ENSG00000236289 NR_126559 GRCh38_2:16050427-16085801 colorectal cancer C19.9 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (FHC, HT29, HCT116,SW480, LoVo, and 293T), CRC tissues up-regulated GACAT3 was highly expressed in CRC tissues and cell lines. Si-GACAT3 significantly decreased cell proliferation, motility, and invasiveness both in vitro and in vivo. We confirmed that downregulated GACAT3 significantly increased the expression of miR-149, and miR-149 binds to GACAT3 in a sequence-specific manner using luciferase reporter assays and pull-down assay. Further functional experiments indicated that GACAT3 could directly upregulate SP1 and STAT3 expressions by functioning as a competing endogenous RNA for miR-149, and consequentially, promoting CRC cell proliferation and invasion in vitro. 29593420 2018 Novel long noncoding RNA GACAT3 promotes colorectal cancer cell proliferation, invasion, and migration through miR-149. 450 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 esophageal cancer C15 NA qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown EC cell lines (ECA109, TE-1, TE-3 and EC9706), esophageal epithelia cell line (SHEE) up-regulated GAS5 expression was increased in EC cells (ECA109, TE-1, TE3 and EC9706) compared to SHEE cells.Knockdown of GAS5 decreased cell viability,migration,invasion,and induced apoptosis in EC9706 cells.Moreover,miR-301a was directly sponged to GAS5,and miR-301a suppression obviously alleviated the pro-tumor effects of GAS5.Furthermore,miR-301a positively regulated CXCR4 expression,and overexpression of CXCR4 induced apoptosis and abolished the promoting effect of miR-301a inhibition on cell viability,migration and invasion.Besides,miR-301a blocked Wnt/β-catenin and NF-κB signal pathways by regulation of CXCR4. 29386089 2018 Long non-coding RNA GAS5 promotes proliferation, migration and invasion by regulation of miR-301a in esophageal cancer. 451 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 osteosarcoma NA M9180/3 qPCR, Western blot cell lines (MG-63 and OS-732, hFOB1.19) down-regulated LncRNA GAS5 was down-regulated in MG-63 and OS-732 cells compared to hFOB1.19 cells.Silence of lncRNA GAS5 significantly promoted MG-63 cells viability,migration and invasion,and up-regulated Cyclin D1,Cyclin B1,CDK1 and CDK4 expressions.miR-203a was negatively regulated by lncRNA GAS5.The promoting activities of lncRNA GAS5 silence on MG-63 cells growth and metastasis were reversed by miR-203a suppression.lncRNA GAS5 silence,miR-203a overexpression,and TIMP2 silence could activate PI3K/AKT/GSK3β signaling while block NF-κB signaling.LncRNA GAS5 might be a tumor suppressor in osteosarcoma via sponging miR-203a,sequestering miR-203a away from TIMP2. 29414815 2018 LncRNA GAS5 Represses Osteosarcoma Cells Growth and Metastasis via Sponging MiR-203a. 452 Gas5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 papillary thyroid cancer NA M8260/3 qPCR, Luciferase reporter assay, Western blot papillary thyroid carcinoma tissues, cell lines ( BHP5-16, TPC, K1 and BHP2-7, Nthy-ori 3-1) down-regulated Over-expression of Gas5 remarkably suppressed PTC cells proliferation in vitro and inhibited the growth of tumor cells in vivo likewise. Gas5 was identified as a target of miR-222-3p which was aberrantly high in PTC cells.Enhanced expression of miR-222-3p promoted the proliferation of PTC cells while knocking down miR-222-3p could inhibit it. The advanced effects of miR-222-3p on the proliferation of PTC cells could be partly reversed by the upregulation of Gas5 expression.Gas5 increased the protein level of the PTEN,one of miR-222-3p's targets, which further activated PTEN/AKT pathway. 29423063 2017 LncRNA Gas5 acts as a ceRNA to regulate PTEN expression by sponging miR-222-3p in papillary thyroid carcinoma. 453 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 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. 454 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 endometrial cancer NA M8380/3 qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay etc. endometrial carcinoma tissues, cell lines (HHUA, JEC) down-regulated We identified that GAS5 was down-regulated in endometrial cancer cells and stimulated the apoptosis of endometrial cancer cells. In summary, we demonstrate that GAS5 acts as an tumor suppressor lncRNA in endometrial cancer. Through inhibiting the expression of miR-103, GAS5 significantly enhanced the expression of PTEN to promote cancer cell apoptosis, and, thus, could be an important mediator in the pathogenesis of endometrial cancer. 26511107 2015 LncRNA-GAS5 induces PTEN expression through inhibiting miR-103 in endometrial cancer cells. 455 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 osteosarcoma NA M9180/3 qPCR, Luciferase reporter assay, Western blot, RIP osteosarcoma tissues, cell lines (KHOS, 143B, SAOS-2, U2OS,MG-63,hFOB 1.19, HEK-293T) down-regulated GAS5 and ARHI levels were significantly reduced, while miR-221 increased, both in osteosarcoma tissues and cells. Overexpression of GAS5 suppressed the proliferation, migration, and epithelial-mesenchymal transition (EMT) of osteosarcoma cells.GAS5 could directly bind to miR-221 to decrease miR-221 expression and enhance ARHI expression. The effect of GAS5 overexpression on the proliferation, migration and EMT was reversed by miR-221 mimics or ARHI siRNA in osteosarcoma cells.GAS5 suppressed tumor volume, Ki-67 and PCNA staining, and EMT process in the development of osteosarcoma in vivo.Taken together, lncRNA GAS5 functions as a competing endogenous RNA for miR-221 to suppress cell growth and EMT in osteosarcoma by regulating the miR-221/ARHI pathway. 28519068 2017 Long Noncoding RNA GAS5 Suppresses Cell Growth and Epithelial-Mesenchymal Transition in Osteosarcoma by Regulating the miR-221/ARHI Pathway. 456 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 cervical cancer C53 NA qPCR, Western blot, RIP etc. cervical cancer tissues, cell lines (SiHa, HT-3, SW756 and ME-180) down-regulated GAS5 expression was decreased in cervical cancer tissues and cells.GAS5 overexpression suppressed cervical cancer cell proliferation, invasion, and apoptosis. GAS5 was able to directly bind to miR-196a and miR-205 to downregulate their expression.Moreover, GAS5 induced forkhead box protein O1 and phosphatase and tensin homolog expression by repressing miR-196a and miR-205, respectively. Exogenous expression of GAS5 hindered tumor growth in vivo by downregulating miR-196a and miR-205. Upregulation of GAS5 suppressed cell proliferation, invasion, and apoptosis of cervical cancer cells by downregulating miR-196a and miR-205, contributing to our understanding the pathogenesis of cervical cancer and development of long non-coding RNA-mediated clinical therapy against this disease. 28671039 2017 LncRNA GAS5 suppresses the tumorigenesis of cervical cancer by downregulating miR-196a and miR-205. 457 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay etc. GC tissues down-regulated We showed that GAS5 expression was decreased in GC tissue and inversed correlated with up-regulated expression of miR-23a. GAS5 negatively regulated miR-23a expression in GC cells. The bio-informatics prediction showed putative miR-23a binding sites within GAS5 transcripts. Furthermore, our data indicated the positive regulation of GAS5 on the miR-23a target, MT2A, wherein GAS5 suppressed the negative regulation of miR-23a on MT2A by binding its 3'UTR. Additionally, the expression of MT2A was also decreased in GC tissues, showing a positive or negative correlation with GAS5 or miR-23a, respectively. 27827524 2016 Long non-coding RNA GAS5 acts as a molecular sponge to regulate miR-23a in gastric cancer. 458 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA qPCR, RNAi, Western blot, ISH, MTT assay etc. cell lines (MCF-7 and MDA-MB-231) down-regulated This negative correlation between miR-21 and GAS5 is also seen in breast tumor specimens. Of interest, GAS5 can also repress miR-21 expression. Whereas ectopic expression of GAS5 suppresses, GAS5-siRNA increases miR-21 expression. Experiments with in vitro cell culture and xenograft mouse model suggest that GAS5 functions as a tumor suppressor. 23933812 2013 Negative regulation of lncRNA GAS5 by miR-21. 459 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 melanoma NA M8720/3 qPCR melanoma tissues, cell lines (A2058, B16, M21, MM200, MEL-RM and A375) down-regulated the expression of GAS5 was down-regulated in melanoma tissues compared to adjacent normal tissues. Finally, we suggested that GAS5 inhibited the growth of melanoma through miR-137 in vivo. 28386376 2017 Long non-coding RNA GAS5 inhibits tumorigenesis via miR-137 in melanoma 460 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 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. 461 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 non small cell lung cancer C34 M8046/3 qPCR, Dual-luciferase reporter assay, MTT assay etc. NSCLC tissues, cell lines (A549, H838, H157, HCC827) down-regulated GAS5 was down-regulated in NSCLC tissues and cells and was negatively correlated with miR-23a expression.GAS5 directly interacted with miR-23a and reversely regulate its expression. miR-23a overexpression markedly promoted NSCLC cell proliferation and invasion, while GAS5 overexpression dramatically inhibited NSCLC cell proliferation, invasion and promoted apoptosis. 28059053 2017 Long noncoding RNA GAS5 suppresses tumorigenesis by inhibiting miR-23a 5 expression in non-small cell lung cancer. 462 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 prostate cancer C61.9 NA qPCR, RNAi, Western blot, Dual-luciferase reporter assay, Cell proliferation assay, ISH etc. prostate cancer tissues, cell lines (PC3, DU145, and LNCaP) down-regulated The lncRNA GAS5 levels were reduced significantly in the PCa tissues and cell lines. A low exposure of lncRNA GAS5 caused AKT/mTOR signaling pathway activation in PC3 cells. In addition, over-exposure of lncRNA GAS5 was proven to significantly decelerate PCa cell progression in vitro and tumor growth in vivo through inactivating the AKT/mTOR signaling pathway.In this research, the exposure levels of the main components of the AKT/mTOR signaling pathway, including AKT, mTOR, and S6K1, all of which are tumorrelated genes, were assessed at total and at phosphorylation protein levels in vitro and in vivo. 27743383 2016 LncRNA GAS5 inhibits proliferation and progression of prostate cancer by targeting miR-103 through AKT/mTOR signaling pathway. 463 GCASPC lnc-SOD2-1, RP1-56L9.7-001, TCONS_00011605 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. 464 Gm15290 NA NA NA NA non small cell lung cancer C34 M8046/3 qPCR, Western blot cell lines (SK-MES-1, A549, NCI-H460) up-regulated First,lncRNA Gm15290 was markedly upregulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively. The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p. Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2 and SHMT2. 28474572 2017 LncRNA Gm15290 Promotes Cell Proliferation and Invasion in Non-Small Cell Lung Cancer Through Directly Interacting With and Suppressing the Tumor Suppressor miR-615-5p 465 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 neuroblastoma NA M9500/3 qRT-PCR, Western blot Human neuroblastoma cell line (SH-SY5Y), 293T cells up-regulated Expressions of lncRNA-H19 and miR-675 were upregulated in neuroblastoma cells,and were downregulated by AP.AP was also identified to upregulate CD44.We next found AP affected SH-SY5Y cells through downregulating miR-675.Key kinases in the PI3K/AKT and JAK/STAT pathways were downregulated by AP stimulation,while these downregulations were abrogated by miR-675 overexpression. KIF1B isoform β (KIF1Bβ) is proved to be a target of miR-675. 29465760 2018 Angelica sinensis polysaccharide inhibits proliferation, migration, and invasion by downregulating microRNA-675 in human neuroblastoma cell line SH-SY5Y. 466 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 nasopharyngeal cancer C11 NA qPCR, Western blot, RIP etc. cell lines (NP69, NPC, CNE2) up-regulated Herein, we found that H19 was overexpressed in NPC tissues and poorly differentiated cell lines. Knockdown of H19 significantly inhibited the invasive ability of NPC cells. Moreover, H19 affected the expression of enhancer of zeste homolog 2 (EZH2), which has also been observed to be up-regulated in NPC and to promote cell invasion. Rather than direct interaction, H19 regulated EZH2 expression by suppressing the activity of miR-630, which is a repressor of EZH2 and interacts with H19 in a sequence-specific manner. Furthermore, H19 inhibited E-cadherin expression and promoted cell invasion of NPC cells via the miR-630/EZH2 pathway 27040767 2016 Long noncoding RNA H19 regulates EZH2 expression by interacting with miR-630 and promotes cell invasion in nasopharyngeal carcinoma 467 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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 468 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 cholangiocarcinoma NA M810/3 qPCR, Western blot, RIP, Luciferase reporter assay cell line (QBC939) differential expression We identified that two lncRNAs, H19 and HULC, were differentially expressed among all the samples under the treatment of hypoxic or inflammatory factors, and they were shown to be stimulated by short-term oxidative stress responses to H2O2 and glucose oxidase in CCA cell lines. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4. 27809873 2016 LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner 469 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 liver cancer C22.0 NA qPCR, RNAi, Western blot, ChIP, Dual-luciferase reporter assay, Cell proliferation assay etc. cell lines (Hep3B and HepG2) up-regulated Herein, we demonstrate miR675 overexpression promotes and silencing miR675 attenuated liver cancer cell growth in vitro and in vivo. Mechanistically, miR675 inhibits the heterochromatin1 isoform HP1α expression in human liver cancer cells which causes a dramatically decrease of the total histone H3 lysine 9 trimethylation (H3K9me3), histone H3 lysine 27 trimethylation (H3K27me3) and a increase of histone H3 lysine 27 acetylation(H3K27Ac). Notably, a significant reduction of the H3K9me3 and H3K27me3 and the increment of H3K27Ac occupancy on the promoter region of EGR1 triggers EGR1 transcription, translation, sumoylation and activation which upregulates lincRNA H19. 26376677 2015 miR675 upregulates long noncoding RNA H19 through activating EGR1 in human liver cancer. 470 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 tongue squamous cell carcinoma C02 M8070/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown cell line (CAL27, SCC9, SCC15, SCC25, FaDu), TSCC tissues up-regulated Depletion of H19 impaired the migration and invasion ability of TSCC cells.Mechanisticlly,H19 functions as a competing endogenous RNA (ceRNA) to sponge miRNA let-7a,leading to an increase in a let-7a target, the key regulator of tumor metastasis HMGA2,which is enriched in TSCC tissues and cell lines.Intriguingly,inhibition of let-7a significantly rescued short hairpin H19 (shH19) induced decrease of TSCC migration and invasion.H19/let-7a/HMGA2/EMT axis plays a critical role in the regulation of TSCC migration and invasion,which may provide a new therapeutic target for TSCC cancers. 29523225 2018 H19 facilitates tongue squamous cell carcinoma migration and invasion via sponging miR-let-7. 471 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 prostate cancer C61.9 NA qPCR, Western blot etc. cell lines (P69, M12) down-regulated In this study, we found that long non-coding RNA H19 (H19) and H19-derived microRNA-675 (miR-675) were significantly downregulated in the metastatic prostate cancer cell line M12 compared with the non-metastatic prostate epithelial cell line P69. Upregulation of H19 in P69 and PC3 cells significantly increased the level of miR-675 and repressed cell migration; however, ectopic expression of H19 in M12 cells could not increase the level of miR-675 and therefore had no effect on cell migration. 24988946 2014 lncRNA H19/miR-675 axis represses prostate cancer metastasis by targeting TGFBI. 472 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, Luciferase reporter assay, Western blot, RIP, RNAi clear cell renal cell carcinoma tissues, cell lines (786-O) up-regulated lncRNA-H19 was high expressed and negatively correlated with miR-29a-3p in ccRCC.miR-29a-3p was identified as a direct target of lncRNA-H19. down-regulated lncRNA-H19 could affect the expression of miR-29a-3p targeting E2F1 with competitively binding miR-29a-3p.lncRNA-H19 knockdown inhibited cells migration and invasion, but this effect was attenuated by co-transfection of lncRNA-H19 siRNA and miR-29a-3p inhibitor. Over expression of E2F1 could rescue lncRNA-H19 siRNA induced suppression on cell migration and invasion in ccRCC cells.These results show a possible competing endogenous RNAs regulatory network involving lncRNA-H19 regulates E2F1 expression by competitively sponging endogenous miR-29a-3p in ccRCC. 29214011 2017 Long non-coding RNA H19 regulates E2F1 expression by competitively sponging endogenous miR-29a-3p in clear cell renal cell carcinoma. 473 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 osteosarcoma NA M9180/3 qPCR, Western blot, MTT assay etc. cell line (hFOB1.19) down-regulated Both H19 and miR-675 levels in hFOB1.19 cells were significantly decreased by overexpression of miR-141 than that in control group, but their expression were reversed by miR-141 inhibitor. In addition, expression of H19 and miR-675 in adjacent tissues were both significantly higher than that in tumor tissues. However, cell viability was significantly decreased by co-transfection of siRNA-H19/miR-675 inhibitor and miR-141 inhibitor compared with the miR-141 inhibitor group with time increasing, suggesting that the promote role of miR-141 inhibitor on cell proliferation may be suppressed by silencing H19 or miR-675 inhibitor. 27186302 2016 miR-141 modulates osteoblastic cell proliferation by regulating the target gene of lncRNA H19 and lncRNA H19-derived miR-675. 474 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 osteosarcoma NA M9180/3 qPCR, RNAi, RIP, ChIP, Flow cytometry assay etc. cell line (MG63) up-regulated H19 is overexpressed after transfection with H19 lentivirus in MG63 cells, while silenced after transfection with shH19 lentivirus. Functionally, overexpression of H19 promoted cell migration and invasion of MG63 cells compared with the control. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family. 27008415 2016 H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma. 475 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 thyroid cancer C73.9 NA qPCR, Luciferase reporter assay etc. thyroid cancer tissues, cell lines (TPC-1, NIM, Nthy-ori 3-1 and BCPAP) up-regulated Our results suggest that H19 functions as a competitive endogenous RNA (ceRNA) by acting as a sink for miR-17-5p, revealing a potential ceRNA regulatory network involving H19 and miR-17-5p with a role in the modulation of YES1 expression. This mechanism may contribute to a better understanding of thyroid cancer pathogenesis and provide new insights into the treatment of this disease. 27093644 2016 Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer 476 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colon cancer C18 NA qPCR, Northern blot, ISH etc. CRC tissues up-regulated By quantitative reverse transcription-polymerase chain reaction, both H19 and miR-675 were found to be upregulated in human colon cancer cell lines and primary human colorectal cancer (CRC) tissues compared with adjacent non-cancerous tissues. Our findings demonstrate that H19-derived miR-675, through downregulation of its target RB, regulates the CRC development and thus may serve as a potential target for CRC therapy. 19926638 2010 Oncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal cancer. 477 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 acute myeloid leukemia NA M9861/3 Western blot, luciferase reporter assay, etc. acute myelocytic leukemia tissues, cell lines (HL-60, HEK-193T) up-regulated it was demonstrated that the knockdown of lncRNA H19 resulted in increased expression of hsa-microRNA-19a/b and decreased expression of inhibitor of DNA binding 2 (ID2) in AML cells. 28765931 2017 LncRNA H19 regulates ID2 expression through competitive binding to hsa-miR-19a/b in acute myelocytic leukemia. 478 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gallbladder cancer C23.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. GBC tissues, cell lines (GBC-SD, EHGB-1 and NOZ) up-regulated We demonstrated H19 was overexpressed and negatively correlated with miR-342-3p in GBC. H19 silencing down-regulated, whereas over-expression enhanced the expression of miR-342-3p targeting FOXM1 through competitively 'sponging' miR-342-3p. Furthermore, H19 knockdown inhibited both cells invasion and proliferation, but this effects was attenuated by co-transfection of siRNA-H19 and miR-342-3p inhibitor in GBC cells. 27716361 2016 Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancer. 479 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gallbladder cancer C23.9 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. GBC tissues, cell lines (GBC-SD, EH-GB1, and NOZ) up-regulated The expression of H19 and AKT2 were significantly elevated in GBC tissues, and the level of miR-194-5p is markedly decreased. Moreover, H19 elevation was significantly associated with tumor size. In addition, overexpression of H19 in GBC-SD cells downregulated miR-194-5p and markedly increased AKT2 expression, and miR-194-5p mimic reversed these effects. Eventually, GBC cells were arrested in G0/G1-phase after H19 knockdown, inhibition of miR-194-5p markedly promoted cells into S-phase and co-transfection of siH19, and miR-194-5p inhibitor exerted mutually counter-regulated effects on cell cycle. 26803515 2016 Long noncoding RNA H19 contributes to gallbladder cancer cell proliferation by modulated miR-194-5p targeting AKT2. 480 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, RNAi, Western blot etc. pancreatic cancer tissues, cell lines (PANC-1, SW1990, AsPC-1, BxPC-3, CFPAC-1 etc.) up-regulated The levels of H19 was overexpressed in PDAC and was upregulated remarkably in primary tumors which subsequently metastasized, compared to those did not metastasis. H19 promoted PDAC cell invasion and migration. An important role of H19 in regulating metastasis of PDAC and provides some clues for elucidating the lncRNAmiRNA functional network in cancer. 24920070 2014 H19 promotes pancreatic cancer metastasis by derepressing let-7's suppression on its target HMGA2-mediated EMT. 481 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 non small cell lung cancer C34 M8046/3 qPCR, RNAi, ChIP, Luciferase reporter assay, Flow cytometry assay etc. cell lines (A549, L78, H460, 16HBE) up-regulated The mRNA levels of lncRNA H19 in NSCLC tissues and cells were significantly higher than the adjacent tissues and normal cells, respectively. The expression of H19 increased or decreased accordingly with the overexpression and knockdown of c-Myc. The activity of the promoter of H19 was strengthened by c-Myc. While the expression of miR-107 increased or decreased with the overexpression and knockdown of H19, respectively. The number of cells in G2/M stage decreased significantly with the knockdown of H19 and miR-107 compared with the control group. 26722426 2015 c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer. 482 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioblastoma NA M9440/3 RT-qPCR, Western blot, in vitro knockdown, RIP glioblastoma tissues, cell lines (A172, LN229, U87MG, LN18 and T98G) up-regulated Most importantly,we provide a mechanistic perspective about the role of H19 in glioblastoma cells,by showing that its expression is inversely linked to that of NKD1,a negative regulator of Wnt pathway, suggesting that H19 might regulate NKD1 transcription via EZH2-induced H3K27 trimethylation of its promoter.Indeed, we showed that H19 binds EZH2 in glioblastoma cells,and that EZH2 binding to NKD1 and other promoters is impaired by H19 silencing.The molecular mechanisms described so far for an oncogenic role of H19 in GBM range from H19 processing to produce miR-675 to a function as sponge for miR-29a, in turn boosting tumor angiogenesis. 29643989 2018 The lncRNA H19 positively affects the tumorigenic properties of glioblastoma cells and contributes to NKD1 repression through the recruitment of EZH2 on its promoter. 483 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colon cancer C18 NA qPCR, western blot, luciferase reporter assay colon cancer tissues, cell lines (SW480, HT-29, colon26, HCT-8, and RKO) differential expression H19 shRNA strongly reduced the tumor growth and tumor volume. H19 shRNA also inhibited metastasis via suppressing hepatic metastases and the expression of metastasis-related proteins. Taken together, our research indicated an H19-miR138-HMGA1 pathway in regulating the migration and invasion of colon cancer, 28358427 2017 H19 promotes the migration and invasion of colon cancer by sponging miR-138 to upregulate the expression of HMGA1 484 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 lung cancer C34 NA qPCR, Western blot etc. lung cancer tissues, cell lines (A549, H1975, HCC827, Calu-3, 2BS and MRC-5) up-regulated H19 was highly expressed in both lung cancer tissues and cells. Suppression of H19 significantly decreased A549 cell viability, migration, and invasion, but promoted apoptosis. Overexpression of H19 promoted cell migration, invasion, and EMT process.miR-484 was a target of H19 and overexpression of it reversed the effects of H19 on EMT. miR-484 regulated the expression of ROCK2.Mechanistic study revealed that suppressing H19 decreased the expression of proteins in JNK pathway, and ROCK2 was the main downstream molecule of H19.H19 promoted EMT in lung cancer A549 cells by negatively regulating miR-484. 29219208 2018 LncRNA H19 promotes epithelial-mesenchymal transition (EMT) by targeting miR-484 in human lung cancer cells. 485 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot etc. cell lines (Huh-7, MHCC-97H, HepG2 etc.) up-regulated The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells as compared with the control group. Inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3β/Cdc25A signaling pathway. 24939300 2014 Downregulation of LncRNAH19 and MiR-675 promotes migration and invasion of human hepatocellular carcinoma cells through AKT/GSK-3β/Cdc25A signaling pathway. 486 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA qPCR, Northern blot, ISH etc. CRC tissues up-regulated By quantitative reverse transcription-polymerase chain reaction, both H19 and miR-675 were found to be upregulated in human colon cancer cell lines and primary human colorectal cancer (CRC) tissues compared with adjacent non-cancerous tissues. Our findings demonstrate that H19-derived miR-675, through downregulation of its target RB, regulates the CRC development and thus may serve as a potential target for CRC therapy. 19926638 2010 Oncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal cancer. 487 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioma NA M9380/3 qRT-PCR, Luciferase reporter assay glioma tissues, human glioma cell lines (A172, U251, U87, U373 and U563) up-regulated H19 expression was upregulated and miR 152 expression was downregulated in human glioma cell lines.H19 downregulation or miR-152 upregulation suppressed glioma cell proliferation and invasion in vitro.Moreover, H19 and miR-152 directly regulated each other.Furthermore,decreased miR-152 expression alleviated si-H19-induced inhibitory effects on proliferation and invasion in glioma cells.As expected, H19 silencing hindered glioma growth in vivo. 29422115 2018 Long non-coding RNA H19 promotes proliferation and invasion in human glioma cells by downregulating miR-152. 488 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioma NA M9380/3 qPCR, Cell transfection, Western blot etc. glioma tissues, cell line (HEK294) up-regulated H19 was up-regulated in microvessels from glioma tissues and glioma-associated endothelial cells (GEC) cultured in glioma conditioned medium. Knockdown of H19 suppressed glioma-induced endothelial cell proliferation, migration and tube formation in vitro and meanwhile up-regulated the expression of miR-29a. Bioinformatics analysis and luciferase reporter assay defined that H19 mediated the above effects via directly binding to miR-29a. 27543358 2016 Long non-coding RNA H19 regulates glioma angiogenesis and the biological behavior of glioma-associated endothelial cells by inhibiting microRNA-29a. 489 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay, MTT assay etc. primary glioma tissues, cell lines (U373, A172, U251, T98G and U87MG) up-regulated lncRNA-H19 was specifically upregulated in glioma cell lines and promoted glioma cell growth through targeting miR-140. Knockdown of H19 inhibited the proliferation and invasion of human glioma cell and suppressed its metastasis in vitro and in vivo. In addition, miR-140 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) regulation was required in H19 induced glioma cell growth. These findings indicated that H19 might regulate the tumor growth and metastasis via miR-140 dependent iASPP regulation. 27693036 2016 The lncRNA H19 interacts with miR-140 to modulate glioma growth by targeting iASPP. 490 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioma NA M9380/3 microarray, qPCR, RNAi, Western blot, Luciferase reporter assay etc. glioma tissues, cell lines (U87, U251 etc.) up-regulated By analyzing glioma gene expression data sets, we found increased H19 in high grade gliomas. H19 depletion via siRNA inhibited invasion in glioma cells. Further, we found H19 positively correlated with its derivate miR-675 expression and reduction of H19 inhibited miR-675 expression. 24466011 2014 Long non-coding RNA H19 promotes glioma cell invasion by deriving miR-675. 491 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric cancer C16 NA qPCR, RNAi, Luciferase reporter assay etc. gastric cancer tissues up-regulated H19 expression was found to be inversely correlated to miR-141 expression in gastric cancer cells and tissues. H19 promotes malignancy including proliferation and invasion whereas miR-141 suppresses malignancy in human cancer cells. MiR-141 binds to H19 in a sequence specific manner, and suppresses H19 expression and functions including proliferation and invasion. MiR-141 could also regulate H19 target genes and miR-141 inhibitor restores H19 siRNA function, while H19 regulates miR-141 target gene ZEB1 26160158 2015 The Interaction Between MiR-141 and lncRNA-H19 in Regulating Cell Proliferation and Migration in Gastric Cancer 492 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 493 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 bladder cancer C67 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. bladder cancer tissues, cell lines (RT4, HT-1376, 5637, 253J, TCCSUP, T24,and J82) up-regulated We found that miR-675 expression levels were remarkably increased in bladder cancer tissues as compared with adjacent noncancerous tissues or normal bladder tissue from health donors; moreover, enhanced miR-675 expression was also observed in bladder cancer cell lines. Ectopic expression of H19 significantly increased bladder cancer cell proliferation and miR-675 expression in vitro 26198047 2015 H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation 494 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, RNAi, Flow cytometry assay, Cell proliferation assay etc. cell lines (U87 and U252) up-regulated We showed that overexpression of H19/miR-675 enhanced the aggressive phenotype of breast cancer cells including increased cell proliferation and migration in vitro, and increased tumor growth and metastasis in vivo. Moreover, we identified ubiquitin ligase E3 family (c-Cbl and Cbl-b) as direct targets of miR-675 in breast cancer cells. Using a luciferase assay, we demonstrated that H19, through its microRNA, decreased both c-Cbl and Cbl-b expression in all breast cancer cell lines tested. 26353930 2015 H19 non coding RNA-derived miR-675 enhances tumorigenesis and metastasis of breast cancer cells by downregulating c-Cbl and Cbl-b. 495 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 bladder cancer C67 NA qPCR, Western blot, Luciferase reporter assay etc. bladder carcinoma tissues, cell lines (BIU, 5673, EJ, T24) up-regulated up-regulating H19 antagonized miR-29b-3p-mediated proliferation, migration and EMT suppression in BC cells. Furthermore,H19 knockdown partially reversed the function of miR-29b-3p inhibitor on DNMT3B and facilitated miR-29b-3p-induced MET. Taken together, we demonstrated for the first time that H19 might function as ceRNA (competing endogenous RNA) for miR-29b-3p and relieve the suppression for DNMT3B, which led to EMT and metastasis of BC. Our findings highlight a novel mechanism of H19 in progression of BC and provide H19/miR-29b-3p/ DNMT3B axis as a promising therapeutic target for BC. 28779971 2017 lncRNA H19 regulates epithelial–mesench mal transition and metastasis of bladder cancer by miR-29b-3p as competing endogenous RNA 496 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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 β-catenin in CRC. 28164117 2017 The lncRNA H19 Promotes Cell Proliferation by Competitively Binding to miR-200a and Derepressing β-Catenin Expression in Colorectal Cancer. 497 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA qPCR, Western blot, RIP, Luciferase reporter assay etc. CRC tissues, cell lines (SW620, HCT-116) up-regulated We showed that overexpression of H19/miR-675 enhanced the aggressive phenotype of breast cancer cells including increased cell proliferation and migration in vitro, and increased tumor growth and metastasis in vivo. Moreover, we identified ubiquitin ligase E3 family (c-Cbl and Cbl-b) as direct targets of miR-675 in breast cancer cells. Using a luciferase assay, we demonstrated that H19, through its microRNA, decreased both c-Cbl and Cbl-b expression in all breast cancer cell lines tested. 26068968 2015 The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer. 498 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric cancer C16 NA qPCR, Western blot GC tissues, GC cell lines (BGC823 and SGC7901) up-regulated the expression levels of H19 lncRNA in GC tissue samples were significantly higher when compared with that in matched benign adjacent tissue samples.H19 silenced GC cells exhibited significantly increased let-7c expression and decreased HER2 protein expression levels. 29207111 2017 H19 functions as a competing endogenous RNA to regulate human epidermal growth factor receptor expression by sequestering let?7c in gastric cancer. 499 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric cancer C16 NA qPCR, Western blot etc. Gastric Cancer tissues, cell lines (AGS and GES-1) up-regulated we found that H19 depended on miR-675 to enhance the proliferation and invasion of gastric cancer AGS cells, and the expression of miR-675 was positively correlated with H19 in patients with gastric cancer. Subsequently, the tumor-suppressor runt domain transcription factor 1 (RUNX1) was confirmed to be a downstream molecule of H19/miR-675 axis, since overexpression of H19 or miR-675 significantly decreased RUNX1 expression in AGS cells, and knockdown of H19 or miR-675 enhanced RUNX1 expression. 26931432 2016 Long Noncoding RNA H19-Derived miR-675 Enhances Proliferation and Invasion via RUNX1 in Gastric Cancer Cells 500 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric cancer C16 NA qPCR, RNAi, Western blot etc. gastric cancer tissues, cell lines (AGS, MGC803 etc.) up-regulated The expression levels of H19 and miR-675 in five gastric cancer cell lines were correlated with each other. We next assessed the correlation of miR-675 and H19 expression in 24 human gastric cancer tissues. The expression of H19 and miR-675 in gastric cancer tissues was correlated with each other. 24388988 2014 The long non-coding RNA H19-derived miR-675 modulates human gastric cancer cell proliferation by targeting tumor suppressor RUNX1. 501 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 502 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 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. 503 HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 ENSG00000241388 NR_024345 GRCh38_12:120941728-120980965 non small cell lung cancer C34 M8046/3 qRT-PCR, Luciferase reporter assay NSCLC tissues, NSCLC cell lines (H1299, H1650, A549, and PC9) up-regulated HNF1A-AS1 was upregulation in NSCLC tissues and cell lines.High HNF1A-AS1 expression was associated with patients' advanced TNM stage and lymph node metastasis.Reduced HNF1A-AS1 expression inhibited lung cancer cells proliferation, invasion and increased cells apoptosis rate. Bioinformatics analysis and luciferase reporter assay revealed that HNF1A-AS1 interacted with miR-17-5p by directly targeting it. Rescue experiments showed that miR-17-5p suppression reversed the tumor-suppressing role of HNF1A-AS1 knockdown on NSCLC progression. 29289833 2017 Long non-coding RNA HNF1A-AS1 promotes cell proliferation and invasion via regulating miR-17-5p in non-small cell lung cancer. 504 HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 ENSG00000241388 NR_024345 GRCh38_12:120941728-120980965 esophageal squamous cell cancer NA NA qPCR, Western blot etc. ESCC tissues, cell lines (KYSE70, KYSE450, EC109 and EC970) up-regulated upregulated expression of HAS1 was detected in ESCC tissues and four human ESCC cell lines (KYSE70, KYSE450, EC109 and EC970) compared with normal tissues and cell lines.HAS1-siRNA counteracted the effect of miR-214 inhibitor on cell viability and mobility in EC109 cells. HAS1-siRNA abated the role of miR-214 inhibitor in promoting tumor growth and metastasis. HAS1-miR-214-SOX-4 pathway in regulating the growth and metastasis of ESCC, providing a promising target for ESCC therapy. 28656277 2017 HNF1A?AS1 promotes growth and metastasis of esophageal squamous cell carcinoma by sponging miR?214 to upregulate the expression of SOX-4. 505 HNF1A-AS1 HNF1A-AS1, C12orf27, NCRNA00262 ENSG00000241388 NR_024345 GRCh38_12:120941728-120980965 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. fresh tumor tissues, cell lines (HepG2, SMMC-7721, PLC/PRF/5, Huh7) down-regulated First, we revealed: HNF1A-AS1 was frequently overexpressed in HCC tissues and cell lines and its relative high expression was closely related to larger tumor size, multiple tumor lesions, poor differentiation and advanced TNM stage. Then we found: HNF1A-AS1 functioned as an oncogene in tumor growth and apoptosis through sponging tumor-suppressive hsa-miR-30b-5p (miR-30b) and de-repressing Bcl-2. Further experiments identified: HNF1A-AS1-miR-30b axis significantly promoted autophagy under starvation and ATG5 was first proved to be a target of miR-30b. 27084450 2016 Long non-coding RNA HNF1A-AS1 functioned as an oncogene and autophagy promoter in hepatocellular carcinoma through sponging hsa-miR-30b-5p 506 HOST2 CERNA2, HOST2, lncRNA-HOST2 NR_134505 NA breast cancer C50 NA qPCR, Western blot etc. breast cancer tissues, cell lines(MDA-MB-231, MDA-MB-468, SK-BR-3, MCF-7, and MCF-10A) up-regulated Compared with adjacent normal tissues,HOST2 expression was higher but let-7b expression lower in breast cancer tissues. HOST2 expression in breast cancer cells was remarkably increased compared with that in the normal breast epithelial MCF-10A cells.In MCF-7 cells,in comparison with the blank and NC groups,expressions of HOST2 and c-Myc were reduced,but let-7b expression was remarkably elevated in the siHOST2 and let-7b mimic groups,the let-7b inhibitor group exhibited higher expressions of HOST2 and c-Myc but lower let-7b expression.Overexpression of HOST2 could promote cell motility,migration and invasion,thus enhancing the growth of breast cancer tumor. By inhibiting HOST2,opposite trends were found.LncRNA HOST2 promotes cell migration and invasion by inhibiting let-7b in breast cancer patients. 29236319 2018 Effects of long non-coding RNA HOST2 on cell migration and invasion by regulating MicroRNA let-7b in breast cancer. 507 HOST2 CERNA2, HOST2, lncRNA-HOST2 NR_134505 NA ovarian cancer C56.9 NA qPCR, Western blot etc. ovarian cancer tissues, cells lines (OVCAR3) up-regulated The data showed that HOST2 was obviously upregulated in an EOCderived cell line, OVCAR-3, compared with the other tested cell lines, including MKN28, Huh-7, HepG2, McF-7,DU145, A357, MG63, Hep-2, ARK2 and Hela. HOST2 promotes tumor cell migration, invasion and proliferation in epithelial ovarian cancer by working in key aspetcs of biological behaviors. 25292198 2014 LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b. 508 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 renal cancer C64.9 NA qPCR, Western blot, RIP etc. cell lines (86-O, ACHN) up-regulated We found that HOTAIR expression is inversely correlated to miR-141 expression in renal carcinoma cells. HOTAIR promotes malignancy, including proliferation and invasion, whereas miR-141 suppresses malignancy in human cancer cells. miR-141 binds to HOTAIR in a sequence-specific manner and suppresses HOTAIR expression and functions, including proliferation and invasion. 24616104 2014 Long non-coding RNA HOTAIR is targeted and regulated by miR-141 in human cancer cells. 509 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, RNAi, ChIP, MTT assay etc. cell lines (BxPC3, CAPAN2, CFPAC1, PANC04.03, PANC1, SW1990 and HEK293T) differential expression we studied the effect of ectopic EZH2 expression to the silencing of miR-34a, and identified HOTAIR as an interacting partner to induce heterochromatin formation during miR-34a repression.We then showed that HOTAIR played a critical role in EZH2-mediated repression of miR-34a, as knockdown of HOTAIR attenuated the miR-34a inhibition effect in EZH2-overexpressing HPDE cells.HOTAIR physically interacted with miR-34a promoter,and the EZH2-interacting region located at 5' HOTAIR RNA was essential in repressing miR-34a and promoting cell proliferation. 27594424 2017 EZH2 coupled with HOTAIR to silence MicroRNA-34a by the induction of heterochromatin formation in human pancreatic ductal adenocarcinoma. 510 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 chondrosarcoma NA M9220/3 qPCR, RNAi, Western blot, Luciferase reporter assay, CCK-8 assay etc. chondrosarcoma tissues, cell lines (HC-a, SW1353, OUMS-27, HCS-2/8, JJ012) up-regulated HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. Functional experiments reveal that HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo. In addition to cycle arrest and apoptosis, knockdown of HOTAIR inhibits autophagy, which favors cell death. Mechanistically, we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions,which markedly silences miR-454-3p expression. Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p,initiate HOTAIR deficiency-induced apoptosis and reduce autophagy. 28182000 2017 Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth. 511 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gallbladder cancer C23.9 NA qPCR, Northern blot, RIP, in vitro knockdown etc. gallbladder cancer tissues, cell lines (GBC-SD, SGC-996,NOZ, EH-GB2 etc.) up-regulated The HOTAIR transcripts were expressed at higher levels in the tumor tissues compared with adjacent normal tissues, indicating that HOTAIR was frequently up-regulated in GBC.A positive correlation between c-Myc and HOTAIR mRNA levels was observed in gallbladder cancer tissues. HOTAIR is a c-Myc-activated driver of malignancy, which acts in part through repression of miRNA-130a. 24953832 2014 Long non-coding RNA HOTAIR, a c-Myc activated driver of malignancy, negatively regulates miRNA-130a in gallbladder cancer. 512 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 513 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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 514 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 endometrial cancer NA M8380/3 qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP Human EC cell lines (HEC-1-A and Ishikawa) up-regulated MiR-646 expression was significantly decreased both in human EC tissues and cell lines compared with the control.Moreover, miR-646 expression was negatively related to HOTAIR in human EC tissues.miR-646 overexpression considerably attenuated the E2-promoted viability, migration and invasion of Ishikawa and HEC-1-A cells in vitro.In addition, HOTAIR was confirmed to regulate the viability, migration and invasion of EC cells through negative regulating miR-646.More importantly, we also demonstrated that NPM1 was the target of miR-646,and HOTAIR promoted NPM1 expression through interacting with miR-646 in EC cells.HOTAIR was well documented in recruiting PRC2 components and subsequent chromosomal gene silencing via coordinated histone H3K27 methylation and H3K4 demethylation. 29466670 2018 Long non-coding RNA HOTAIR mediates the estrogen-induced metastasis of endometrial cancer cells via miR-646/NPM1 axis. 515 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 lung cancer C34 NA qPCR, Western blot, Flow cytometry assay etc. cell lines (A549, 95D, NCI-H460, HLamp and H838) up-regulated By using siRNAs and luciferase assays, we also demonstrated that Phox2a is a functional target of miR-326, and that miR-326 is regulated by long non-coding RNA HOTAIR through silencing HOTAIR. Enforced expression of miR-326 inhibited cell proliferation and migration in vitro and tumor growth in nude mice, decreased proportion of cells in S phase and increased cell apoptosis in both A549 and H838 cells. In addition, we found miR-326 bound to 3'UTR of Phox2a but not KLF3, and enforced expression of miR-326 decreased accumulation of Phox2a in both A549 and H838. Moreover, exogenous expression of Phox2a compromised inhibitory effects of miR-326 on cell proliferation and migration. We also found silencing of HOTAIR caused increased expression of miR-326. 27186394 2016 MiR-326 regulates cell proliferation and migration in lung cancer by targeting phox2a and is regulated by HOTAIR. 516 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 prostate cancer C61.9 NA qPCR, Western blot, in vitro knockdown etc. cell lines (DU145, PC3) down-regulated Silenced HOTAIR reduced EZH2 and DNMT1 protein expressions.On the contrary, exogenously expressed HOTAIR resisted PPI-inhibited EZH2 and DNMT1 protein expressions, EZH2 promoter activity and cell growth. Moreover, excessive EZH2 antagonized PPI-suppressed DNMT1 protein expression or vice versa.The interactions among HOTAIR, DNMT1 and EZH2, and reciprocal regulation of DNMT1 and EZH2 contribute to the overall responses of PPI. HOTAIR induced DNA methylation of miR-454-3p via recruiting EZH2 and DNMT1 to the promoter regions of miR-454-3p, this largely reduced miR-454-3p expression,thereby reducing apoptosis and inducing autophagy in human chondrosarcoma cells 29221985 2018 HOTAIR-mediated reciprocal regulation of EZH2 and DNMT1 contribute to polyphyllin I-inhibited growth of castration-resistant prostate cancer cells in vitro and in vivo. 517 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 bladder cancer C67 NA qPCR, Western blot, Northern blot etc. cell lines (HCV29, 5637, T24, J82, SW780) up-regulated We have identified cyclin J (CCNJ) gene, which is involved in cell cycle regulation, as a novel target for miR-205. Furthermore, a long non-coding RNA HOTAIR (HOX transcript antisense RNA) was observed to participate in the silencing of miR-205 in bladder cancer cells by breaking the balance of histone modification between H3K4me3 (histone H3 at lysine 4 methylation) and H3K27me3 on miR-205 promoter. 26469956 2015 Long non-coding RNA HOTAIR regulates cyclin J via inhibition of microRNA-205 expression in bladder cancer 518 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 519 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioma NA M9380/3 qPCR, Western blot etc. cell lines (U-87 MG) down-regulated The present study further demonstrated that miR-15b, HOTAIR, and p53 formed a mutually regulated loop. MiR-15b upregulated the expression of p53 but inhibited the expression of HOTAIR.In addition,miR-15b was able to regulate the expression of HOTAIR through p53.Furthermore,the examination of cell proliferation,apoptosis,and invasion revealed that both miR-15b and p53 inhibited the proliferation and invasion,but promoted the apoptosis,of glioma cells. In contrast,HOTAIR exerted effects that were the opposite of those exerted by miR-15b and p53 on glioma cells.The upregulation of HOTAIR suppressed the inhibitory effects of miR-15b and p53 on cell proliferation and invasion as well as the promoting effect of miR-15b and p53 on apoptosis. 29323737 2018 MiR-15b/HOTAIR/p53 form a regulatory loop that affects the growth of glioma cells. 520 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 renal cell carcinoma C64.9 NA qPCR, Western blot, RIP renal cell carcinoma tissues, cell lines (769-P and ACHN) up-regulated HOTAIR expression was upregulated, which was correlated with tumor progression, and miR-217 downregulated in Rcc tissues and cells.Importantly,HOTAIR expression was negatively correlated with miR-217 expression in Rcc tissues. 28492542 2017 LncRNA HOTAIR regulates HIF-1α/AXL signaling through inhibition of miR-217 in renal cell carcinoma 521 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (H1299, H23, H292, A549) up-regulated Down-regulation of HOTAIR suppressed tumorigenesis and metastasis of NSCLC via up-regulating the expression of miR-613. 29187267 2017 LncRNA-HOTAIR affects tumorigenesis and metastasis of non-small cell lung cancer by up-regulating miR-613 522 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colorectal cancer C19.9 NA qPCR, Luciferase reporter assay etc. cell lines (HCT116, SW480, LOVO, HT29, FHC) up-regulated HOTAIR knockdown promoted apoptosis and inhibited cell proliferation, migration and invasion in vitro and in vivo.Moreover, HOTAIR modulated the progression of colorectal cancer by competitively binding miR-197.Taken together, our study has identified a novel pathway through which HOTAIR exerts its oncogenic role,and provided a molecular basis for potential applications of HOTAIR in the prognosis and treatment of colorectal cancer. 29137688 2017 The long noncoding RNA HOTAIR promotes colorectal cancer progression by sponging miR-197 523 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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 524 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 pancreatic cancer C25 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. pancreatic cancer tissues, cell lines (BXPC3, CFPAC-1, Panc-1 and L3.6pl) up-regulated The long non-coding RNA, HOTAIR, was up-regulated in both pancreatic cancer cells and tissues, and HOTAIR suppressed the expression of miR-663b in pancreatic cancer by histone modification on H3K4me3 and H3K27me3 on miR-663b promoter. Further in vivo studies demonstrated that the stable overexpression of miR-663b or knock-down of HOTAIR inhibited tumor growth and was associated with IGF2 expression. 27895308 2016 Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2. 525 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (LNCaP, PC3, DU145, RWPE-1 etc.) up-regulated LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells. Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa. 23936419 2013 Genistein inhibits prostate cancer cell growth by targeting miR-34a and oncogenic HOTAIR. 526 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. cell lines (SKOV3, OVCAR3, and A2780) up-regulated The expression of HOTAIR and PIK3R3 in ovarian SKOV3 and OVCAR3 was increased compared with A2780 cells. The mRNA level of HOTAIR and PIK3R3 in ovarian cancer SKOV3 cells was decreased when transected with miR-214 or miR-217 compared to negative control. The mRNA and protein level of PIK3R3 was decreased when HOTAIR was silenced and the mRNA level of HOTAIR was decreased when PIK3R3 was silenced. The proliferation, migration and invasion was decreased in ovarian SKOV3 when HOTAIR or PIK3R3 was silenced. 26826873 2016 HOTAIR Promotes Proliferation, Migration, and Invasion of Ovarian Cancer SKOV3 Cells Through Regulating PIK3R3. 527 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, Western blot etc. cell lines (SKOV3, ES-2, OVCAR3, A2780, and COC1) down-regulated In this study, we report that HOTAIR may function as a ceRNA to regulate the expression of MAPK1 through competition for miR-1, miR-214-3p, or miR-330-5p in ovarian SKOV3 cells, providing a new insight in the treatment of ovarian cancer. 26117268 2015 HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion 528 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. cell lines (HepG2, Bel7404, PLC5, Huh7 etc.) up-regulated We found that Hotair was increased in HCC tissues compared to their adjacent non-tumor tissues and the normal liver tissues. Increased Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis. Further investigation revealed that Hotair knockdown dramatically inhibited cell viability and induced G1-phase arrest in vitro and suppressed tumorigenicity in vivo by promoting miR-218 expression. 26024833 2015 Hotair Mediates Hepatocarcinogenesis through Suppressing MiRNA-218 Expression and Activating P14 and P16 Signaling. 529 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 esophageal squamous cell cancer NA NA qPCR, Western blot, RIP, Luciferase reporter assay, Cell proliferation assay etc. ESCC tissues, cell lines (KYSE30, KYSE140, KYSE150, KYSE180, KYSE410, and KYSE510) up-regulated We found that HOTAIR was aberrantly upregulated in ESCC cells and that HOTAIR depletion inhibited proliferation and led to G1 cell cycle arrest in ESCC cells. Besides, we found that HOTAIR acted as an endogenous sponge to downregulate miR-1 expression by directly binding to miR-1. Furthermore, HOTAIR overturned the effect of miR-1 on the proliferation and cell cycle profile in ESCC cells, which involved the derepression of cyclin D1 (CCND1) expression, a target of miR-1. Taken together, our study elucidated a novel HOTAIR /miR-1/CCND1 regulatory axis in which HOTAIR acted as a competing endogenous RNA by sponging miR-1 and upregulated CCND1 expression, thereby facilitating the tumorigenesis of ESCC. 27816685 2016 Long Noncoding RNA HOTAIR Controls Cell Cycle by Functioning as a Competing Endogenous RNA in Esophageal Squamous Cell Carcinoma. 530 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioma NA M9380/3 Microarray, qRT-PCR, Western blot, Luciferase reporter assay glioma tissues, glioma cell lines (U87 and U251) up-regulated HOTAIR was aberrantly up-regulated in glioma tissues and was negatively correlated with miR-126-5p expression.Next, we determined that HOTAIR promote glioma progression by sponging miR-126-5p.Subsequently,glutaminase (GLS) was confirmed to be a direct target of miR-126-5p.Moreover,HOTAIR could modulate GLS expression by functioning as a competing endogenous RNA (ceRNA) for miR-126-5p. 29319172 2018 Long non-coding RNA HOTAIR acts as a competing endogenous RNA to promote glioma progression by sponging miR-126-5p. 531 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioma NA M9380/3 qPCR, RNAi, Luciferase reporter assay, Flow cytometry assay etc. glioma tissues, cell lines (HA1800, A172) up-regulated The results confirmed that HOTAIR mRNA expression was inversely correlated with miR-148b-3p expression in A172 glioma cells. The results showed that HOTAIR promotes factors associated with malignancy, including cell proliferation, cell cycle progression and invasion, whereas miR-148b-3p suppresses malignancy. Bioinformatics and luciferase reporter assays showed that miR-148b-3p modulates HOTAIR expression by directly targeting the HOTAIR gene sequence. 27446363 2016 miR-148b-3p inhibits malignant biological behaviors of human glioma cells induced by high HOTAIR expression. 532 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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 533 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 534 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, RNAi, Cell migration assay etc. ovarian cancer tissues, cell lines (SKOV3, A2780 and CP70) up-regulated HOTAIR was significantly upregulated. Furthermore, the upregulation of HOTAIR increased the proliferation, migration and invasion of ovarian cancer cells. By contrast, the knockdown of HOTAIR repressed cell invasion and viability. HOTAIR functioned as a ceRNA, and acted as a sink for miR-373, thereby regulating the expression of Rab22a. The upregulation of HOTAIR contributed to the malignant progression of ovarian cancer cells. 27484896 2016 LncRNA HOTAIR controls the expression of Rab22a by sponging miR-373 in ovarian cancer. 535 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, ChIP, Luciferase reporter assay etc. HCC tissues, cell lines (HepG2 and LO2) up-regulated The relative levels of FOXC1 and HOTAIR expression in HCC tissues and HepG2 cells were significantly higher than those in normal liver LO2 cells and adjacent carcinoma tissues. Overexpression of HOTAIR promoted HCC cell proliferation and progression of tumor xenografts. The present authors have demonstrated that FOXC1 binds to the upstream region of HOTAIR in HCC cells and that FOXC1 activates lncRNA HOTAIR expression in HCC HepG2 cells. 27895772 2016 HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma. 536 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, Western blot, CHIP-PCR, Dual-luciferase reporter assay etc. cell lines (MDA-MB-231 and MCF-7) up-regulated To explore why miR-7 expression was downregulated in breast cancer cells and BCSCs, we examined HOTAIR expression and found that the downregulation of miR-7 was closely related to the high level of HOTAIR expression in breast cancer patients. HOTAIR inhibits many tumor suppression genes including HoxD10 in MDA-MB-231 cells. We downregulated the expression of HOTAIR by RNA interference in MDA-MB-231 cells and found that the expression of HoxD10 along with miR-7 were enhanced. 25070049 2014 MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway. 537 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, RNAi, Luciferase reporter assay, ELISA etc. gastric cancer tissues, cell lines (SGC7901, MGC-803) up-regulated Significant HOTAIR overexpression was observed in GC tissues, as well as strong positive correlations with HLA-G levels in both tissue and peripheral blood samples. HOTAIR overexpression might also get involved in tumor escape mechanisms, involving HLA-G upregulation via inhibiting miR-152. 26187665 2015 Long non-coding RNA HOTAIR promotes HLA-G expression via inhibiting miR-152 in gastric cancer cells. 538 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, Western blot, Luciferase reporter assay, RIP etc. cervical cancer tissues, cell lines (SiHa, HeLa, Caski, c4-1 and HaCaT) up-regulated HOTAIR expression was elevated while miR-143-3p expression was reduced in cervical cancer tissues and cell lines.HOTAIR knockdown suppressed proliferation and enhanced apoptosis in cervical cancer cells.Moreover, HOTAIR could function as a sponge for miR-143-3p.The inhibitory effect of HOTAIR knockdown on cervical cancer cells growth was abolished following decrease of miR-143-3p expression.Furthermore, HOTAIR promoted BCL2 expression by modulating miR-143-3p.BCL2 overexpression attenuated the tumor-suppressive effect of miR-143-3p in cervical cancer.Finally, the carcinogenicity of HOTAIR was validated in mice.HOTAIR acted as a ceRNA to modulate BCL2 expression via competitively binding to miR-143-3p. 29336659 2018 Long non-coding RNA HOTAIR promotes cervical cancer progression through regulating BCL2 via targeting miR-143-3p. 539 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown Tumor tissues, cervical cancer cell lines (SiHa, HeLa, Caski, and C4-1) up-regulated the expressions of HOTAIR and miR-23b were detected by real-time PCR in 33 paired cervical cancer tissue samples and cervical cell lines. The effects of HOTAIR on the expressions of miR-23b and mitogen-activated protein kinase 1 (MAPK1) were studied by overexpression and RNAi approaches.HOTAIR expression was significantly increased in cervical cancer cells and tissues.In contrast,the expression of miR-23b was obviously decreased.HOTAIR knockdown promoted apoptosis and inhibited cell proliferation and invasion in vitro and in vivo Moreover, our data indicated that HOTAIR may competitively bind miR-23b and modulate the expression of MAPK1 indirectly in cervical cancer cells. 29335299 2018 HOTAIR contributes to cell proliferation and metastasis of cervical cancer via targetting miR-23b/MAPK1 axis. 540 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 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. 541 HOTAIRM1 HOTAIRM1, HOXA-AS1, HOXA1-AS1, NCRNA00179 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. 542 HOTAIRM1 HOTAIRM1, HOXA-AS1, HOXA1-AS1, NCRNA00179 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. 543 HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 papillary thyroid cancer NA M8260/3 qPCR, Western blot, RIP etc. Papillary thyroid carcinoma tissues, cell lines (TPC-1 and HTH83) up-regulated HOTTIP was upregulated in human PTC tissues and PTC cell lines.In addition,HOTTIP knockdown inhibited the proliferation, invasion and migration in vitro together with in vivo tumorigenesis of PTC cells.Additionally, HOTTIP knockdown downregulated Akt1 expression and suppressed cell proliferation, invasion and migration in PTC cells by regulating miR-637. In contrast, miR-637 inhibitor reversed above-mentioned tendencies caused by HOTTIP knockdown. 29474928 2018 LncRNA HOTTIP promotes papillary thyroid carcinoma cell proliferation, invasion and migration by regulating miR-637. 544 HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 malignant glioma NA M9380/3 qPCR, luciferase reporter assay etc. glioma tissues, cell lines (U87, U251) up-regulated HOTTIP was the most upregulated lncRNA in glioma cells treated by hypoxia. High levels of HOTTIP and HIF-1α were correlated with glioma metastasis and poor patient prognosis. Knockdown of HIF-1α and HOTTIP blocked hypoxia-induced EMT, and suppressed invasion and migration of glioma cells. Finally, HOTTIP sponged endogenous miR-101 and inhibited its activity, which resulted in increased ZEB1 expression and promoted process of EMT. HIF-1α/HOTTIP/miR-101/ZEB1 axis plays essential role in hypoxia-induced EMT and metastasis of glioma, and HOTTIP may serve as a therapeutic target to reverse EMT and prevent glioma progression. 28886531 2017 Long non-coding RNA HOTTIP promotes hypoxia-induced epithelialmesenchymal transition of malignant glioma by regulating the miR-101/ZEB1 axis 545 HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 esophageal squamous cell cancer NA NA Western blot, RIP, ChIP, qPCR etc. ESCC tissues, cell lines (Eca-109, KYSE-30, KYSE-150,KYSE-180, KYSE-410, KYSE-450, KYSE-510, TE-10 and TE-13) up-regulated HOTTIP modulated HOXA13 at both the transcriptional and posttranscriptional levels in ESCC cells and HOTTIP-miR-30b-HOXA13 axis may serve as potential diagnostic markers or drug targets for ESCC therapies. 28534516 2017 Transcriptional and posttranscriptional regulation of HOXA13 by lncRNA HOTTIP facilitates tumorigenesis and metastasis in esophageal squamous carcinoma cells 546 HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay etc. cell lines (BEL7402, MHCC97H, MHCC97H-Luc) up-regulated In our profiling study, HOTTIP was identified as the most significantly up-regulated lncRNA in human HCCs, even in early stage of HCC formation. HOTTIP is a novel oncogenic lncRNA, which negatively regulated by miR-125b. Overexpression of HOTTIP contributes to hepatocarcinogenesis by regulating the expression of its neighboring protein-coding genes.Knock-down of HOTTIP significantly suppressed the expression of a number of HOXA genes. 25424744 2014 Long non-coding RNA HOTTIP is frequently up-regulated in hepatocellular carcinoma and is targeted by tumor suppressive miR-125b. 547 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 lung cancer C34 NA qPCR etc. cell line (A549) up-regulated The transfection efficiency was ~100%,and the knockdown efficiency of HOXA11 AS in NSCLC cell lines was >75%, as determined by a reverse transcription quantitative polymerase chain reaction.Following the knockdown of HOXA11-AS,miR-642b-3p was significantly downregulated in A549 NSCLC cells.The ROC curve revealed that the area under curve (AUC) of HOXA11-AS was 0.700 for patients with lung adenocarcinoma and 0.964 for patients with squamous cell carcinoma,which may gain a moderate or high diagnostic value of HOXA11-AS level in lung cancer. 29616096 2018 A comprehensive analysis of the predicted targets of miR-642b-3p associated with the long non-coding RNA HOXA11-AS in NSCLC cells. 548 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 uveal melanoma C69.9 M8720/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (OCM-1A, MUM-2C, C918, MUM-2B, D78) up-regulated The aim of this study was to explore the critical role of lncRNA HOXA11-AS in uveal melanoma (UM) progression.Briefly, we found that HOXA11-AS is overexpressed in UM tissues and cells; HOXA11-AS could regulate UM cell growth, invasion, and apoptosis. Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression. In addition, we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS. Collectively, our findings reveal an oncogenic role for HOXA11-AS in UM tumorigenesis. 28749709 2017 LncRNA HOXA11-AS Exerts Oncogenic Functions by Repressing p21 and miR-124 in Uveal Melanoma 549 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 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. 550 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. hepatocellular carcinoma tissues, cell lines(Hep3B, SMMC-7721, MHCC97-H, BEL-7402 and HL-7702) up-regulated HOXA11-AS expression was up-regulated in the HCC tissues,and the higher expression of HOXA11-AS was associated with the advanced stage in the HCC samples. In addition,the expression of HOXA11-AS was up-regulated in HCC cell lines compared with normal liver cell lines. Ectopic expression of miR-214-3p suppressed HCC cell proliferation and invasion.Furthermore,we indicated that overexpression of HOXA11-AS decreased the miR-214-3p expression and the expression of miR-214-3p was negatively related with the HOXA11-AS expression in HCC samples. Ectopic expression of HOXA11-AS increased HCC proliferation and invasion and induced EMT through inhibiting miR-214-3p expression.These data suggested that HOXA11-AS/miR-214-3p axis was responsible for development of HCC.We ndemonstrated that miR-214-3p expression was down-regulated in the HCC tissues and the expression of miR-214-3p was negatively correlated with the expression of HOXA11-AS. 29761918 2018 LncRNA HOXA11-AS promotes hepatocellular carcinoma progression by repressing miR-214-3p. 551 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. lung tissues, cell lines (A549,H1299, H460) up-regulated HOXA11-AS expression was upregulated in non-small cell lung cancer tissues and cell lines. High levels of HOXA11-AS expression were correlated with larger tumor size and lymph node metastasis. Functional analysis revealed that HOXA11-AS promotes non–small cell lung cancer cell proliferation and invasion. In particular, HOXA11-AS functions as a competing endogenous RNA to regulate transcriptional factor Sp1 expression via sponging miR-124. Collectively, our findings reveal an oncogenic role for HOXA11-AS in non–small cell lung cancer tumorigenesis. 29034803 2017 LncRNA HOXA11-AS promotes proliferation and invasion by targeting miR-124 in human non–small cell lung cancer cells 552 HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 non small cell lung cancer C34 M8046/3 qPCR, RIP, Western blotting etc. NSCLC tissues, cell lines (A549, H1299, 95D) up-regulated upregulation of lncRNA HOXA11-AS predicted a poor prognosis and lncRNA HOXA11-AS promoted cell epithelial-mesenchymal transition (EMT) by inhibiting miR-200b expression in NSCLC. 28615992 2017 Overexpression of lncRNA HOXA11-AS promotes cell epithelial–mesenchymal transition by repressing miR-200b in non-small cell lung cancer 553 HOXA-AS2 HOXA-AS2, HOXA3as ENSG00000253552 NR_122069 GRCh38_7:27107777-27134302 breast cancer C50 NA qPCR, Luciferase report assay etc. breast cancer tissues, cell lines (MCF-10A, MDA-MB-231, MDA-MB-453, and MCF-7) up-regulated HOXA-AS2 was up-regulated in human breast cancer tissues and cell lines and associated with clinicopathological characteristics. HOXA-AS2 may be a potential prognostic and therapeutic target in breast cancer. HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells. 28545023 2017 Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge. 554 HOXD-AS1 HAGLR, HOXD-AS1, Mdgt ENSG00000224189 NA GRCh38_2:176164051-176188958 glioblastoma NA M9440/3 qPCR, Western blot, Luciferase reporter assay etc. glioma tissues, cell line (HEK-293T) up-regulated HOXD-AS1 expression was upregulated in glioma tissues and in glioma cell lines.HOXD-AS1 overexpression promoted cell migration and invasion in vitro, whereas knockdown of HOXD-AS1 expression repressed these cellular processes. Mechanistic studies further revealed that HOXD-AS1 could compete with the transcription factor E2F8 to bind with miR-130a,thus affecting E2F8 expression. Additionally, reciprocal repression was observed between HOXD-AS1 and miR-130a,and miR-130a mediated the tumor-suppressive effects of HOXD-AS1 knockdown. 29341117 2018 HOXD-AS1/miR-130a sponge regulates glioma development by targeting E2F8. 555 HOXD-AS1 HAGLR, HOXD-AS1, Mdgt ENSG00000224189 NA GRCh38_2:176164051-176188958 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay etc. HCC tissues, cell lines (HCCLM3, MHCC97H, MHCC97L, SMMC7721 and L02) up-regulated remarkable overexpression of HOXD-AS1 in metastatic cancer tissues.In vitro and in vivo gain- or loss-of-function studies re-affirmed that HOXD-AS1 is able to facilitate cancer metastasis and inhibit apoptosis. HOXD-AS1 is an oncogenic lncRNA that promotes HCC metastasis and that its pro-metastatic phenotype can partially be attributed to the HOXD-AS1/miR19a/ARHGAP11A signaling axis. downregulated by ectopic HOXD-AS1 overexpression, leading to a remarkably reduced apoptotic effect. OXD-AS1 functions as a competing endogenous RNA (ceRNA) by “sponging” miR19a during HCC metastasis/recurrence. 28724429 2017 The noncoding RNA HOXD-AS1 is a critical regulator of the metastasis and apoptosis phenotype in human hepatocellular carcinoma. 556 HULC HULC, HCCAT1, LINC00078, NCRNA00078 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 rectal adenocarcinoma NA M8140/0 qPCR etc. rectal adenocarcinoma tissues up-regulated HULC,CRNDE and PVT1 expression levels were increased,and the expression level of ADAMTS9 AS2 was decreased in READ tumor tissues compared to adjacent non tumor tissues. 29512732 2018 Construction of a ceRNA network reveals potential lncRNA biomarkers in rectal adenocarcinoma. 557 HULC HULC, HCCAT1, LINC00078, NCRNA00078 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 cholangiocarcinoma NA M810/3 qPCR, Western blot, RIP, Luciferase reporter assay cell line (QBC939) differential expression We identified that two lncRNAs, H19 and HULC, were differentially expressed among all the samples under the treatment of hypoxic or inflammatory factors, and they were shown to be stimulated by short-term oxidative stress responses to H2O2 and glucose oxidase in CCA cell lines. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4. Our study revealed that H19 and HULC, up-regulated by oxidative stress, regulate CCA cell migration and invasion by targeting IL-6 and CXCR4 via ceRNA patterns of sponging let-7a/let-7b and miR-372/miR-373, respectively. 27809873 2016 LncRNAs H29 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner 558 HULC HULC, HCCAT1, LINC00078, NCRNA00078 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 liver cancer C22.0 NA qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay etc. HCC tissues, cell lines (HepG2, Huh7, HepG2.2.15 etc.) up-regulated Levels of HULC were positively correlated with levels of SPHK1 and its product, sphingosine-1-phosphate (S1P), in patients HCC samples. HULC increased SPHK1 in hepatoma cells. Mechanistically, HULC activated the promoter of SPHK1 in hepatoma cells through the transcription factor E2F1. Chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) further showed that E2F1 was capable of binding to the E2F1 element in the SPHK1 promoter. HULC increased the expression of E2F1 in hepatoma cells and levels of HULC were positively correlated with those of E2F1 in HCC tissues. Intriguingly, HULC sequestered miR-107, which targeted E2F1 mRNA 3'UTR, by complementary base pairing. Functionally, si-SPHK1 remarkably abolished the HULC-enhanced tumor angiogenesis in vitro and in vivo. 26540633 2015 Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1). 559 HULC HULC, HCCAT1, LINC00078, NCRNA00078 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 liver cancer C22.0 NA qPCR, Western blot, Luciferase reporter assay etc. liver cancer tissues, cell lines (CREB, HULC, Prkacb etc.) up-regulated The study elucidates that fine tuning of HULC expression is part of an auto-regulatory loop in which it's inhibitory to expression and activity of miR-372 allows lncRNA up-regulated expression in liver cancer. 20423907 2010 CREB up-regulates long non-coding RNA, HULC expression through interaction with microRNA-372 in liver cancer. 560 HULC HULC, HCCAT1, LINC00078, NCRNA00078 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 hepatocellular carcinoma C22.0 M8170/3 qPCR, Cell transfection, Western blot, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc. HCC tissues, cell lines (PLC, HepG2, SMMC-7721, Huh7 and Bel-7402) up-regulated We also confirmed that miR-203 and oncogene ADAM9 (a disintegrin and metalloproteinase 9)/oncogenic long non-coding RNA HULC (highly up-regulated in liver cancer) were inversely expressed in hepatocellular carcinoma (HCC) tissues or cell lines. More intriguingly, up-regulation of miR-203 diminished the expression of ADAM9 and HULC in HCC cancer cells. Over-expression of miR-203 could markedly inhibit cell proliferation, invasion and induce cell apoptosis. Furthermore, we identified that miR-203 modulated ADAM9 and HULC in a novel post-transcriptional regulatory mechanism. Over-expression of HULC partly rescued the miR-203-mediated antitumor effects. 26179263 2016 miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC. 561 HULC HULC, HCCAT1, LINC00078, NCRNA00078 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell lines (H7402, Huh7, HepG2, and HepG2.2.15) up-regulated HULC modulated the deregulation of lipid metabolism in HCC by activating the acyl-CoA synthetase subunit ACSL1. Moreover, HULC mRNA levels correlated positively with ACSL1 levels in 60 HCC cases according to real-time PCR analysis. Mechanistic investigations showed that HULC upregulated the transcriptional factor PPARA, which activated the ACSL1 promoter in hepatoma cells. HULC also suppressed miR-9 targeting of PPARA mRNA by eliciting methylation of CpG islands in the miR-9 promoter. We documented the ability of HULC to promote lipogenesis, thereby stimulating accumulation of intracellular triglycerides and cholesterol in vitro and in vivo. 25592151 2015 Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. 562 KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 glioma NA M9380/3 qPCR, Western blot, RIP, Luciferase reporter assay brain tumor tissues, cell lines (U87, U251) up-regulated KCNQ1OT1 expression was up-regulated in glioma tissues and cells.These results provided a comprehensive analysis of KCNQ1OT1-miR-370-CCNE2 axis in human glioma cells and might provide a novel strategy for glioma treatment. 28381990 2017 Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells’ Malignancy by Activating miR-370/CCNE2 Axis 563 KLKP1 KLKP1, KARMA, KLK31P, KRSP1, PsiKLK1, YKLK1 ENSG00000197588 NA GRCh38_19:50882096-50896398 prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (LNCaP) up-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. 564 LINC00052 LINC00052, NCRNA00052, TMEM83 ENSG00000259527 NR_026869 GRCh38_15:87576929-87579866 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RIP etc, hepatocellular carcinoma tissues, cell lines (L02, SMMC7721, SK-hep1, Huh7, HepG2) up-regulated We found that overexpression of LINC00052 could upregulate the EPB41L3 expression and it might serve as a tumor suppressor gene in HCC. Database analysis showed that miR-452-5P could target LINC00052. The binding regions between LINC00052 and miR-452-5P were confirmed by luciferase assays. Moreover, LINC00052 inhibited cell malignant behavior by increasing miR-452-5P expression, suggesting that LINC00052 was negatively regulated by miR-452-5P.In addition, overexpression of miR-452-5P resulted in a decrease of EPB41L3 expression, suggesting that EPB41L3 was as a target of miR-452-5P. In conclusion, these results demonstrated that a novel pathway was mediated by LINC00052 in HCC. 28969024 2017 LINC00052 upregulates EPB41L3 to inhibit migration and invasion of hepatocellular carcinoma by binding miR-452-5p. 565 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA GRCh38_2:87454781-87636740 pancreatic cancer C25 NA qPCR, RNAi, Western blot etc. PDAC tissues up-regulated The upregulation of LINC00152 (MACE log2fc: 2.3, qPCR: 1.5) and downregulation of LINC00261 (MACE log2fc: 5.3, qPCR: 4.4) in PDAC tissues was confirmed by qPCR.In silico target analysis of miR-802 revealed potential binding sites in the 3′ UTR of TCF4, encoding a transcription factor that controls Wnt-signalling genes. Overexpression of miR-802 in MiaPaCa pancreatic cancer cells reduced TCF4 protein levels. 25910082 2015 Next-generation sequencing reveals novel differentially regulated mRNAs, lncRNAs, miRNAs, sdRNAs and a piRNA in pancreatic cancer. 566 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA GRCh38_2:87454781-87636740 renal cell carcinoma C64.9 NA qPCR, RNAi, Western blot, RIP, ChIP, Luciferase reporter assay, Flow cytometry assay etc. RCC tissues, cell lines (ACHN, Caki-1, Caki-2 and 786-O) up-regulated LINC00152 expression was up-regulated in RCC tissues compared with adjacent normal tissues.Furthermore, knockdown of LINC00152 inhibited RCC cell proliferation and S phase cell proportion in vitro. Mechanistically,LINC00152 may contribute to RCC progression by epigenetically repressing P16 expression and interacted with miR-205. 28337379 2017 Long intergenic non-coding RNA 00152 promotes renal cell carcinoma progression by epigenetically suppressing P16 and negatively regulates miR-205. 567 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA GRCh38_2:87454781-87636740 gallbladder cancer C23.9 NA qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. GBC tissues, cell lines (GBC-SD and H69) up-regulated LINC00152 is overexpressed in gallbladder cancer (GBC) tissue samples and cell lines.Functionally, LINC00152 dramatically promoted cell migration,invasion and epithelial-mesenchymal transition (EMT) progression in vitro. In vivo, LINC00152 overexpression significantly promoted tumour peritoneal spreading and metastasis. LINC00152 functions as a molecular sponge for miR-138, which directly suppresses the expression of HIF-1α.We revealed that miR-138 is a suppressor of GBC cell metastasis and EMT progression, and a similar phenomenon was observed in HIF-1α knockdown NOZ cells. 28077595 2017 Long non-coding RNA LINC00152 promotes gallbladder cancer metastasis and epithelial-mesenchymal transition by regulating HIF-1α via miR-138. 568 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA GRCh38_2:87454781-87636740 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc. cell line (SMMC7721) down-regulated We found one LncRNA which called intergenic non-protein coding RNA 52 (LINC00052) has the ability to inhibit invasion and migration of hepatocarcinoma cells. We found that invasion, migration and proliferation abilities in SMMC7721 cell were inhibited after up-expressing LINC00052. We identified that NTRK3 was the target gene of LINC00052. Down-expression of NTRK3 could increase SMMC7721 cell invasion, migration and proliferation. Meanwhile, we discovered that LINC00052 could regulate NTRK3 expression by forming complementary base pairing with miR-128 and miR-485-3p to reduce the luciferase activity of NTRK3 3'UTR. 27351280 2016 LINC00052 regulates the expression of NTRK3 by miR-128 and miR-485-3p to strengthen HCC cells invasion and migration. 569 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA GRCh38_2:87454781-87636740 glioma NA M9380/3 qPCR, Luciferase reporter assay, in vitro knockdown glioma tissues, cell lines (U87, LN229, U251, and T98G, NHAs) up-regulated LINC00152 was found to be significantly upregulated in human glioma cell lines and clinical samples.Knockdown of LINC00152 suppressed glioma cell proliferation, migration, and invasion in vitro.LINC00152 knockdown inhibits tumor growth.LINC00152 binds to miR-16 in a sequence-specific manner and suppresses its expression. miR-16 inhibition strongly attenuated LINC00152 knockdown-mediated suppressive effects on proliferation, migration, and invasion.LINC00152 induced BMI1 expression by sponging miR-16,this effect further promoted glioma cell proliferation and invasion.LINC00152 as an oncogenic lncRNA promoting glioma cell proliferation and invasion and as a potential target for human glioma treatment. 29669323 2018 Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16. 570 LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 ENSG00000222041 NA GRCh38_2:87454781-87636740 colorectal cancer C19.9 NA qPCR, Flow cytometry assay, CCK-8 assay etc. CRC tissues, cell lines (CACO2, HCT-116, HT-29, SW480, and SW620) down-regulated We found that LINC00152 expression was significantly decreased in CRC tissues and CRC cell lines. Overexpression of LINC00152 resulted in decreased cell viability and increased apoptosis in CSC cell lines. Interestingly, miR-376c-3p down-regulated the expression of LINC00152 in CSC cells. In addition, miR-376c-3p suppressed the effect of LINC00152 on the viability and apoptosis of CSC cells. 28078002 2016 LncRNA-LINC00152 down-regulated by miR-376c-3p restricts viability and promotes apoptosis of colorectal cancer cells. 571 LINC00261 LINC00261, ALIEN, C20orf56, DEANR1, HCCDR1, NCRNA00261, onco-lncRNA-17 ENSG00000259974 NR_001558 GRCh38_20:22547671-22578642 pancreatic cancer C25 NA qPCR, RNAi, Western blot etc. PDAC tissues down-regulated The upregulation of LINC00152 (MACE log2fc: 2.3, qPCR: 1.5) and downregulation of LINC00261 (MACE log2fc: 5.3, qPCR: 4.4) in PDAC tissues was confirmed by qPCR.In silico target analysis of miR-802 revealed potential binding sites in the 3′ UTR of TCF4, encoding a transcription factor that controls Wnt-signalling genes. Overexpression of miR-802 in MiaPaCa pancreatic cancer cells reduced TCF4 protein levels. 25910082 2015 Next-generation sequencing reveals novel differentially regulated mRNAs, lncRNAs, miRNAs, sdRNAs and a piRNA in pancreatic cancer. 572 LINC00312 LINC00312, ERR-10, ERR10, LMCD1DN, LOH3CR2A, NAG-7, NAG7, NCRNA00312 NA NR_024065 NA bladder cancer C67 NA qPCR, Western blot etc. bladder cancer tissues, cell lines (T24, BIU87, and 5637) down-regulated qRT-PCR indicated that LINC00312 expression was lower but miR-197-3p expression was higher in BC tissues compared with adjacent tissues; LINC00312 was negatively correlated with miR-197-3p. The migration test revealed that the downregulation of miR-197-3p and overexpression of LINC00312 inhibited cell migration and invasion abilities, while the overexpression of miR-197-3p and the upregulation of LINC00312 promoted cell migration and invasion. 27631965 2016 LINC00312 inhibits the migration and invasion of bladder cancer cells by targeting miR-197-3p. 573 LINC00472 LINC00472, C6orf155 ENSG00000233237 NR_121612 GRCh38_6:71344344-71420769 lung adenocarcinoma C34 M8140/3 qPCR lung adenocarcinoma tissues down-regulated Our study sheds novel light on the roles of lncRNA-related ceRNA network in LAD and facilitates the detection of potential lncRNA biomarkers for LAD diagnosis and treatment. Remarkably, in our study, LINC00472, HCP5, and SNHG12 might be potential biomarkers for LAD management.As we all know, histones constantly undergo post-translational modifications, for instance, methylation, acetylation.Typically, lncRNA functions are characterized using a ‘guilt by association’strategy. It has been reported that lncRNAs harboring miRNA response elements (MREs) serve as competing endogenous RNAs (ceRNAs) to exchange with mRNAs via competing for common miRNAs. 28793054 2017 Revealing potential long non-coding RNA biomarkers in lung adenocarcinoma using long non-coding RNA-mediated competitive endogenous RNA network. 574 LINC00472 LINC00472, C6orf155 ENSG00000233237 NR_121612 GRCh38_6:71344344-71420769 lung adenocarcinoma C34 M8140/3 qPCR lung adenocarcinoma tissues down-regulated lncRNAs LINC00472, and HCP5 were down-regulated in LAD tissues.a hub lncRNA LINC00472 functioned as a hub to compete with 12 mRNAs 28793054 2017 Revealing potential long non-coding RNA biomarkers in lung adenocarcinoma using long non-coding RNA-mediated competitive endogenous RNA network 575 Linc00483 C17orf73, FLJ20694 ENSG00000167117 NA GRCh38_17:50761029-50767557 gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissues, cell lines (SGC7901, BGC823, MGC803, MNK28 and GES-1) up-regulated linc00483 promoted gastric cancer cell proliferation,invasiveness and metastasis in vitro and in vivo.Mechanistically, upregulated expression of linc00483 in gastric cancer acts as a sponge to absorb endogenous tumour suppressor miR-30a-3p. Furthermore,it restores SPAG9 expression, which is negatively regulated by miR-30a-3p,and actives MAPK signaling pathway in gastric cancer cells.Thus,linc00483 is an oncogenic lncRNA in gastric cancer and targeting linc00483 or its pathway can potentially be useful in development of targeted therapies for patients with gastric cancer.linc00483 is an important regulator in carcinogenesis and may be a useful biomarker to predict prognosis of gastric cancer patients.Linc00483 regulates SPAG9 by acting as a ceRNA and interacting with miR-30a-3p. 29761936 2018 Linc00483 as ceRNA regulates proliferation and apoptosis through activating MAPKs in gastric cancer. 576 LINC00511 LINC00511, LCAL5, onco-lncRNA-12 ENSG00000227036 NR_033876 GRCh38_17:72323123-72640472 tongue squamous cell carcinoma C02 M8070/3 Microarray, qPCR, Western blot, Luciferase reporter assay etc. tongue squamous cell carcinoma tissues, cell lines (HOEC, Tca-8113, SCC-9, SCC-4 and CAL-2) up-regulated LINC00511 was obviously upregulated in TSCC tissues and cell lines.Moreover,it was found that LINC00511 served as a competing endogenous RNA (ceRNA) through sponging miR-765 and ultimately modulated the derepression of laminin subunit gamma 2 (LAMC2).The inhibitory effects of miR-765 on TSCC cells proliferation,invasion as well as cell cycle distribution can be restored by the ectopic overexpression of LINC00511. Additionally, the restored capacity of LINC00511 promoted the expression of LAMC2, which was a downstream target of miR-765 and can be negatively regulated by miR-765. A novel molecular axis of LINC00511/miR-765/LAMC2 was investigated to regulate the tumor development of TSCC. LINC00511 promoted the expression of LAMC2 via the ceRNA mechanism of sponging miR-765. 29315846 2018 LINC00511 interacts with miR-765 and modulates tongue squamous cell carcinoma progression by targeting LAMC2. 577 LINC00673 LINC00673, HI-LNC75, HILNC75, LUCAIR1, SLNCR, SLNCR1 NA NR_036488 GRCh38_17:72403322-72592804 pancreatic cancer C25 NA qPCR, Flow cytometry assay etc. pancreatic cancer tissues, cell lines (BXPC-3 and CFPAC-1) up-regulated Flow cytometry analysis indicated that LINC00673 overexpression resulted in a substantial accumulation of PDAC cells in G0/G1 phase, accompanied by a substantial decrease in the number of cells in S phase. LINC00673 is able to reinforce the interaction of PTPN11 with PRPF19, an E3 ubiquitin ligase, and promote PTPN11 degradation through ubiquitination, which causes diminished SRC-ERK oncogenic signaling and enhanced activation of the STAT1-dependent antitumor response. A G>A change at rs11655237 in exon 4 of LINC00673 creates a target site for miR-1231 binding, which diminishes the effect of LINC00673 in an allele-specific manner and thus confers susceptibility to tumorigenesis. 27213290 2016 Pancreatic cancer risk variant in LINC00673 creates a miR-1231 binding site and interferes with PTPN11 degradation. 578 LINC00858 LINC00858 ENSG00000229404 NR_038220 GRCh38_10:84279980-84294659 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Luciferase reporter assay, RNA pull-down assay, CCK-8 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 LINC00858 levels were remarkably higher in NSCLC tissues and cell lines. Ectopic expression of LINC00858 in NSCLC cells promoted cell proliferation and induced cell migration and invasion. Moreover, LINC00858 functioned as a competitive endogenous RNA (ceRNA),effectively becoming sponge for miR-422a and thereby modulating the expression of kallikrein-related peptidase 4 (KLK4). In NSCLC patients, high expression of LINC00858 closely correlated with tumor progression. 28177876 2017 Long intergenic non-protein coding RNA 00858 functions as a competing endogenous RNA for miR-422a to facilitate the cell growth in non-small cell lung cancer. 579 LINC00969 NA NA NA NA prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (LNCaP) up-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. 580 LINC01016 NA ENSG00000249346 NR_038989 GRCh38_6:33867506-33896914 endometrial cancer NA M8380/3 qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown endometrial cell lines (Ishikawa and RL-95-) up-regulated LINC01016 was substantially upregulated in endometrial cancer tissues,and LINC01016 silencing abolished the malignant behavior of endometrial cancer cells.LINC01016 positively rescued the downstream gene nuclear factor YA (NFYA) by competitively "sponging" miR-302a-3p and miR-3130-3p.In turn, these two miRNAs could inhibit LINC01016 transcription,thus forming two reciprocal repression cycles,which influenced the biological behavior of endometrial cancer cells. miR-3130-3p could specifically bind with the 3'-UTR regions of NFYA, and NFYA could upregulate the expression of special AT-rich sequence-binding protein 1 (SATB1) as a transcriptional factor. 29467441 2018 LINC01016 promotes the malignant phenotype of endometrial cancer cells by regulating the miR-302a-3p/miR-3130-3p/NFYA/SATB1 axis. 581 LINC01021 NA NA NA GRCh38_5:27472292-27496401 colorectal cancer C19.9 NA RNA-seq, qPCR, Western blot, Luciferase reporter assay, pSILAC etc. cell line (SW480) up-regulated Ectopic LINC01021 expression inhibited proliferation in SW480 cells. 26183718 2015 p53-regulated networks of protein, mRNA, miRNA and lncRNA expression revealed by integrated pSILAC and NGS analyses. 582 LINC01133 NA ENSG00000224259 NR_038849 GRCh38_1:159961218-159984750 osteosarcoma NA M9180/3 qPCR osteosarcoma tissues, cell lines (MG63, Saos-2, HOS, and U2-OS) up-regulated we found that the expression level of LINC01133 was statistically upregulated in OS tumor tissue and cell lines compared to noncancerous tissues and a normal human osteoplastic cell line. In summary, our study discovered that lncRNA LINC01133 aggravates the proliferation, migration, and invasion of OS by sponging miR-422a, which provides a novel insight in the tumorigenesis of OS. 28390115 2017 Long Noncoding RNA LINC01133 Functions as an miR-422a Sponge to Aggravate the Tumorigenesis of Human Osteosarcoma 583 LINC01138 LINC01138, LINC00875 ENSG00000274020 NR_027468 GRCh38_1:148290889-148519604 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. 584 linc-223 NA NA NA NA acute myeloid leukemia NA M9861/3 qPCR, Luciferase reporter assay, in vitro knockdown cell lines (HL-60, K562) down-regulated we show that linc-223 directly binds to miR-125-5p and that its knockdown increases the repressing activity of miR-125-5p resulting in the downregulation of its target interferon regulatory factor 4 (IRF4), which it was previously shown to inhibit the oncogenic activity of miR-125-5p in vivo. Furthermore, data from primary AML samples show significant downregulation of linc-223 in different AML subtypes 27517498 2016 The miR-223 host non-coding transcript linc-223 induces IRF4 expression in acute myeloid leukemia by acting as a competing endogenous RNA 585 lnc34a NA NA NA NA colon cancer C18 NA qPCR, Western blot, RIP etc. cell lines (Colo205, SW480, HT29, SW620, LS174T, DLD1 etc.) up-regulated Here we report a novel LncRNA, Lnc34a, that is enriched in colon cancer stem cells (CCSCs) and initiates asymmetric division by directly targeting the microRNA miR-34a to cause its spatial imbalance. Lnc34a recruits Dnmt3a via PHB2 and HDAC1 to methylate and deacetylate the miR-34a promoter simultaneously, hence epigenetically silencing miR-34a expression independent of its upstream regulator, p53. Lnc34a levels affect CCSC self-renewal and colorectal cancer (CRC) growth in xenograft models. Lnc34a is upregulated in late-stage CRCs, contributing to epigenetic miR-34a silencing and CRC proliferation. 27077950 2016 A long non-coding RNA targets microRNA miR-34a to regulate colon cancer stem cell asymmetric division 586 LOC101927497 NA NA NA NA gastric cancer C16 NA RNA-seq, qRT-PCR, in vitro knockdown gastric cancer cell lines(MKN28 and MGC-803) down-regulated LncRNA LOC101927497 functions as a suppressor by interacting with miR-574-5p, thus inhibiting the malignant phenotype of GES-1-T cells. 29223541 2017 Functional role of lncRNA LOC101927497 in N-methyl-N'-nitro-N-nitrosoguanidine-induced malignantly transformed human gastric epithelial cells. 587 LOC150622 LINC01105 ENSG00000232044 NR_026832 GRCh38_2:5932687-6001275 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. 588 LOC553103 MIR3936HG, SLC22A5-AS1 ENSG00000233006 NR_110997 GRCh38_5:132311285-132369916 gastric cancer C16 NA microarray, qPCR, RNAi, Luciferase reporter assay etc. cell line (AGS) up-regulated We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT. 27584792 2016 Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103. 589 LOC553103 MIR3936HG, SLC22A5-AS1 ENSG00000233006 NR_110997 GRCh38_5:132311285-132369916 nasopharyngeal cancer C11 NA microarray, qPCR, RNAi, Luciferase reporter assay etc. cell lines (5-8F and HNE2) up-regulated We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT. 27584792 2016 Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103. 590 LOC554202 MIR31HG, hsa-lnc-31 ENSG00000171889 NR_027054 GRCh38_9:21455642-21559669 laryngeal squamous cell cancer C32.3 NA qPCR, Western blot, RNAi etc. laryngeal squamous cell carcinomatissues, cell line (Hep2) up-regulated lncRNA LOC554202 expression was overexpressed in LSCC tissues compared with the paired adjacent samples and higher LOC554202 expression was associated with the advanced stage.In addition,we demonstrated that the expression level of miR-31 was downregulated in LSCC tissues compared to the paired adjacent samples and lower miR-31 expression was correlated with the advanced stage. Moreover, the expression of miR-31 was negatively correlated with the expression of LOC554202 in LSCC tissues. Ectopic expression of LOC554202 promoted LSCC cell growth, cell cyle and cell invasion and overexpression of miR-31 inhibited LSCC cell growth,cell cyle and cell invasion.Elevated expression of LOC554202 suppressed miR-31 expression and promoted RhoA expression in LSCC cell,which was a direct target gene of miR-31. 29737563 2018 Long non-coding RNA LOC554202 promotes laryngeal squamous cell carcinoma progression through regulating miR-31. 591 LOC554202 MIR31HG, hsa-lnc-31 ENSG00000171889 NR_027054 GRCh38_9:21455642-21559669 breast cancer C50 NA qPCR etc. cell line (MCF10A) down-regulated Both miR-31 and the host gene LOC554202 are down-regulated in the TNBC cell lines of basal subtype and over-expressed in the luminal counterparts. Treatment of the TNBC cell lines with either a de-methylating agent alone or in combination with a de-acetylating agent resulted in a significant increase of both miR-31 and its host gene, suggesting an epigenetic mechanism for the silencing of these two genes by promoter hypermethylation. Finally, both methylation-specific PCR and sequencing of bisulfite-converted DNA demonstrated that the LOC554202 promoter-associated CpG island is heavily methylated in the TNBC cell lines and hypomethylated in the luminal subtypes. 22289355 2012 miR-31 and its host gene lncRNA LOC554202 are regulated by promoter hypermethylation in triple-negative breast cancer. 592 LUCAT1 LUCAT1, SCAL1 ENSG00000248323 NR_103548 GRCh38_5:91303029-91314402 osteosarcoma NA M9180/3 RNAi, qPCR, Western blot, Luciferase reporter assay cell lines (MG-63, U2OS, HOS, SAOS-2, hFOB, MG63/MTX, HOS/MTX, U2OS/MTX) up-regulated LUCAT1 was up-regulated in MTX-resistant cells (MG63/MTX, HOS/MTX) compared to that in parental cells. LncRNA LUCAT1 and ABCB1 protein expression levels were both up-regulated when induced by different concentration of methotrexate. In vitro and vivo, LUCAT1 knockdown decreased the expression levels drug resistance related genes (MDR1, MRP5, LRP1), proliferation, invasion and tumor growth of osteosarcoma cells.the modulation of LUCAT1 on ABCB1 through sponging miR-200c. 29170124 2017 Long non-coding RNA LUCAT1 modulates methotrexate resistance in osteosarcoma via miR-200c/ABCB1 axis 593 LUCAT1 LUCAT1, SCAL1 ENSG00000248323 NR_103548 GRCh38_5:91303029-91314402 glioma NA M9380/3 qPCR, Luciferase reporter assay, in vitro knockdown etc. cell lines (LN229, U251, SNB19, U87, H4), glioma tissues up-regulated LUCAT1 was substantially upregulated in glioma tissues and cells.LUCAT1 inhibition significantly suppressed the proliferation and invasion of glioma cells. The lncRNA LUCAT1 was critical for the proliferation and invasion of glioma cells by regulating miR-375. 29089067 2017 Knockdown of Long Noncoding RNA LUCAT1 Inhibits Cell Viability and Invasion by Regulating miR-375 in Glioma. 594 M59227 COL3A1, EDS4A NA NA NA gastric cancer C16 NA microarray, qPCR, RNAi etc. gastric cancer tissues up-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. 595 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 renal cancer C64.9 NA qPCR etc. ccRCC tissues up-regulated We found that MALAT1 exist a higher fold change (Tumor/Normal) in clear cell kidney carcinoma (KIRC) from The Cancer Genome Atlas (TCGA) Data Portal and a negative correlation with miR-200s family. We further demonstrated MALAT1 promote KIRC proliferation and metastasis through sponging miR-200s in vitro and in vivo. In addition, miR-200c can partly reverse the MALAT1's stimulation on proliferation and metastasis in KIRC. In summary we unveil a branch of the MALAT1/miR-200s/ZEB2 pathway that regulates the progression of KIRC. 26461224 2015 LncRNA MALAT1 functions as a competing endogenous RNA to regulate ZEB2 expression by sponging miR-200s in clear cell kidney carcinoma 596 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 retinoblastoma C69.2 M9510/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (Y79, Weri-Rb1, SO-Rb50 and HXO-RB44) up-regulated Through direct targeting miR-124,MALAT1 promotes retinoblastoma cell autophagy.Further,we investigated whether Syntaxin 17 (STX17),a Soluble NSF Attachment Protein receptor (SNARE) of the autophagosome,is involved in MALAT1/miR-124 regulation of retinoblastoma cell autophagy, and the underlying mechanism. 29073720 2018 MALAT1 modulates the autophagy of retinoblastoma cell through miR-124-mediated stx17 regulation. 597 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 tongue cancer C02 NA qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc. tongue cancer tissues, cell lines (CAL-27, SCC-9, SCC-4, SCC-15 and SCC-25) up-regulated MALAT1 was specifically upregulated in tongue cancer cell lines and overexpression promoted tongue cancer cell growth by targeting miR-124. Knockdown of MALAT1 suppressed the growth and invasion of human tongue cancer cells and inhibited metastasis in vitro and in vivo. In addition, miR-124-dependent jagged1 (JAG1) regulation was required for MALAT1-induced tongue cancer cell growth. 28260102 2017 Long non-coding RNA MALAT1 interacts with miR-124 and modulates tongue cancer growth by targeting JAG1. 598 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 uveal melanoma C69.9 M8720/3 qPCR, Western blot, Cell proliferation assay, Cell migration and invasion assay etc. uveal melanoma tissues, cell lines (MUM-2C, OCM-1A, MUM-2B and C918) up-regulated The expression of MALAT1 was upregulated in the uveal melanoma tissues compared to normal tissues. Among them, MALAT1 was upregulated in 72% uveal melanoma tissues compared to their paired normal tissues. Knockdown of MALAT1 suppressed uveal melanoma cell proliferation, colony information, invasion and migration. Moreover, we showed that knockdown of MALAT1 promoted miR-140 expression and suppressed Slug and ADAM10 expression in the MUM-2C cell. In addition, we demonstrated that miR-140 was downregulated in the uveal melanoma tissues compared to normal tissues and cell lines. The expression level of MALAT1 was inversely correlated with the expression level of miR-140 in uveal melanoma tissues. 27725873 2017 Long noncoding RNA MALAT1 promotes uveal melanoma cell growth and invasion by silencing of miR-140. 599 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 retinoblastoma C69.2 M9510/3 qPCR, Western blot, Luciferase Reporter Assays cell line (Y79) up-regulated Results showed that the expression of - MALAT1 was significantly higher in Y79 cell line than ARPE-19 cell line (P<0.01). MiR-124 was up-regulated by MALAT1 silence and hence was identified as a target of MALAT1 (P<0.05 or P<0.001). 28550678 2017 Knockdown of Long Noncoding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Inhibits Proliferation, Migration, and Invasion and Promoted Apoptosis By Targeting miR-124 in Retinoblastoma 600 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 endometrioid endometrial cancer NA M8930/0 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell proliferation assay etc. EEC tissues, cell lines (RL-952, HEC-1-B and JEC) down-regulated In the present study, we first showed that miR-200c levels were higher in most EEC specimens than in non-tumor tissues, while MALAT1 levels were lower. Moreover, we found that miR-200c bound directly to MALAT1 using luciferase reporter and qRT-PCR assays. MALAT1 and miR-200c are reciprocally repressed, and TGF-β increased MALAT1 expression by inhibiting miR-200c. When the interaction between miR-200c/MALAT1 was interrupted, the invasive capacity of EEC cells was decreased and EMT markers expression were altered in vitro. 27693631 2016 Disrupting MALAT1/miR-200c sponge decreases invasion and migration in endometrioid endometrial carcinoma. 601 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 malignant melanoma NA M8720/3 qPCR, RNAi, Western blot, Luciferase reporter assay, Cell migration and invasion assay etc. primary malignant melanoma tissues, cell lines (A375, SK-MEL-5 and SK-MEL-2) up-regulated In this study, the aberrant up-regulation of MALAT1 was detected in melanoma. We determined that MALAT1 promotes melanoma cells proliferation, invasion and migration by sponging miR-22. MiR-22 was decreased and acted as a tumor suppressor in melanoma, and MMP14 and Snail were the functional targets of miR-22. Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22. 27564100 2016 Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22. 602 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 colon cancer C18 NA qPCR, Luciferase reporter assay, Western blot cell lines (Lovo, HCT116, SW480, HT29, HIEC) up-regulated miR-129-5p mimics were able to restrain the progression of colon cancer cells. In addition, high motility group box protein 1 (HMGB1), was predicted as a mRNA target of miR-129-5p. Furthermore, we found that MALAT1 exerted its biological functions through regulating HMGB1 by sponging miR-129-5p in vitro. Silencing MALAT1 greatly inhibited HMGB1 expression which can be reversed by miR-129-5p inhibitors.MALAT1 may serve as a competing endogenous lncRNA (ceRNA) to mediate HMGB1 by sponging miR-129-5p in colon cancer. 29226325 2017 LncRNA MALAT1 induces colon cancer development by regulating miR-129-5p/HMGB1 axis. 603 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 melanoma NA M8720/3 qPCR, Western blot melanoma tissues, cell lines (A375, C32, EDMEL3, G361, HBL, WM1115, SK-MEL-1, M14, MV3, A875, M21) differential expression We further found that the expression and function of miR-183 were suppressed by MALAT1. We also illustrated that MALAT1 may function as a sponge competitive endogenous RNA (ceRNA) for miR-183, and thus regulate the molecular expression of ITGB1. 27966454 2017 Deregulation of miR-183 promotes melanoma development via lncRNA MALAT1 regulation and ITGB1 signal activation 604 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 nasopharyngeal cancer C11 NA qPCR, Western blot, Luciferase reporter assay etc. cell line (HNEpC, 5-8F, CNE-2, C666-1, HONE-1) up-regulated MALAT1 and Capn4 were upregulated while miR-124 expression was downregulated in NPC cell lines.MALAT1 knockdown inhibited proliferation, invasion and EMT of NPC cells. Moreover, MALAT1 improved Capn4 expression by sponging miR-124. MALAT1 upregulation abated miR-124-induced repression on NPC cell proliferation, invasion and EMT. Furthermore, Capn4 overexpression reversed the inhibitory effect of MALAT1 silencing on proliferation, invasion and EMT of NPC cells. 28857668 2017 MALAT1/miR-124/Capn4 axis regulates proliferation, invasion and EMT in nasopharyngeal carcinoma cells 605 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 nasopharyngeal cancer C11 NA microarray, qPCR, Luciferase reporter assay, Cell migration and invasion assay etc. primary NPC tumor tissues differential expression In this study, we found that RNA-binding protein 24 (RBM24) was frequently downregulated in nasopharyngeal carcinoma (NPC). The restoration of RBM24 expression suppressed NPC cellular proliferation, migration and invasion and impeded metastatic colonization in mouse models. Microarray analyses revealed that miR-25 expression was upregulated by RBM24 expression in NPC cells. Similarly, ectopic miR-25 expression suppressed NPC cellular growth and motility by targeting the pro-oncogenic lncRNA MALAT1, and the knockdown of MALAT1 expression exhibited similar effects as RBM24 restoration in NPC cells. 27584791 2016 RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal carcinoma. 606 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 bladder cancer C67 NA qPCR, Western blot etc. cell lines (T24, 5637) up-regulated MALAT1 is capable of suppressing mature miR-125b and increasing the expression of its target genes (Bcl-2 and MMP-13), but has no effect on pri-miR-125b and pre-miR-125b.We observe that the biotin-labeled MALAT1–RNA probe is able to pull down Ago2 and miR-125b and that the negative regulation of miR-125b by MALAT1 is dependent on Ago2. Importantly, the results of flow cytometry assay and transwell assay reveal that the MALAT1-mediated cancer progression is in part due to specific suppression of miR-125b and activation of its two target genes. All together, these data suggest that the “MALAT1-miR-125b-Bcl-2 / MMP-13” axis plays an important role in the progression of BCa, thereby may provide a potential therapeutic strategy for the treatment of human BCa. 29151968 2017 LncRNA MALAT1 Inhibits Apoptosis and Promotes Invasion by Antagonizing miR-125b in Bladder Cancer Cells 607 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 multiple myeloma C42.1 M9732/3 qPCR, Luciferase reporter assays, Western blot, RIP etc. cell lines (MM.1S, OPM-2, NCI-H929, U266, RPMI-8226) up-regulated MALAT1 expression was upregulated in MM samples and cell lines. In function assays, we confirmed that MALAT1 inhibition significantly suppressed cells proliferation, induced cells apoptosis, arrested cells in G1/S phase, and inhibited MM cells growth in vivo. Furthermore, MALAT1 was identified to function as a competitive endogenous RNA (ceRNA) for miR-509-5p to promote MM cell viability. Additionally, our results suggested that miR-509-5p targeted the 3’-UTR of FOXP1 to suppress MM cells progression. Meanwhile, our results showed that miR-509-5p inhibitors significantly abrogated the decreased expression of FOXP1 induced by MALAT1 suppression, indicating that MALAT1 could positively regulate FOXP1 expression by sponging miR-509-5p. 29254219 2017 LncRNA MALAT1 acts as an oncogene in multiple myeloma through sponging miR-509-5p to modulate FOXP1 expression 608 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay etc. PDAC tissues, cell lines (PANC-1, BxPC3, Aspc-1, SW1990 and CFPAC-1) up-regulated We confirmed significantly higher MALAT1 expression in PDAC tissues than in the normal tissues. The following in vitro cell assay further confirmed a direct binding between miR-216a and MALAT1 and the suppressive effect of miR-216a on MALAT1 expression. MiR-216a overexpression had similar effects as MALAT1 siRNA on restoring p21 and p27 expression and inhibiting B-MYB, RAF1 and PCNA1 expression in both PANC-1 and BxPC3 cells. MiR-216a overexpression and MALAT1 knockdown induced cell cycle arrest at G2/M phase. 28034748 2017 MiR-216a decreases MALAT1 expression, induces G2/M arrest and apoptosis in pancreatic cancer cells. 609 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 610 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 esophageal squamous cell cancer NA NA qPCR, Luciferase reporter assay etc. ESCC tissues, cell lines (KYSE30, KYSE150, KYSE450) up-regulated In this study, we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated upregulation of P21 and P27 expression and the inhibition of B-MYB expression. 25538231 2014 Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217inhibits proliferation, migration and invasion of esophageal squamous cell carcinoma cells. 611 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 bladder cancer C67 NA qPCR, Western blot, ChIP, Luciferase reporter assay, Cell proliferation assay etc. bladder urothelial carcinoma tissues, cell lines (T24, 5737, SV-HUC-1, HEK 293T) up-regulated Hsa-miR-125b was down-regulated in bladder cancer compared with matched normal urothelium. Both SIRT7 and MALAT1 were up-regulated in bladder cancer compared with matched normal urothelium. Upregulation of hsa-miR-125b or downregulation of SIRT7 inhibited proliferation, motility and increased apoptosis. 24512851 2013 Hsa-miR-125b suppresses bladder cancer development by down-regulating oncogene SIRT7 and oncogenic long noncoding RNA MALAT1. 612 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR, Cell proliferation assay etc. cell line (MG-63) down-regulated Consistent with a previous study, high dose of E2 treatment dramatically downregulated expressing level of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT-1). The observation of upregulation of miR-9 after a high dose of E2 treatment indicated the cause of MALAT-1 reduction. Downregulation of MALAT-1 promoted the combination of SFPQ/PTBP2 complex. Furthermore, the abolishment of the effects on these physiological processes caused by ectopic expression of miR-9 ASOs suggested the necessity of miR-9 in MALAT-1 regulation. 25592968 2015 17β-estradiol regulates cell proliferation, colony formation, migration, invasion and promotes apoptosis by upregulating miR-9 and thus degrades MALAT-1 in osteosarcoma cell MG-63 in an estrogen receptor-independent manner. 613 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 cervical cancer C53 NA qPCR, RNAi, Western blot, MTT assay etc. cell line (HeLa) up-regulated The levels of MALAT1 were also significantly higher in the MALAT1 transfection group compared to the control group. Low levels of miRNA-143 and high levels of MALAT1 could potentiate proliferation of the cervical cancer cell line HeLa, and accelerate its invasion and migration via enhancement of vimentin and reduction of E-cadherin levels, respectively. 28252165 2017 Effects of miRNA-143 and the non-coding RNA MALAT1 on the pathogenesis and metastasis of HeLa cells. 614 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 cervical cancer C53 NA qPCR, Cell transfection, Western blot, Dual-luciferase reporter assay, Flow cytometry assay etc. cell lines (SiHa and CaSki) differential expression MiR-375 overexpression or MALAT1 siRNA partly restored E-cadherin expression and also significantly reduced N-cadherin. Following immunofluorescent staining confirmed these trends. Since EMT is an important mechanism of enhanced tumor cell invasion and metastasis, we further detected how miR-375 and MALAT1 modulate invasion capacity of SiHa cells. Transwell assay showed that both miR-375 overexpression and MALAT1 knockdown significantly reduced invasion capacity of SiHa cells. 27658300 2016 MiR-375 Is Epigenetically Downregulated by HPV-16 E6 Mediated DNMT1 Upregulation and Modulates EMT of Cervical Cancer Cells by Suppressing lncRNA MALAT1. 615 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioma NA M9380/3 qPCR, Western blot, RIP, ChIP, Luciferase reporter assay etc. glioma tissues, cell lines (hCMEC/D3, ECs) up-regulated Our results proved that MALAT1 expression was up-regulated in brain microvessels of human glioma and glioma endothelial cells (GECs) which were obtained by co-culturing endothelial cells with glioma cells. Functionally, knockdown of MALAT1 resulted in an impairment and increased the permeability of BTB as well as decreased the expression of ZO-1, occludin and claudin-5 in GECs. Further, there was reciprocal repression between MALAT1 and miR-140, and miR-140 mediated the effects that MALAT1 knockdown exerted. Mechanistic investigations defined that nuclear factor YA (NFYA), a CCAAT box-binding transcription factor, was a direct and functional downstream target of miR-140, which was involved in the MALAT1 knockdown induced regulation of BTB function. 26619802 2015 Knockdown of long non-coding RNA MALAT1 increases the blood-tumor barrier permeability by up-regulating miR-140 616 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 cervical cancer C53 NA qPCR, RNAi, RIP, Flow cytometry assay, RNA pull-down assay etc. HR-HPV+ cervical cancer tisssue, cell lines (HeLa, CaSki) up-regulated We found MALAT1 expression was significantly higher in radioresistant than in radiosensitive cancer cases. In addition, MALAT1 and miR-145 expression inversely changed in response to irradiation in HR-HPV+ cervical cancer cells. We found CaSki and Hela cells with knockdown of MALAT1 had significantly lower colony formation, higher ratio of G2/M phase block and higher ratio of cell apoptosis. Next, we confirmed that miR-145 and MALAT1 were in the same Ago2 complex and there was a reciprocal repression between them. Then, we explored the function of MALAT1-miR-145 in radiosensitivity of cervical cancers cells and demonstrated that si-MALAT1 and miR-145 had some level of synergic effect in reducing cancer cell colony formation, cell cycle regulation, and inducing apoptosis. 26311052 2015 Long non-coding RNA MALAT1 modulates radiosensitivity of HR-HPV+ cervical cancer via sponging miR-145. 617 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 cervical cancer C53 NA qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay etc. HR-HPV+ cervical cancer tisssue, cell lines (HeLa, CaSki, SiHa) up-regulated Findings of this study confirmed higher MALAT1 expression in HR-HPV (+) cervical cancer. Knockdown of endogenous MALAT1 significantly reduced cell growth rate and invasion and increased cell apoptosis of Hela and siHa cells. Besides, knockdown of MALAT1 increased the expression of miRNA-124, while ectopic expression of miR-124 decreased MALAT1 expression. MALAT1 can indirectly modulate GRB2 expression via competing miR-124. Knockdown of GRB2 reduced cell invasion and increased cell apoptosis. In conclusion, MALAT1 can promote HR-HPV (+) cancer cell growth and invasion at least partially through the MALAT1-miR-124-RBG2 axis. 26242259 2015 MALAT1-miR-124-RBG2 axis is involved in growth and invasion of HR-HPV-positive cervical cancer cells. 618 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 ovarian cancer C56.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc. ovarian cancer tissues, cell lines (SKOV3, A2780, HO8910, and CAOV3) up-regulated lncRNA-MALAT1 was specifically upregulated in ovarian cancer cell lines and promoted ovarian cancer-cell growth through targeting microRNA (miR)-506. Knockdown of MALAT1 inhibited the proliferation and DNA synthesis of human ovarian cancer cell in vitro. In addition, miR-506-dependent iASPP regulation was required in MALAT1-induced ovarian cancer-cell growth. 28031721 2016 Long noncoding RNA MALAT1-regulated microRNA 506 modulates ovarian cancer growth by targeting iASPP. 619 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 hepatocellular carcinoma C22.0 M8170/3 RT-PCR, Western blot, Luciferase reporter assay HCC cell lines (HepG2 and MHCC97) up-regulated MALAT1 was highly expressed in HCC cell lines when compared to normal liver cells. Malat1 silence suppressed HCC cells viability, migration and invasion, induced apoptosis, and arrested more cells in G0/G1 phase. Malat1 acted as a circular endogenous RNA (ceRNA) for miR-195. Malat1 silence could not suppress HCC cell growth and motility when miR-195 was knocked down. EGFR was a direct target of miR-195. miR-195 overexpression could not suppress HCC cell growth and motility when the 3'UTR site of EGFR was overexpressed. Furthermore, Malat1 silence blocked the activation of PI3K/AKT and JAK/STAT pathways, while EGFR overexpression activated them. 28722813 2017 Knockdown of long non-coding RNA MALAT1 inhibits growth and motility of human hepatoma cells via modulation of miR-195. 620 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, Luciferase reporter assay, Western blot cell lines (Lovo, HCT116, SW480, HT29, HIEC) up-regulated MALAT1 was upregulated in human colon cancer cell lines.miR-129-5p was downregulated in colon cancer cells with a significant increase of HMGB1 expression.miR-129-5p was identified and confirmed as a direct regulator of MALAT1 and miR-129-5p mimics were able to restrain the progression of colon cancer cells. In addition, high motility group box protein 1 (HMGB1), was predicted as a mRNA target of miR-129-5p. MALAT1 may serve as a competing endogenous lncRNA (ceRNA) to mediate HMGB1 by sponging miR-129-5p in colon cancer. 29130936 2017 JAK2-binding long noncoding RNA promotes breast cancer brain metastasis. 621 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, Western blot, Luciferase reporter assay, Immunofluorescent assay etc. cell lines (HBL-100, MCF-7, MDA-MB-231) up-regulated In this study we identified long non-coding RNA (lncRNA) MALAT1 can function as a ceRNA of cell division cycle 42 (cdc42) 3'UTR in inducing migration and invasion of breast cancer cells via miR-1. We found that miR-1 bound both MALAT1 and cdc42 3'UTR directly. Further study showed that MALAT1 induced migration and invasion of breast cancer cells while reduced the level of cdc42. 26926567 2016 MALAT1 induced migration and invasion of human breast cancer cells by competitively binding miR-1 with cdc42 622 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, Western blot, Luciferase reporter assay etc. breast cancer tissues down-regulated The effects of up-regulation of miR-1 were similar to that of silencing K-RAS and MALAT1 in breast cancer cells 26275461 2015 Hsa-miR-1 suppresses breast cancer development by down-regulating K-ras and long non-coding RNA MALAT1 623 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell proliferation assay etc. gastric cancer tissues, cell lines (MKN28, MKN45 and SGC-7901) up-regulated MALAT1 was upregulated in GC tissues and higher MALAT1 expression was correlated with larger tumor size, lymph node metastasis, and TNM stage. Moreover, we revealed that MALAT1 was a direct target of miR-202 and knockdown of MALAT1 significantly decreased the expression of Gli2 through negatively regulating miR-202. In addition, knockdown of Malat1 inhibited GC cells proliferation, S-phase cell number, and induced cell apoptosis via negatively regulating miR-202 in vitro. 27887846 2017 Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 regulates the expression of Gli2 by miR-202 to strengthen gastric cancer progression. 624 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR, Cell transfection, Western blot, Luciferase reporter assay, Flow cytometry assay, MTT assay etc. osteosarcoma tissues, cell lines (Saos2, MG63, U2OS, SW1353, HOS) up-regulated MALAT1 and HMGB1 were significantly increased in human OS cell lines and knockdown of MALAT1 reduced HMGB1 expression. Moreover, knockdown of MALAT1 decreased HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on HMGB1 expression, OS cell growth and the promotion of apoptosis. 28346809 2017 MALAT1 promotes osteosarcoma development by regulation of HMGB1 via miR-142-3p and miR-129-5p. 625 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 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. 626 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR, Cell transfection, Western blot, Luciferase reporter assay, MTT assay etc. osteosarcoma tissues, cell lines (Saos2, MG63, U2OS, SW1353, hFOB) up-regulated Here, we showed that MALAT1 was increased in human OS cell lines and tissues and promoted OS cell growth, while MALAT1 knockdown suppressed OS cell growth. TGFA expression was positively correlated with MALAT1 expression, and both were negatively correlated with MIR376A expression. There was a direct interaction between MIR376A and MALAT1 via a putative MIR376A binding site within the MALAT1 3'-untranslated region (3'-UTR). There was also a direct interaction between MIR376A and the TGFA 3'-UTR. Thus, MALAT1 may promote OS cell growth through inhibition of MIR376A, leading to increased expression of TGFA. 27458156 2016 MALAT1 promotes osteosarcoma development by targeting TGFA via MIR376A. 627 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay etc. hepatocellular carcinoma tissues, cell lines (LO2, Bel7404, Huh7, and HepG2) up-regulated microRNA-204 was significantly downregulated in sh-MALAT1 HepG2 cell and 15 hepatocellular carcinoma tissues by quantitative real-time polymerase chain reaction analysis.microRNA-204 as a potential interacting partner for MALAT1. Functionally, wound-healing and transwell assays revealed that microRNA-204 significantly inhibited the migration and invasion of hepatocellular carcinoma cells.Notably,sirtuin 1 was recognized as a direct downstream target of microRNA-204 in HepG2 cells. Moreover, si-SIRT1 significantly inhibited cell invasion and migration process. These data elucidated, by sponging and competitive binding to microRNA-204, MALAT1 releases the suppression on sirtuin 1, which in turn promotes hepatocellular carcinoma migration and invasion. 28720061 2018 The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1. 628 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 hepatocellular carcinoma C22.0 M8170/3 qPCR, luciferase reporter assay hepatocellular carcinoma tissues, cell lines (MHCC97-H, SMMC-7721, Hep3B and HepG2) differential expression Furthermore, we identified long non-coding RNA MALAT1 as a molecular sponge of miR-146b-5p to down-regulate its expression in HCC. 28404923 2017 Down-regulation of miR-146b-5p by long noncoding RNA MALAT1 in hepatocellular carcinoma promotes cancer growth and metastasis 629 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc. breast cancer tissues, cell lines (MCF-7, Bcap-37 and MDAMB-435S) up-regulated We also found that MALAT1 was increased in most breast cancer cells. In contrast, miR-124 was downregulated in the MCF-7 cells with MALAT1 overexpression. We found that MALAT1 expression had no effect in breast cancer cells treated with the miR-124 mimic or miR-124 inhibitor. Taken together, our results reveal that MALAT1 may act as an endogenous potent regulator that reduces miR-124 expression. 26918449 2016 miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation. 630 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 breast cancer C50 NA qPCR, RNAi, Western blot etc. breast cancer tissues, cell lines (MDA-MB-231, MDA-MB-453, HS578T, T47D, AU565 and SKBr3) up-regulated KDM5B induces the expression of MALAT1 and its effector metastasis- associated genes in triple negative breast carcinoma cells. KDM5B interacts with MALAT1 to modulate its expression in triple negative breast carcinoma cells and consequently facilitate invasion and associated metastatic activities. 26917489 2016 Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448. 631 MCM3AP-AS1 NA ENSG00000215424 NR_002776 GRCh38_21:46229217-46259390 glioblastoma NA M9440/3 qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP glioma tissues, GBM cell line U87 up-regulated lncRNA antisense 1 to Micro-chromosome maintenance protein 3-associated protein (MCM3AP-AS1) was upregulated whereas miR-211 was downregulated in glioma-associated endothelial cells (GECs).Furthermore, knockdown of MCM3AP-AS1 increased the expression of miR-211.miR-211 targeted KLF5 3'-UTR and consequently inhibited KLF5 expression.Besides,in this study we found that MCM3AP-AS1 knockdown decreased KLF5 and AGGF1 expression by upregulating miR-211.In addition, KLF5 was associated with the promoter region of AGGF1.Knockdown of KLF5 decreased AGGF1 expression by transcriptional repression, and also inhibited the activation of PI3K/AKT and ERK1/2 signaling pathways. 29375300 2018 The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis. 632 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 liver cancer C22.0 NA RT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP liver cancer tissue, liver cancer cell line (Hep3B) down-regulated Mechanistically, MEG3 promotes the expression and maturition of miR122 which targets PKM2.Therefore,MEG3 decreases the expression and nuclear location of PKM2 dependent on miR122.Furthermore,MEG3 also inhibits CyclinD1 and C-Myc via PKM2 in liver cancer cells.On the other hand,MEG3 promotes β-catenin degradation through ubiquitin-proteasome system dependent on PTEN. Strikingly, MEG3 inhibits β-catenin activity through PKM2 reduction and PTEN increase.Significantly,we also found that excessive β-catenin abrogated the effect of MEG3 in liver cancer.MEG3 overexpression increased the PTEN 3-UTR mRNA methylation compared to control. MEG3 may be an underlying therapeutic target for LUAD functioning as ceRNAs for the regulation of miRNA-mRNA in lung adenocarcinoma. 29449541 2018 Long noncoding RNA MEG3 suppresses liver cancer cells growth through inhibiting β-catenin by activating PKM2 and inactivating PTEN. 633 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 gastric cardia adenocarcinoma C16.0 M8140/3 qPCR, Cell transfection, Cell proliferation assay etc. GCA tissues, cell lines (MKN45, SGC7901, BGC823, and AGS) down-regulated MEG3 and miR-770 was significantly downregulated in GCA patients and cell lines. Overexpression of MEG3 and miR-770 inhibited gastric cancer cell proliferation and invasion in vitro. Furthermore, the expression level of MEG3 and miR-770 was significantly increased in cancer cells after treated with 5-Aza-dC. The aberrant hypermethylation of proximal promoter and enhancer region of MEG3 was detected in GCA tissues. 28345805 2017 Promoter hypermethylation-mediated downregulation of miR-770 and its host gene MEG3, a long non-coding RNA, in the development of gastric cardia adenocarcinoma. 634 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 T-cell lymphoblastic lymphoma NA M9729/3 qPCR, Western blot, Luciferase report assay etc. T-LBL tissues, cell lines (CCRF-CEM, Jurkat, SUP-T1, H9) down-regulated Down-regulated level of MEG3 was also found in three T-LBL cell lines (CCRF-CEM, Jurkat and SUP-T1) compared with human T-cell line H9. MEG3 worked as an anti-oncogene in T-LBL, and the MEG3-miR-214-AIFM2 pathway regulated the growth of T-LBL, providing potential prognosis markers as well as new potential targets for T-LBL treatment. MEG3 effectively suppressed tumor growth and the expression of proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA). 28534937 2017 The inhibitory effect of MEG3/miR-214/AIFM2 axis on the growth of T-cell lymphoblastic lymphoma. 635 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 testicular germ cell tumor C62 M9065/3 qPCR, RNAi, Western blot, Luciferase reporter assay, ISH, MTT assay etc. TGCT tissues, cell line (NCCIT) down-regulated Compared to paired adjacent non-tumor tissue (NT), and found that Meg3 levels were significantly decreased and miR-1297 levels were unchanged in TGCT. Luciferase report assay showed that Meg3 overexpression abolished the effects of miR-1297 on 3'-UTR of PTEN mRNA, possibly through competitive binding, which was supported by double fluorescent in situ hybridization showing co-localization of intracellular Meg3 and miR-1297 signals in TGCT cells. Moreover, Meg3 overexpression abolished the inhibitory effects of miR-1297 on PTEN, resulting in deactivation of Akt and decreases in cell growth. 27158395 2016 Crosstalk between Meg3 and miR-1297 regulates growth of testicular germ cell tumor through PTEN/PI3K/AKT pathway. 636 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 tongue squamous cell carcinoma C02 M8070/3 microarray, MSP-PCR, RNAi, Western blot etc. TSCC tissues, cell lines (SCC-15, CAL27 etc.) down-regulated We report here that miR-26a and lncRNA MEG3 gene expression were both strongly reduced in TSCC compared with levels in matched nonmalignant tissues, and combined low expression levels of both miR-26a and MEG3 emerged as an independent prognostic factor for poor clinical outcome in TSCC patients. 24343426 2014 Expression, regulation and roles of miR-26a and MEG3 in tongue squamous cell carcinoma. 637 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 pancreatic neuroendocrine tumor C25 M8246/3 qPCR, Western blot cell line (BON1, QGP-1) down-regulated MEG3 was low expressed in BON1 and QGP-1 cells, when compared to three normal cell lines (HEK293, CCL-153, and EC-304). miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells. 29132136 2017 MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183 638 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 osteosarcoma NA M9180/3 qPCR cell line (hFOB 1.19, U-2 OS) down-regulated the expression level of MEG3 gene was increased while the expression level of miR-664a was decreased.In addition, changes in expression level of MEG3 and miR-644a interferes with the migration of osteosarcoma cells migration speed of osteosarcoma cells.As a result of this study, it was shown that the upregulated expression of miR-664a could have an inhibitory effect on MEG3 gene expression and migration of osteosarcoma cells. 28669734 2017 Inhibition of miR-664a interferes with the migration of osteosarcoma cells via modulation of MEG3. 639 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 lung cancer C34 NA qPCR, RIP, ChIP, Cell migration assay etc. cell lines (A549 and LC-2/ad) up-regulated The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-β (TGF-β)-induced EMT of human lung cancer cell lines. Knockdown of MEG3 inhibited TGF-β-mediated changes in cell morphology and cell motility characteristic of EMT and counteracted TGF-β-dependent changes in the expression of EMT-related genes such as CDH1, ZEB family, and the microRNA-200 family. Overexpression of MEG3 influenced the expression of these genes and enhanced the effects of TGF-β in their expressions. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. 27852821 2017 MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. 640 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 gastric cancer C16 NA qPCR, Western blot, RNAi etc. cell lines (AGS, NCI?N87, SGC7901, MKN45, TMK1 and GES1) down-regulated MEG3 was downregulated while miR?21 was upregulated in gastric cancer tissues and cell lines by qRT-PCR.Overexpression of MEG3 suppressed cell mobility of gastric cancer cells (AGS) by downregulating the expression of MMP?3, MMP?9 and VEGF.overexpression of MEG3 also suppressed epithelial?mesenchymal transition (EMT) by increasing the expression of an epithelial marker (E?cadherin) and downregulating the expression of mesenchymal markers,indicating that MEG3 suppressed cell mobility through the inhibition of EMT in gastric cancer.The expression of miR?21 was negatively regulated by MEG3 and overexpression of miR-21 promoted cell mobility of AGS through activation of EMT.Co?transfection of lncRNA?MEG3 and miR?21 mimic counteracted the inhibitory effect on the cell mobility attributed to MEG3,suggesting that the MEG3/miR-21 axis affects cell mobility by suppressing EMT in gastric cancer. 29749532 2018 MEG3/miR?21 axis affects cell mobility by suppressing epithelial?mesenchymal transition in gastric cancer. 641 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay, Western blot etc. cell lines (Huh7, 7721, HepG2, 7402, LO2) up-regulated MEG3 over-expression imposes another level of post-transcriptional regulation, whereas MEG3 overexpression increase the expression of the miR-664 target gene, ADH4, through competitive ‘sponging’ miR-664. In addition,NF-κB may affect transcription of MEG3 by directly binding to the promoter region. Our data revealed that NF-κB may affect the transcript of MEG3. MEG3 overexpression inhibited the proliferation of HCC cells, at least in part by affecting miR-664mediated regulation of ADH4. Together, these results suggest that MEG3 is a suppressor of tumor which acts in part through ‘sponging’ miR-664. 28374914 2017 Overexpression of long non-coding RNA MEG3 inhibits proliferation of hepatocellular carcinoma Huh7 cells via negative modulation of miRNA-664 642 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 hepatocellular carcinoma C22.0 M8170/3 qPCR, MTT assay etc. cell lines (HepG2 and HuH-7) up-regulated In result we found that the DNC dependent overexpression of miR-29a and miR-185 can down-regulate the expression of DNMT1, 3A and 3B and subsequently overexpresses MEG3. 26321746 2015 Dendrosomal curcumin increases expression of the long non-coding RNA gene MEG3 via up-regulation of epi-miRs in hepatocellular cancer. 643 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues down-regulated RNA in situ hybridization showed intense cytoplasmic expression of MEG3 in non-neoplastic liver with absent or very weak expression in HCC tissues. Enforced expression of MEG3 in HCC cells significantly decreased both anchorage-dependent and -independent cell growth, and induced apoptosis. We confirmed a similar miR-29a-dependent modulation of DNMT protein expression in HCC cells. 21625215 2011 microRNA-29 can regulate expression of the long non-coding RNA gene MEG3 in hepatocellular cancer. 644 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay etc. cell lines (MKN74, MKN45, SGC7901, AGS), GC tissues down-regulated MEG3 suppressed proliferation and metastasis of GC cells through inhibiting miR-21 expression.MiR-21 was a target of MEG3. 29710493 2018 LncRNA-MEG3 inhibits proliferation and metastasis by regulating miRNA-21 in gastric cancer. 645 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 cervical cancer C53 NA qPCR, RNAi, Western blot etc. cervical cancer tissues, cell lines (HeLa, CaSki) down-regulated We observed that MEG3 was downregulated in cervical cancer tissues, compared to the adjacent normal tissues, and was negatively related with FIGO stages, tumor size, lymphatic metastasis, HR-HPV infection and the expression of homo sapiens microRNA-21 (miR-21). Furthermore, we focused on the function and molecular mechanism of MEG3, finding that overexpression of MEG3 reduced the level of miR-21-5p expression, causing inhibition of proliferation and increased apoptosis in cervical cancer cells. In summary, our findings indicate that MEG3 function as a tumor suppressor by regulating miR-21-5p, resulting in the inhibition of tumor growth in cervical cancer. 26574780 2015 Long noncoding RNA MEG3 is downregulated in cervical cancer and affects cell proliferation and apoptosis by regulating miR-21. 646 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissues, cell line (GES-1) down-regulated We found that expression of both miR-141 and MEG3 was significantly reduced in GC compared with levels in matched nonmalignant tissues. Positive correlation between miR-141 and MEG3 was found in both tumor tissues and control tissues. Furthermore, the over-expression of either miR-141 or MEG3 in 7901 and MKN45 cells inhibited cell proliferation and cell cycle progression and promoted cell apoptosis. E2F3 was identified as a target of miR-141, and its inhibition significantly reduced MEG3 expression. E2F3 over-expression partly reversed the changes caused by transfection of miR-141 mimic, and inhibition of miR-141 or MEG3 overrides MEG3- or miR-141-induced modulation of cell growth in GC. 26233544 2015 MiR-141 Inhibits Gastric Cancer Proliferation by Interacting with Long Noncoding RNA MEG3 and Down-Regulating E2F3 Expression. 647 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 gastric cancer C16 NA qPCR, Luciferase reporter assay, RNA pull-down assay etc. gastric cancer tissues, cell lines (MGC-803, HGC-27, MKN-45, SGC-7901, BGC-823, AGS) down-regulated MEG3 is decreased in GC patients and cell lines, and its expression was associated with metastatic GC. Furthermore, ectopic expression of MEG3 in HGC-27 and MGC-803 cells inhibited cell proliferation, migration, invasion, and promoted cell apoptosis, which might be due to MEG3 sequestering oncogenic miR-181 s in GC cells. Furthermore, MEG3 could up-regulated Bcl-2 via its competing endogenous RNA (ceRNA) activity on miR-181a. 26253106 2015 Long non-coding RNA MEG3 functions as a competing endogenous RNA to regulate gastric cancer progression. 648 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 gastric cancer C16 NA qPCR, RNAi, Western blot etc. gastric cancer tissues, cell lines (SGC-7901, BGC-823, GES-1 etc.) down-regulated We examined the expression of MEG3 in 52 gastric cancer samples using quantitative qPCR and found the down-regulation of MEG3 in both gastric cancer tissues and cell lines. The positive correlation of MEG3 and miR-148a was further confirmed in SGC-7901 and BGC-823 gastric cancer cell lines. Hypermethylation of MEG3 differentially methylated regions was identified by methylation-specific PCR, and MEG3 expression was increased with the inhibition of methylation with siRNA to DNMT-1 in gastric cancer cells. In addition, transfection of MEG3 siRNA into gastric cancer cells diminished the suppression of proliferation induced by overexpression of miR-148a. 24515776 2014 MiR-148a regulates MEG3 in gastric cancer by targeting DNA methyltransferase 1. 649 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 glioma NA M9380/3 qPCR, Cell transfection, Western blot, Luciferase reporter assay, Cell proliferation assay etc. glioma tissues, cell lines (U251, U87, NHA) down-regulated MEG3 was down-regulated and miR-19a was up-regulated in malignant glioma tissues and cell lines. MiR-19a represses the expression of PTEN and promotes glioma cell proliferation, migration and invasion. However, MEG3 could directly bind to miR-19a and effectively act as a competing endogenous RNA (ceRNA) for miR-19a to suppress tumorigenesis. 28276316 2017 Long Noncoding RNA MEG3 Suppresses Glioma Cell Proliferation, Migration, and Invasion By Acting As Competing Endogenous RNA of MiR-19a. 650 MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT ENSG00000225783 NR_003491 GRCh38_22:26646428-26676475 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RNAi etc. hepatocellular carcinoma tissues, cell lines (HepG2, Huh7, SK-HEP-1, HLE and L02) up-regulated Upregulation of MIAT is related to the proliferation and invasion of HCC,and downregulating MIAT expression inhibited HCC cell proliferation and invasion.The H3/H4 histone acetylation level of MIAT promoter in HCC tissues was higher than that in normal tissues.MIAT negatively regulated miR-214 in HCC cells. Inhibition of miR-214 reversed the influence of MIAT downregulation on HCC cell proliferation and invasion.In nude mouse xenograft models,downregulation of MIAT markedly suppressed the tumor growth of HCC via releasing miR-214.In conclusion, lncRNA MIAT promotes the proliferation and invasion of HCC cells through sponging miR-214, which brings a novel target for the therapy and prognosis of hepatocellular carcinoma.NEW & NOTEWORTHY This is the first research showing long noncoding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) to have a regulatory effect on hepatocellular carcinoma. 29097358 2018 lncRNA MIAT promotes proliferation and invasion of HCC cells via sponging miR-214. 651 MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT ENSG00000225783 NR_003491 GRCh38_22:26646428-26676475 colorectal cancer C19.9 NA qPCR, Western blot, Luciferase reporter assay etc. colorectal cancer tissues, cell lines (HcoEpic, HT-29, SW480, and LOVO) up-regulated MIAT was highly expressed in CRC tissues and cells.MIAT knockdown inhibited proliferation,migration and invasion and enhanced apoptosis of CRC cells.Further,we demonstrated that MIAT acted as a competing endogenous RNA for miR-132, antagonized its functions,and resulted in the de-repression of its target gene Derlin-1,which acted as an oncogene in promoting growth and metastasis of CRC cells.In LOVO and SW480 cells with si-MIAT, miR-132 inhibitor resulted in an increase of cell proliferation, migration and invasion and a decrease of cell apoptosis, which was partially abolished by transfection of Derlin-1 shRNA.Our data indicated that highly expressed MIAT was an oncogenic lncRNA that promoted the growth and metastasis of CRC through miR-132/Derlin-1 axis. 29686537 2018 Long non-coding RNA MIAT promotes growth and metastasis of colorectal cancer cells through regulation of miR-132/Derlin-1 pathway. 652 MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT ENSG00000225783 NR_003491 GRCh38_22:26646428-26676475 non small cell lung cancer C34 M8046/3 qPCR, luciferase reporter assay etc. cell lines (A549, L78, H226) up-regulated MIAT indirectly regulated ZEB1 expression through sponging and suppressing microRNA (miR)-150, which represses ZEB1 and interacts with MIAT in a sequence-specific manner. Thus, MIAT may inhibit ZEB1 expression and promote cell invasion of NSCLC cells via the miR-150/ ZEB1 pathway. Taken together, our findings suggested that MIAT plays an oncogenic role in NSCLC through the ZEB1 signaling pathway by sponging miR-150, and MIAT may therefore serve as a valuable prognostic biomarker and therapeutic target for NSCLC. 28843520 2017 The long non-coding RNA MIAT regulates zinc finger E-box binding homeobox 1 expression by sponging miR-150 and promoteing cell invasion in non-small-cell lung cancer 653 MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT ENSG00000225783 NR_003491 GRCh38_22:26646428-26676475 gastric cancer C16 NA qPCR, RIP, Western blot, Luciferase reporter assayin vitro knockdown etc. cell line (BGC-823, MGC-803), gastric cancer tissues up-regulated MIAT was highly expressed in GC tissues and cell lines and correlated with differentiation degree, TNM stage, distant metastasis, and lymph node metastasis.MIAT knockdown inhibited GC growth and metastasis both in vitro and in vivo.MIAT acted as miR-141 sponge and regulated its target gene DDX5 expression.In BGC-823 and MGC-803 cells with si-MIAT,DDX5 overexpression resulted in an increase of cell proliferation,migration and invasion.Our data indicated that MIAT played an oncogenic role in GC growth and metastasis,and could serve as a novel molecular target for treating GC. 29540201 2018 Long non-coding RNA MIAT promotes gastric cancer growth and metastasis through regulation of miR-141/DDX5 pathway. 654 MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT ENSG00000225783 NR_003491 GRCh38_22:26646428-26676475 breast cancer C50 NA qPCR, Western blot, Luciferase report assay etc. breast tumor tissues, cell lines (MCF-10A, MCF-7) 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. 29100300 2017 Long non-coding RNA MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p. 655 MIF GIF, GLIF ENSG00000240972 NA GRCh38_22:23894004-23895227 cervical cancer C53 NA qPCR, Luciferase reporter assay etc. cell line (Hela) differential expression In this study, we demonstrate that lncRNA‐MIF (Myc inhibitory factor), which is transcribed by c‐Myc, is able to reduce c‐Myc expression. Mechanistically, lncRNA‐MIF competes with coding mRNA Fbxw7 for miR‐586 and relieves the inhibitory effect of miR‐586 on Fbxw7, thereby leading to increased Fbxw7 expression and decreased c-Myc level. 27317567 2016 LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw7-mediated c-Myc degradation 656 MIF GIF, GLIF ENSG00000240972 NA GRCh38_22:23894004-23895227 colon cancer C18 NA qPCR, Luciferase reporter assay etc. cell line (HCT116) differential expression In this study, we demonstrate that lncRNA‐MIF (Myc inhibitory factor), which is transcribed by c‐Myc, is able to reduce c‐Myc expression. Mechanistically, lncRNA‐MIF competes with coding mRNA Fbxw7 for miR‐586 and relieves the inhibitory effect of miR‐586 on Fbxw7, thereby leading to increased Fbxw10 expression and decreased c-Myc level. 27317567 2016 LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw10-mediated c-Myc degradation 657 MIF GIF, GLIF ENSG00000240972 NA GRCh38_22:23894004-23895227 breast cancer C50 NA qPCR, Luciferase reporter assay etc. cell line (MCF7) differential expression In this study, we demonstrate that lncRNA‐MIF (Myc inhibitory factor), which is transcribed by c‐Myc, is able to reduce c‐Myc expression. Mechanistically, lncRNA‐MIF competes with coding mRNA Fbxw7 for miR‐586 and relieves the inhibitory effect of miR‐586 on Fbxw7, thereby leading to increased Fbxw11 expression and decreased c-Myc level. 27317567 2016 LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw11-mediated c-Myc degradation 658 MIF GIF, GLIF ENSG00000240972 NA GRCh38_22:23894004-23895227 lung cancer C34 NA qPCR, Luciferase reporter assay etc. cell line (A549) differential expression In this study, we demonstrate that lncRNA‐MIF (Myc inhibitory factor), which is transcribed by c‐Myc, is able to reduce c‐Myc expression. Mechanistically, lncRNA‐MIF competes with coding mRNA Fbxw7 for miR‐586 and relieves the inhibitory effect of miR‐586 on Fbxw7, thereby leading to increased Fbxw8 expression and decreased c-Myc level. 27317567 2016 LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw8-mediated c-Myc degradation 659 MIF GIF, GLIF ENSG00000240972 NA GRCh38_22:23894004-23895227 lung cancer C34 NA qPCR, Luciferase reporter assay etc. cell line (H1299) differential expression In this study, we demonstrate that lncRNA‐MIF (Myc inhibitory factor), which is transcribed by c‐Myc, is able to reduce c‐Myc expression. Mechanistically, lncRNA‐MIF competes with coding mRNA Fbxw7 for miR‐586 and relieves the inhibitory effect of miR‐586 on Fbxw7, thereby leading to increased Fbxw9 expression and decreased c-Myc level. 27317567 2016 LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw9-mediated c-Myc degradation 660 MIR17HG MIR17HG, C13orf25, FGLDS2, LINC00048, MIHG1, MIRH1, MIRHG1, NCRNA00048, miR-17-92 ENSG00000215417 NR_027349 GRCh38_13:91347820-91354579 prostate cancer C61.9 NA microarray, qPCR etc. prostate cancer tissues, cell lines (LNCaP) up-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. 661 MIR222HG NA ENSG00000270069 NA GRCh38_X:45745211-45770274 prostate cancer C61.9 NA qPCR, luciferase reporter assay, RIP, in vitro knockdown etc. cell line (LNCaP, LNCaP-Abl), PCa tumor tissues up-regulated Upon promoter activation, a set of polyadenylated long non-coding RNA (lncRNA) MIR222HGs was transcribed from this promoter region. Over-expression of these MIR222HGs increased androgen-independent cell growth and repressed the expression of androgen receptor-regulated dihydrotestosterone (DHT)-induced KLK3, TMPRSS2, and FKBP5 in HSPC LNCaP cells, hallmarks of the CRPC phenotype. Clinically, increased expression of MIR222HG is associated with PCa progression to CRPC.MIR222HG may potentially affect miR-mediated expression silencing, subsequently leading to AR reprogramming. Our study highlights an essential role of a non-coding RNA in CRPC development and that differential activation of a single promoter can up-regulate two different types of non-coding RNAs, miR-221/222 and lncRNA MIR222HG, in CRPC. 29540675 2018 Expression of lncRNA MIR222HG co tra Source Oncogenesis SO 2018 Mar 13 7 3 30[PMIDT29540675] 662 MIR31HG MIR31HG, hsa-lnc-31, LOC554202 ENSG00000171889 NR_027054 GRCh38_9:21455642-21559669 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, RNAi, Western blot, RIP, Dual-luciferase reporter assay, ISH etc. cell lines (AsPC-1, PANC-1, CFPAC-1, Hs 766T, SW 1990, MIA PaCa-2, and BxPC-3) up-regulated In this study, we discovered that lncRNA MIR31HG is markedly upregulated in PDAC. Knockdown of MIR31HG significantly suppressed PDAC cell growth, induced apoptosis and G1/S arrest, and inhibited invasion, whereas enhanced expression of MIR31HG had the opposite effects. Inhibition of miR-193b expression significantly upregulated the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b. 26549028 2016 Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b. 663 MIR4697HG MIR4697HG, LINC00947 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. 664 MIR503HG MIR503HG, H19X, MIR503HG2 ENSG00000223749 NR_024607 GRCh38_X:134543337-134546632 anaplastic large-cell lymphoma NA M9714/3 qPCR etc. cell lines (SR-786, KARPAS, MAC-1 and FePD) up-regulated MIR503HG (miR-503 host gene) was highly expressed in ALK-negative cell lines and was significantly upregulated in tumors in mice formed from ALK-negative ALCL cell lines.Depletion of MIR503HG suppressed tumor cell proliferation in vivo and in vitro;conversely, its overexpression enhanced tumor cell growth. MIR503HG-induced proliferation was mediated by the induction of microRNA-503 (miR-503) and suppression of Smurf2, resulting in stabilization of the tumor growth factor-β receptor (TGFBR) and enhanced tumor cell growth. Collectively, these findings support a potential role for MIR503HG in cancer cell proliferation through the miR-503/Smurf2/TGFBR axis and indicate that MIR503HG is a potential marker in ALK-negative ALCL. 29758012 2018 The Long Non-Coding RNA MIR503HG Enhances Proliferation of Human ALK-Negative Anaplastic Large-Cell Lymphoma. 665 MNX1-AS1 MNX1-AS1, CCAT5 ENSG00000243479 NR_038835 GRCh38_7:157010805-157016426 glioblastoma NA M9440/3 qPCR etc. glioblastoma tissues, cell lines (U138, LN229, T98 and U251) up-regulated the expression of MNX1-AS1 was significantly upregulated in GBM tissues and cell lines.Knockdown of MNX1-AS1 significantly inhibited the proliferation,migration and invasion of GBM cells. In terms of mechanism,we found that MNX1-AS1 could bind to miR-4443 in GBM cells.Overexpression of miR-4443 significantly inhibited the expression of MNX1-AS1, and vice versa. Moreover,there was an inverse correlation between the expression levels of MNX1-AS1 and miR-4443 in GBM tissues. Moreover,we found that overexpression of miR-4443 inhibited the proliferation, migration and invasion of GBM cells. Besides,we showed that inhibition of miR-4443 reversed the effects of MNX1-AS1 knockdown on GBM cell proliferation, migration and invasion. 29678219 2018 LncRNA MNX1-AS1 promotes glioblastoma progression through inhibition of miR-4443. 666 MSTO2P NA ENSG00000203761 NA GRCh38_1:155745829-155750137 gastric cancer C16 NA qPCR etc. gastric cancer tissues, blood, cell lines (NCI-N87, SNU-1, SNU-16, AGS, and KATO-III) differential expression The expression levels of misato family member 2, pseudogene were significantly associated with lymphatic metastasis and distal metastasis in 80 paired gastric cancer tissues using real-time quantitative reverse transcription polymerase chain reaction experiments. Long non-coding RNA misato family member 2, pseudogene influenced biologic functions in gastric cancer cells via indirectly regulating the activation of miR-335. 28618927 2017 Long non-coding RNA MSTO2P promotes the proliferation and colony formation in gastric cancer by indirectly regulating miR-335 expression 667 MYCNOS-01 NA NA NA NA rhabdomyosarcoma and neuroblastomacells NA M8900/3 Microarray, qRT-PCR, Western blot, in vitro knockdown Human ARMS cell line (RMS-01), cell line (RH30), The human NB cell lines (KELLY and SY5Y) up-regulated MYCNOS-01 transcript levels were generally higher in NB and RMS tumor samples and cell lines with MYCN genomic amplification. RNA interference of MYCNOS-01 expression did not alter MYCN transcript levels but decreased MYCN protein levels. Conversely, MYCN reduction increased MYCNOS-01 transcript levels,creating a negative feedback loop on MYCN protein levels.Reduction of MYCNOS-01 or MYCN expression decreased cell growth in MYCN-amplified alveolar rhabdomyosarcoma and neuroblastoma cell lines.This is consistent with MYCNOS-01-mediated regulation of MYCN contributing to the phenotype observed.Another possibility therefore is that MYCNOS-01 interacts with an miRNA that targets MYCN for degradation, therefore increasing MYCN protein expression by sequestering away a negative regulating factor. 29466962 2018 The long non-coding RNA MYCNOS-01 regulates MYCN protein levels and affects growth of MYCN-amplified rhabdomyosarcoma and neuroblastoma cells. 668 n335586 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. hepatocellular carcinoma tissues, cell lines (Huh7 and HepG2) up-regulated the expression of n335586 was significantly increased in HBV positive HCC tissues and cells and was induced by HBV in vitro.Function study indicated that lncRNA n335586 remarkably promoted HCC cells migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and metastasis in vivo.Further mechanistic studies showed lncRNA n335586 promoted HCC cells migration and invasion through facilitating the expression of its host gene CKMT1A by competitively binding miR-924. In conclusion,we demonstrated that the n335586/miR-924/CKMT1A axis contributes to HCC cell migration and invasion, which may be helpful for understanding of pathogenesis of HBV-related HCC. Because lncRNA n335586 overlapped with part of CDS and 3′-UTR of CKMT1A,we speculated that it may operate in ceRNA manner. 29753758 2018 LncRNA n335586/miR-924/CKMT1A axis contributes to cell migration and invasion in hepatocellular carcinoma cells. 669 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 esophageal squamous cell cancer NA NA qPCR, Western blot, RIP, Luciferase reporter assay cell line (EC109, EC9706) up-regulated NEAT1 and CTBP2 were upregulated and miR-129 was downregulated in ESCC cells.Moreover, NEAT1 functioned as an endogenous sponge to downregulate miR-129 by competitively binding to miR-129, thereby leading to the derepression of CTBP2, a target of miR-129. 29147064 2017 LncRNA NEAT1 Regulates Cell Viability and Invasion in Esophageal Squamous Cell Carcinoma through the miR-129/CTBP2 Axis 670 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 laryngeal squamous cell cancer C32.3 NA qPCR, Western blot, Luciferase reporter assay etc. LSCC tissues, cell line (Hep-2) down-regulated NEAT1 level was significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues, and patients with neck nodal metastasis or advanced clinical stage had higher NEAT1 expression. Moreover, siRNA mediated NEAT1 knockdown significantly inhibited the proliferation and induced apoptosis and cell cycle arrest at G1 phase in LSCC cells. The growth of LSCC xenografts was significantly suppressed by the injection of NEAT1 siRNA lentivirus. Furthermore, NEAT1 regulated CDK6 expression in LSCC cells which was mediated by miR-107 26822763 2016 Long noncoding RNA NEAT1 promotes laryngeal squamous cell cancer through regulating miR-107/CDK6 pathway 671 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 gastric cancer C16 NA qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP cell lines (BGC823, SGC-7901, AGS, MGC803, MKN28), cell lines (GES-1 and HEK-293T) up-regulated NEAT1 and STAT3 expression were significantly upregulated in human gastric cancer cells including BGC823, SGC-7901,AGS, MGC803 and MKN28 cells compared to normal gastric epithelial cells GES-1 while miR-506 was downregulated.the negative binding correlation between NEAT1 and miR-506. In addition, miR-506 can modulate expression of NEAT1 in vitro. STAT3 was predicted as an mRNA target of miR-506 and miR-506 mimics can suppress STAT3 mRNA expression.downregulation of NEAT1 can restrain gastric cancer development by decreasing STAT3 which can be reversed by miR-506 inhibitors. 29363783 2018 Long noncoding RNA NEAT1-modualted miR-506 regulates gastric cancer development through targeting STAT3. 672 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 ovarian cancer C56.9 NA qPCR, Western blot, Luciferase reporter assay etc. Ovarian cancer tissues up-regulated In this study, we identified that NEAT1 was up-regulated in OC patients and cell lines, and its expression was associated with the FIGO stage and lymph node metastasis. Furthermore, the ectopic expression of NEAT1_1 in OVCAR-3 cell lines promoted cell proliferation and invasion, whereas knockdown of NEAT1_1 did the opposite. Furthermore, NEAT1_1 was stabilized by an RNA-binding protein HuR, but suppressed by miR-124-3p in OC cells. Accordingly, the increased HuR mRNA and decreased miR-124-3p levels were observed in OC patients. 27075229 2016 HuR-regulated lncRNA NEAT1 stability in tumorigenesis and progression of ovarian cancer 673 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 lung cancer C34 NA qPCR, RNAi etc. cell line (A549) differential expression Our result showed that, the level of NEAT1 was up-regulated when the knockdown of miR-449a; on the contrary, the expression of NEAT1 was down-regulated when miR-449a was the overexpression. 25818739 2014 MicroRNA-449a inhibits cell growth in lung cancer and regulates long noncoding RNA nuclear enriched abundant transcript 1. 674 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 glioma NA M9380/3 qPCR etc. cell line (CD133+ U87) up-regulated We found higher NEAT1 RNA expression in CD133+ human glioma primary culture stem cells and CD133+ U87 cells via RT-PCR. Moreover, NEAT1 knockdown in the CD133+ U87 cells resulted in decreased colony formation, increased G1 cell cycle arrest and apoptosis. In addition, these effects were accompanied by miR-107 activation and inactivation of CDK6 protein. 27878295 2017 Silencing of the long non-coding RNA NEAT1 suppresses glioma stem-like properties through modulation of the miR-107/CDK6 pathway. 675 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 glioma NA M9380/3 qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay etc. cell lines (U87 MG, U251MG and HEK 293T) up-regulated NEAT1 was remarkably up-regulated in glioma endothelial cells (GECs). Knockdown of NEAT1 impaired the integrity and increased the permeability of the BTB, accompanied by downregulation of expression of the tight junction proteins ZO-1, occludin and claudin-5 in GECs. Knockdown of NEAT1 also down-regulated the expression of sex determining region Y-box protein 5 (SOX5), which was defined as a direct and functional downstream target of miR-181d-5p. SOX5 interacts with the promoter region of ZO-1, occludin and claudin-5 in GECs. 28185956 2017 Long non-coding RNA NEAT1 regulates permeability of the blood-tumor barrier via miR-181d-5p-mediated expression changes in ZO-1, occludin, and claudin-5. 676 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 papillary thyroid cancer NA M8260/3 Microarray, QRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown PTC tissues, Thyroid papillary cell line NPA87 (BNCC338081), TPC-1(BNCC337912) and KAT-5 (BNCC338083) up-regulated LncRNA NEAT1 was highly expressed in PTC tissues and cell lines and could deteriorate PTC by promoting proliferation, invasion, and migration accompanied by less apoptosis. Besides, miR-129-5p/lncRNA NEAT1 were found to negatively correlate with each other by direct target relationship and their combination suppressed the progression of PTC. KLK7,a highly expressed downstream protein in PTC tissues,could be directly regulated by miR-129-5p in a negative way. KLK7 accelerated the deterioration of PTC in vitro experiments which could be reversed by sh-lnc RNA NEAT1 and miR-129-5p mimics.In vivo experiments, silence of lncRNA NEAT1 restrain tumor growth in weight and volume. 29319165 2018 Long noncoding RNA NEAT1 regulate papillary thyroid cancer progression by modulating miR-129-5p/KLK7 expression. 677 NEAT1_2 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 papillary thyroid cancer NA M8260/3 qPCR，RNAi, Western blot cell line (Nthy-ori 3-1, K1, IHH4, TPC1, BCPAP), PTC tissues up-regulated The relative expression level of NEAT1_2 was positively associated with TNM stage and tumor size. NEAT1_2 knockdown led to a significant inhibition of growth and metastasis, and induced apoptosis in PTC cells. Knockdown of NEAT1_2 significantly inhibited malignant biological behavior by downregulating the oncogene ATAD2. NEAT1_2 could act as a competing endogenous RNA to regulate the expression of ATAD2 through downregulating miR-106b-5p. 29515109 2018 NEAT1_2 functions as a competing endogenous RNA to regulate ATAD2 expression by sponging microRNA-106b-5p in papillary thyroid cancer. 678 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 non small cell lung cancer C34 M8046/3 qPCR, Luciferase activity assay, Western blot etc. cell lines (A549, H1299, H460, H1975) up-regulated NEAT1 was upregulated while hsa-mir-98-5p was downregulated respectively in NSCLC cell lines compared to human normal lung epithelial BES-2B cells. Inhibition of NEAT1 can suppress the progression of NSCLC cells and hsa-mir-98-5p can reverse this phenomenon. Bioinformatics search was used to elucidate the correlation between NEAT1 and hsa-mir-98-5p. Additionally, a novel mRNA target of hsa-mir-98-5p, MAPK6, was predicted. NEAT1 was able to increase MAPK6 expression and hsa-mir-98-5p mimics can inhibit MAPK6 via downregulating NEAT1 levels. We speculated that NEAT1 may act as a competing endogenous lncRNA (ceRNA) to upregulate MAPK6 by attaching hsa-mir-98-5p in lung cancers. Taken these together, NEAT1/has-mir-98-5p/MAPK6 is involved in the development and progress in NSCLC. NEAT1 could be recommended as a prognostic biomarker and therapeutic indicator in NSCLC diagnosis and treatment. 29095526 2017 NEAT1/has-mir-98-5p/MAPK6 axis is involved in non-small-cell lung cancer (NSCLC) development 679 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown cell lines (MCF7, MDAMB453, MDAMB231, SKBR3 and MCF10A) up-regulated NEAT1 levels were significantly increased in human breast cancer cells including MCF-7, MDA-MB-453, MDA-MB-231, and SKBR3 cells compared to normal mammary epithelial cells MCF-10A while miR-448 was decreased. We found that downregulation of NEAT1 was able to inhibit the growth of breast cancer cells and miR-448 mimic exerted the similar function. Bioinformatics analysis and dual luciferase reporter assays confirmed the negative correlation between NEAT1 and miR-448 in vitro. It was speculated in our study that NEAT1 can serve as a competing endogenous lncRNA (ceRNA) to modulate ZEB1 by sponging miR-448 in breast cancer. 29323713 2018 NEAT1 contributes to breast cancer progression through modulating miR-448 and ZEB1. 680 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, RNAi, ChIP etc. cell lines (MCF10A, MCF7 and HCC1937) up-regulated Our studies show that NEAT1 upregulation resulting from BRCA1 deficiency stimulates in vitro and in vivo breast tumorigenicity. NEAT1 epigenetically silences miR-129-5p expression by promoting the DNA methylation of the CpG island in the miR-129 gene. Silencing of miR-129-5p expression by NEAT1 results in upregulation of WNT4 expression, a target of miR-129-5p, which leads to activation of oncogenic WNT signaling. Our functional studies indicate that this NEAT1/miR-129-5p/WNT4 axis contributes to the tumorigenic effects of BRCA1 deficiency. Finally our in silico expression correlation analysis suggests the existence of the BRCA1/NEAT1/miR-129-5p axis in breast cancer. 27556296 2016 Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis. 681 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 glioma NA M9380/3 qPCR, Cell transfection, Western blot, RIP, Dual-luciferase reporter assay, Cell migration and invasion assay etc. glioma tissues, cell lines (U87, T98G, U251, A272 and U373) up-regulated Quantitative real-time PCR demonstrated that NEAT1 was upregulated in GSCs. NEAT1 knockdown inhibited GSC cell proliferation, migration and invasion and promoted GSC apoptosis. A potential binding region between NEAT1 and microRNA let-7e was confirmed by dual-luciferase assays. Upregulation of NEAT1 reduced the expression of let-7e, and there was reciprocal repression between NEAT1 and let-7e in an Argonaute 2-dependent manner. Let-7e expression was lower expression in glioblastoma tissues and GSCs than in normal brain tissues and cells. Restoration of let-7e suppressed tumor function by inhibiting proliferation, migration and invasion while promoting apoptosis in GSCs. 27556696 2016 Knockdown of NEAT1 restrained the malignant progression of glioma stem cells by activating microRNA let-7e. 682 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 glioma NA M9380/3 qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. glioma tissues, cell lines (U87, U373, and U251) up-regulated We suggested that NEAT1 was upregulated in glioma tissues than noncancerous brain tissues. Knockdown of NEAT1 reduced glioma cell proliferation, invasion, and migration. RNA immunoprecipitation assay combined with luciferase reporter assay confirmed miR-449b-5p-specific binding to NEAT1. Furthermore, we verified that c-Met was a directly target of miR-449b-5p. Rescue assays demonstrated NEAT1 functions a molecular sponge for miR-449b-5p and leads to the upregulation of c-Met. 26242266 2016 Long noncoding RNA NEAT1 promotes glioma pathogenesis by regulating miR-449b-5p/c-Met axis. 683 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. lung tissues, cell lines (A549, SPC-A1, H1299, 95D, SK-MES-1, NCI-H520) up-regulated NEAT1 was highly expressed in NSCLC,and high NEAT1 expression was associated with a shorter overall survival.NEAT1 promoted NSCLC cell growth and affected the cell cycle process in vitro. Furthermore, NEAT1 was observed to bind hsa-miR-377-3p, functioning as a competing endogenous RNA, which resulted in de-repression of its target gene E2F transcription factor 3 (E2F3). E2F3, as an oncogene, may promote NSCLC progression.These results suggested that NEAT1 may promote the development of NSCLC through the miR-377-3p-E2F3 pathway. 29085511 2017 Long non?coding RNA NEAT1 regulates E2F3 expression by competitively binding to miR?377 in non?small cell lung cancer 684 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc. breast cancer tissues, cell lines (MCF-7, SKBR3, MDA-MB-453, T-47D and DU4475) up-regulated lncRNA-NEAT1 was specifically upregulated in BC cell lines and promoted BC cell growth through targeting miR-101. Knockdown of NEAT1 inhibited the proliferation and DNA synthesis of human BC cell in vitro. In addition, the regulation of EZH2 by miR-101 was required in NEAT1 induced BC cell growth. These findings indicated that NEAT1 might suppress the tumor growth via miR-101 dependent EZH2 regulation. 28034643 2017 The long non-coding RNA NEAT1 interacted with miR-101 modulates breast cancer growth by targeting EZH2. 685 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay etc. HCC tissue, cell lines (MHCC97H, MHCC97L, SMCC7721, Huh7) up-regulated NEAT1 was notably upregulated in HCC tissues and cells. Higher NEAT1 expression associated with larger tumor size and vascular invasion of HCC patients.Knockdown of NEAT1 significantly suppressed HCC cell proliferation, colony formation and cell invasion. Interestingly, lower miR-613 expression negatively associated with the NEAT1 expression in HCC tissues and was regulated by NEAT1. Additionally, we demonstrated that NEAT1 promoted HCC cell proliferation and invasion by regulating miR-613 expression. 28783584 2017 NEAT1 promotes cell proliferation and invasion in hepatocellular carcinoma by negative regulating miR-613 expression 686 linc-NeD125 MIR100HG, AGD1, linc-NeD125, lncRNA-N2 ENSG00000255248 NR_024430 GRCh38_11:122028327-122556721 neuroblastoma NA M9500/3 qPCR, Cell transfection, Western blot, ChIP, RNA pull-down assay etc. cell lines (BE(2)-C, D283 Med, NB4) down-regulated Linc-NeD125 represents the host gene for miR-125b-1, a microRNA with an established role as negative regulator of human neuroblastoma cell proliferation. Here, we demonstrate that these two overlapping non coding RNAs are coordinately induced during in vitro neuronal differentiation, and that their expression is regulated by different mechanisms. While the production of miR-125b-1 relies on transcriptional regulation, linc-NeD125 is controlled at the post-transcriptional level, through modulation of its stability. 26480000 2015 Identification of linc-NeD125, a novel long non coding RNA that hosts miR-125b-1 and negatively controls proliferation of human neuroblastoma cells. 687 NLC1-C PICSAR, C21orf113, LINC00162, NCRNA00162, NLC1-C, NLC1C, PRED74 ENSG00000275874 NR_024089 GRCh38_21:44999208-45004727 testicular embryonal carcinoma C62 M9070/3 microarray, qPCR, RNAi, Western blot, Northern blot, RIP, RNA pull-down assay etc. testicular tissues, cell lines (NTERA-2, NCCIT, HEK293 T cell) down-regulated NLC1-C, also known as long intergenic non-protein-coding RNA162 (LINC00162), was down-regulated in the cytoplasm and accumulated in the nucleus of spermatogonia and primary spermatocytes in the testes of infertile men with mixed patterns of MA compared with normal control. The accumulation of NLC1-C in the nucleus repressed miR-320a and miR-383 transcript and promoted testicular embryonal carcinoma cell proliferation by binding to Nucleolin. 26539909 2015 Downregulation of miR-320a/383-sponge-like long non-coding RNA NLC1-C (narcolepsy candidate-region 1 genes) is associated with male infertility and promotes testicular embryonal carcinoma cell proliferation. 688 lncRNA-NUTF2P3-001 NUTF2P3 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-1α (HIF-1α) 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. 689 p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay etc. hepatocellular carcinoma tissues, cell lines (L02, HepG2, SMMC7721, Hep3B, MHCC97H and SK-Hep1) down-regulated The effects of miR-9 on HCC cells were studied by using miR-9 inhibitor in vitro. Luciferase assay was used to validate the target of miR-9. The results showed that lincRNA-p21 was downregulated in human HCC tissues and cell lines. LincRNA-p21 overexpression significantly inhibited HCC cell migration and invasion in vitro. Besides, lincRNA-p21 negatively regulated miR-9 expression level, and miR-9 was upregulated in human HCC tissues and cells. MiR-9 knockdown inhibited HCC cell migration and invasion in vitro. Finally,E-cadherin was a direct target of miR-9. The expression level of E-cadherin was found to be regulated by lincRNA-p21 and miR-9. 28721075 2017 LincRNA-p21 inhibits invasion and metastasis of hepatocellular carcinoma through miR-9/E-cadherin cascade signaling pathway molecular mechanism. 690 PCA3 PCA3, DD3, NCRNA00019, PCAT3 ENSG00000225937 NR_015342 GRCh38_9:76691980-76863307 prostate cancer C61.9 NA qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay, Cell proliferation assay etc. prostate cancer tissues, cell lines (RWPE-1, LNCaP) differential expression In the present study, the level of PCA3 expression in prostate cancer cells was reduced by small interfering RNA (siRNA). Subsequently, the ability of LNCaP cell proliferation, invasion, and migration of PCa was compromised both in vivo and in vitro with the occurrence of cell autophagy. The transcription factor, Snail, activated the expression of lncRNA PCA3, which could inhibit the translation of PRKD3 protein via competitive miR-1261 sponging, and thus high expression of PRKD3 further promoted invasion and migration of prostate cancer. 27743381 2016 Snail-activated long non-coding RNA PCA3 up-regulates PRKD3 expression by miR-1261 sponging, thereby promotes invasion and migration of prostate cancer cells. 691 PCAT1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 cholangiocarcinoma NA M810/3 qPCR, Luciferase reporter assay etc. cell lines (QBC939, KMBC, HIBEC) up-regulated PCAT1 is up-regulated in both ECC tissue samples and cell lines. Here, we showed that downregulation of PCAT1 following transfection with silencing RNA reduced ECC cell growth and increased cell apoptosis. Additionally, PCAT1 suppression inhibited ECC cell migration and invasion as determined by transwell assay. Furthermore, we determined that PCAT1 is a competing endogenous for microRNA (miR)-122, with bioinformatics analysis and luciferase-reporter assay results demonstrating that PCAT1 regulated WNT1 expression via miR-122. Moreover, PCAT1 downregulation increased levels of glycogen synthase kinase 3b and significantly decreased b-catenin levels in whole cell lysates and nuclear fractions, indicating that PCAT1 silencing inhibited the Wnt/b-catenin-signaling pathway. We also observed that exogenous expression of WNT1 reversed PCAT1-silencing-induced inhibition of ECC cell growth inhibition. 28753454 2017 Long noncoding RNA PCAT1 regulates extrahepatic cholangiocarcinoma progression via the Wnt/b-catenin-signaling pathway 692 PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 breast cancer C50 NA qPCR etc. BC tissues up-regulated over-expression of PCAT-1 in 12/47 (25.5%) of tumoral tissues compared with their corresponding ANCTs. PCAT-1 is possibly involved in the pathogenesis of fraction of breast cancers. Future studies are needed to evaluate its precise function in breast cancer.In other words, PCAT-1 has a protective effect on cMyc by disruption of MYC regulation by miR-34a. 28989584 2017 Expression Analysis of Long Non-Coding PCAT-1 in Breast Cancer. 693 PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 hepatocellular carcinoma C22.0 M8170/3 qPCR, Luciferase reporter assay, western blot etc. cell lines (MHCC-97H, SMMC-7721, Huh7, HepG2, HCCLM3) up-regulated PCAT-1 could act as an endogenous RNA by directly binding to miR-129-5p. In addition, Luciferase reporter assay and western blotting analyses showed that PCAT-1 repressed inhibitory effect of miR-129-5p and reverse high mobility group box 1 (HMGB1) expression, a target gene of miR-129-5p. PCAT-1 functions as competing endogenous RNA (ceRNA) to provide a better understanding for HCC metastasis, and serves as a potential diagnostic and therapeutic target via PCAT-1/miR-129-5p/HMGB1 regulatory crosstalk for the deadly disease. 28931210 2017 Long noncoding RNA PCAT-1 promotes invasion and metastasis via the miR-129-5p-HMGB1 signaling pathway in hepatocellular carcinoma 694 PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 hepatocellular carcinoma C22.0 M8170/3 qPCR, luciferase reporter assays etc. cell lines (SMMC7721, Huh7) up-regulated Here, we report how miRNAs regulate PCAT-1 expression and also investigate the biological significance of this regulation in hepatocellular carcinoma (HCC). We found that miR-215, a P53-inducible miRNA, is a key regulator of PCAT-1 expression in HCC and identified an interaction between miR-215 and PCAT-1 in dual luciferase reporter gene assays. We also found that posttranscriptional silencing of PCAT-1 by miR-215 or PCAT-1 siRNAs significantly inhibited proliferation of HCC cells and, conversely, that inhibition of endogenous miR-215 upregulated PCAT-1 expression and promoted cell viability. The tumor-suppressing role of miR-215 was further confirmed in an in vivo mouse HCC xenograft model. Of note, gene profiling assays suggested that the kinase CRKlike proto-oncogene, adaptor protein (CRKL) is a potential downstream target of the miR-215- PCAT-1 axis in HCC, and we demonstrated that CRKL silencing significantly suppresses cell proliferation. 28887306 2017 The long noncoding RNA PCAT-1 links the microRNA miR-215 to oncogene CRKL-mediated signaling in hepatocellular carcinoma 695 PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 prostate cancer C61.9 NA qPCR, RNAi, Luciferase reporter assay etc. cell line (LNCaP) up-regulated We show that PCAT-1 promotes prostate cell proliferation and that this phenotype is mediated through up-regulation of the cMyc protein (encoded by the MYC gene). Antagonism of cMyc is able to reverse PCAT-1mediated cell proliferation. We show that PCAT-1 regulates cMyc post-transcriptionally through the MYC 3' untranslated region (UTR). Further, we find a protetcive effetc of PCAT-1 on cMyc by interfering with the regulation of MYC by miR-34a. 25425964 2014 The Long Non-Coding RNA PCAT-1 Promotes Prostate Cancer Cell Proliferation through cMyc. 696 PlncRNA-1 CBR3-AS1, PlncRNA-1, PlncRNA1 ENSG00000236830 NR_038892 GRCh38_21:36131767-36175815 prostate cancer C61.9 NA qPCR, Western blot, Northern blot, RIP, ChIP, Flow cytometry assay etc. prostate cancer tissues, cell lines (22RV1, LNCaP, PC3, DU145) up-regulated In this study, we demonstrated that long non-coding RNA PlncRNA-1, whose expression is promoted by Androgen Receptor (AR), protects AR from microRNA-mediated suppression in PCa cells. PlncRNA-1 knockdown resulted in the up-regulation of a series of AR-targeting microRNAs, among which miR-34c and miR-297 were found to regulate both AR and PlncRNA-1 expression at the post-transcriptional level. Together, the data generated in this study indicate that PlncRNA-1 sponges AR-targeting microRNAs to protect AR from microRNA-mediated down-regulation and that these events form a regulatory feed-forward loop in the development of PCa. 26808578 2016 A feed-forward regulatory loop between androgen receptor and PlncRNA-1 promotes prostate cancer progression. 697 PTCSC3 NA ENSG00000259104 NR_049735 GRCh38_14:36136108-36176468 thyroid cancer C73.9 NA qPCR etc. thyroid cancer tissues, cell lines (BCPAP, FTC133, 8505C etc.) differential expression Following transfection with PTCSC3, all three thyroid cancer cells originating from various pathological types of thyroid cancers demonstrated significant growth inhibition, cell cycle arrest and increased apoptosis. So PTCSC3 as a tumor suppressor was investigated as a competing endogenous RNA for miR-574-5p. 23599737 2013 A long non-coding RNA, PTCSC3, as a tumor suppressor and a target of miRNAs in thyroid cancer cells. 698 PTENP1 PTENP1, PTEN-rs, PTEN2, PTENpg1, PTH2, psiPTEN ENSG00000237984 NA GRCh38_9:33673504-33677499 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. HCC cell lines down-regulated Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation. 25617127 2015 Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation. 699 PTENP1 PTENP1, PTEN-rs, PTEN2, PTENpg1, PTH2, psiPTEN ENSG00000237984 NA GRCh38_9:33673504-33677499 gastric cancer C16 NA qPCR, Cell transfection, Luciferase reporter assay, Cell migration and invasion assay etc. gastric cancer tissues, cell lines (GES-1, AGS, SGC7901, MGC803 and BGC823) down-regulated PTENP1 and PTEN were concurrently downregulated in GC samples. PTENP1 overexpression inhibited cell growth and induced apoptosis in GC cells. We further demonstrated that PTENP1 could act as a ceRNA to sponge miR-106b and miR-93 from targeting PTEN for downregulation using a novel ceRNA in vitro gradient assay. 28212532 2017 Long non-coding RNA PTENP1 functions as a ceRNA to modulate PTEN level by decoying miR-106b and miR-93 in gastric cancer. 700 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 glioma NA M9380/3 qPCR, Western blot Primary glioma tissues up-regulated The long non-coding RNA PVT1 was found to be highly expressed in glioma vascular endothelial cells. PVT1 overexpression increased the expression of Atg7 and Beclin1 by targeting miR-186, which induced protective autophagy, thus promoting glioma vascular endothelial cell proliferation, migration, and angiogenesis. 28351322 2017 PVT1 affects growth of glioma microvascular endothelial cells by negatively regulating miR-186 701 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 esophageal squamous cell cancer NA NA qPCR, Western blot, luciferase reporter assay esophageal squamous cell carcinoma tissues, cell lines (KYSE30, KYSE410, KYSE520, KYSE510, KYSE140, and KYSE150) up-regulated PVT1 expression is significantly up-regulated in ESCC tumor samples compared with their normal counterparts.PVT1 promote ESCC progression via functioning as a molecular sponge for miR-203 and LASP1 and provide the first evidence of dysregulated PVT1/miR-203/LASP1 axis in ESCC. 28404954 2017 Upregulation of the long non-coding RNA PVT1 promotes esophageal squamous cell carcinoma progression by acting as a molecular sponge of miR-203 and LASP1 702 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 glioma NA M9380/3 Western blot, Luciferase reporter assay etc. cell line (HUVEC) differential expression PVT1 affected cell proliferation, migration and in vitro vascular tube formation of HUVECs.In addition,it was determined that PVT1 was able to bind and degrade miR?26b to promote connective tissue growth factor (CTGF) and angiopoietin 2 (ANGPT2) expression.miR?26b was also identified to have a suppressive role in cell proliferation,migration and in vitro vascular tube formation of HUVECs via binding 3'?UTR regions and downregulating CTGF and ANGPT2 expression levels.PVT1 was important in angiogenesis of vascular endothelial cell as ceRNA to bind and degrade miR?26b,which expanded the current understanding of PVT1 as ceRNA to regulate biological processes. 29620147 2018 lncRNA PVT1 promotes the angiogenesis of vascular endothelial cell by targeting miR?26b to activate CTGF/ANGPT2. 703 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 melanoma NA M8720/3 qPCR, RIP etc. cell line (A-375, sk-mel-5,PIG1), melanoma tissue up-regulated PVT1 was highly expressed in the melanoma tissues and cells. Silencing of PVT1 significantly inhibited cell proliferation, migration and invasion, and arrested the cell cycle at the G0/G1 stage. Additionally, PVT1 silencing significantly decreased the cyclin D1 expression in the melanoma cells. 29286144 2017 Effect of long non-coding RNA PVT1 on cell proliferation and migration in melanoma. 704 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 melanoma NA M8720/3 qPCR melanoma tissues, cell lines (M21, B16F10, MM200, MEL-RM, A375, A2058) up-regulated Expression of PVT1 was significantly up-regulated in melanoma tissue and associated with poor prognosis.Overall,our study demonstrates the oncogenic role of PVT1 as a miR-26b sponge, possibly providing a novel therapeutic target for melanoma 28409552 2017 Long Noncoding RNA PVT1 Promotes Melanoma Progression Via Endogenous Sponging MiR-26b 705 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 colorectal cancer C19.9 NA microarray, qPCR etc. cell lines (HT-29, HCT-116 etc.) up-regulated This increase in AA was associated with a marked rise in lncRNA PVT1 (plasmacytoma variant translocation 1), a host gene of miR-1207-5p 26990997 2016 Role of cancer stem cells in racial disparity in colorectal cancer. 706 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, RIP cell lines (HepG2, Hep3B, Huh-7, HCCLM9, SK-Hep1, and SMMC-7721) up-regulated It was determined that plasmacytoma variant translocation 1 was significantly higher, while miR-186-5p was statistically lower in the hepatocellular carcinoma tissues than that in the adjacent normal tissues. 28656879 2017 Long non-coding RNA PVT1 serves as a competing endogenous RNA for miR-186-5p to promote the tumorigenesis and metastasis of hepatocellular carcinoma 707 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 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. 708 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 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. 709 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 prostate cancer C61.9 NA qPCR, MSP-PCR, RNAi etc. prostate cancer tissues, cell lines (LNCaP, PC-3 and DU145) up-regulated Our results showed that miR-146a was downregulated and negatively correlated with PVT1 level in prostate cancer. PVT1 mediated miR-146a expression by inducing the methylation of CpG Island in its promoter. miR-146a overexpression eliminated the effects of PVT1 knockdown on prostate cancer cells. PVT1 regulated prostate cancer cell viability and apoptosis depending on miR-146a. 27794184 2016 LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR-146a. 710 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 colorectal cancer C19.9 NA qPCR, Western blot etc. cell line (FHC,SW480, SW620, HT29, HCT116), colorectal cancer tissues up-regulated PVT1 regulated the growth of CRC tumors by acting as a competing endogenous RNAs (ceRNA) and negatively regulated miR-455. Furthermore, we discovered that RUNX2,a functional transcription factor in CRC,up-regulated PVT1 expression. 29637007 2018 A feedback loop consisting of RUNX2/LncRNA-PVT1/miR-455 is involved in the progression of colorectal cancer. 711 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 non small cell lung cancer C34 M8046/3 qPCR, Western blot NSCLC tissues, cell lines (A549 and SPCA?1) up-regulated PVT1 was overexpressed in the hypoxic lung cancer cells.PVT1 functioned as competing endogenous (ce)RNA for miR?199a?5p, upregulated expression of its endogenous targets HIF?1α and inhibited its function. 29115513 2017 LncRNA PVT1 regulate expression of HIF1α via functioning as ceRNA for miR-199a-5p in non?small cell lung cancer under hypoxia. 712 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 gastric cancer C16 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. gastric cancer tissues, cell lines (SGC7901 and BGC823) up-regulated PVT1 was up-regulated in GC tissues. MiR-152 was negatively associated with PVT1 expression in GC tissues. We found that PVT1 have three binding sequences for miR-152. Moreover, PVT1 might inhibit the expression of miR-152 and increased the expression of CD151 and FGF2 through regulating miR-152. PVT1 was positively associated with CD151 and FGF2 expression in GC tissues. 28258379 2017 Long Noncoding RNA PVT1 Acts as a Sponge to Inhibit microRNA-152 in Gastric Cancer Cells. 713 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 gastric cancer C16 NA qPCR, RNAi, Luciferase reporter assay, MTT assay etc. gastric cancer tissues, cell lines (SGC-7921, AGS and BGC-823) up-regulated PVT1 expression was markedly upregulated in GC tissues and cell lines, and high expression levels of PVT1 were obviously correlated with advanced tumor stage and lymph node metastasis. Further functional experiments indicated up-regulation of PVT1 promoted the GC cell proliferation and invasion, while down-regulation of PVT1 inhibited cell proliferation and invasion. In addition, PVT1 could directly interact with miR-186 in GC cells and this interaction lead to the inhibition of downstream of HIF-1α expression. 28122299 2017 The long noncoding RNA PVT1 functions as a competing endogenous RNA by sponging miR-186 in gastric cancer. 714 PWRN1 NA ENSG00000259905 NR_026646 GRCh38_15:24493137-24652130 gastric cancer C16 NA Microarray, qPCR, Western blot,RIP, Luciferase reporter assay cell line (HEK-293, GES-1, MGC-803, HGC-27, SGC-7901, MKN-45), GC tissues up-regulated PWRN1 affected PTEN/Akt/MDM2/p53 axis via suppressing miR-425-5p.PWRN1 up-regulated could reduce proliferation and metastasis and increased apoptosis in GC cells, while miR-425-5p had reverse effects. PWRN1 may target an oncogene miR-425-5p. 29535266 2018 Prader-Willi region non-protein coding RNA 1 suppressed gastric cancer growth as a competing endogenous RNA of microRNA-425-5p. 715 RMRP RMRP, CHH, NME1, RMRPR, RRP2 ENSG00000269900 NR_003051 GRCh38_9:35657751-35658018 lung adenocarcinoma C34 M8140/3 qPCR, Cell transfection, Western blot etc. LUAD tissues, cell lines (A549, SPC-A1, H1299 and H23) up-regulated RMRP expression was upregulated in 25 cases compared to the adjacent normal tissues. We also showed that RMRP expression was upregulated in lung adenocarcinoma cell lines compared to the bronchial epithelial cell line. Ectopic expression of RMRP promoted lung adenocarcinoma cell proliferation, colony formation and invasion. In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. 27906963 2016 LncRNA-RMRP Acts as an Oncogene in Lung Cancer. 716 RNPC1 HSRNASEB, SEB4D, dJ800J21.2, seb4B, RBM38 ENSG00000132819 NA GRCh38_20:57391407-57409333 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell line (A549), NSCLC tissue down-regulated RNPC1 and long non-coding RNA CASC2 expression levels were significantly downregulated in lung cancer tissues compared with normal adjacent tissues, and their expression levels were positively correlated. Functionally, overexpression of RNPC1 or CASC2 inhibited non-small cell lung cancer cells proliferation, migration and invasion, and promoted cells apoptosis. Mechanistically, RNPC1 was found to harbor binding sites on CASC2 and directly bound to CASC2, and increased CASC2 mRNA stability and expression. Notably, the promotive effects of RNPC1 on CASC2 expression were attenuated by miR-181a overexpression. Moreover, CASC2 3'UTR with mutated miR-181a binding sites did not respond to RNPC1 alteration. Finally, the inhibitory effects of RNPC1 overexpression were attenuated or even reversed by CASC2 knockdown or miR-181a overexpression. 29288351 2017 RNPC1 inhibits non-small cell lung cancer progression via regulating miR-181a/CASC2 axis. 717 linc-ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 endometrial cancer NA M8380/3 qPCR, RNAi, Flow cytometry assay, FISH etc. endometrial carcinoma tissues up-regulated We began by assessing the expression of linc-RoR in ECSC growing under tumorsphere conditions and differentiated conditions (removal of bFGF). In qRT-PCR analyses, a marked reduction of linc-RoR and core TFs was observed in all differentiated tumorspheres. This finding suggested that linc-RoR expression was positively correlated with levels of undifferentiated tumorspheres. The effects of miR-145 could be eliminated after increasing the expression of linc-RoR in ETs or mutated targeted sequences in linc-RoR. 24589415 2014 Linc-RNA-RoR acts as a sponge against mediation of the differentiation of endometrial cancer stem cells by microRNA-145. 718 ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 oral cancer C06.9 NA qPCR oral cancer tissues up-regulated In oral squamous cell carcinomas, for the first time, we observed linc-RoR overexpression, downregulation of miR-145-5p, and overexpression of c-Myc, Klf4, Oct4, and Sox2, suggesting the existence of linc-RoR-mediated competing endogenous RNA network in undifferentiated tumors. 28443494 2017 Expression profiling of long non-coding RNA identifies linc-RoR as a prognostic biomarker in oral cancer 719 ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 triple negative breast cancer C50 NA qPCR etc. Triple-negative breast cancer tissues, cell line (HEK293T, MCF-10A, MCF-7, BT474, MDA-MB-453 and MDA-MB-231) down-regulated lincRNA-ROR was upregulated in TNBC cell lines and tissue samples.The aberrant expression of lincRNA-ROR was shown to increase invasion and metastasis in MDA-MB-231 and loss of function by siRNA reverse these process.Furthermore, lincRNA-ROR functions as a competing endogenous RNAs (ceRNA) which sponges miR-145 and therefore upregulate the expression of Mucin1 (MUC1).Studies showed that downregulated SPRY4-IT1 could facilitate bladder cancer cell apoptosis via acting as a ceRNA for miR-101-3p. 29673594 2018 LincRNA-RoR/miR-145 promote invasion and metastasis in triple-negative breast cancer via targeting MUC1. 720 ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 papillary thyroid cancer NA M8260/3 qPCR, in vitro knockdown cell line(TPC1), FFPE tissue up-regulated ROR was shown to exert regulatory effect in proliferation, invasion, and stemness of gastricc arcinoma stem cells and in breast cancer,pancreatic cancer, hepatocellular cancer, endometrial cancer, and naso- pharyngeal carcinomas.ROR lncRNA had a negative regulatory on miR-145.SiRNA experiments with ROR also led to increased expression of miR-145, supporting the role of ROR as an endogenous miR-145 sponge.There was upregulation of miR-145 after ROR silencing with a specific siRNA. 29280051 2017 Long Non-coding RNA Linc-ROR Is Upregulated in Papillary Thyroid Carcinoma. 721 linc-ROR LINC-ROR, ROR, lincRNA-RoR 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. 722 linc-ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 colon cancer C18 NA qPCR etc. colon cancer tissues, cell lines (NCM460, RKO, Caco2, HCT8, SW480 and SW620) up-regulated In the present study, qRT-PCR was performed to measure the expression levels of lincRNA-ROR in colon cancer tissues and cell lines. Then, the clinicopathological significance and prognostic value of lincRNA-ROR were analyzed. LincRNA-ROR expression correlated with pT stage, pN stage, AJCC stage and vascular invasion. Knockdown of lincRNA-ROR restored the expression of miR-145, and had a significant influence on colon cancer cell proliferation, migration and invasion. Patients of the high lincRNA-ROR/low miR-145 group had significantly poorer outcomes than those of the low lincRNA-ROR/high miR-145 group. 27071407 2016 Long Non-Coding RNA lincRNA-ROR Promotes the Progression of Colon Cancer and Holds Prognostic Value by Associating with miR-145 723 linc-ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 breast cancer C50 NA qPCR, RNAi, Western blot, ChIP, Flow cytometry assay etc. cell lines (MDA-MB-231, MCF10A) up-regulated Untreated MDA-MB-231 cell lines strongly expressed linc-ROR, but linc-ROR knockdown decreased cell viability and expression of p62 and p53 while increasing apoptosis. Linc-ROR knockdown also increased LC3-II/β-actin, Beclin 1, NOTCH1, and Bcl-2 expression, as well as the number of autophagic vesicles in MDA-MB-231 cells. Linc-ROR negatively regulated miR-34a expression by inhibiting histone H3 acetylation in the miR-34a promoter. 27449099 2016 Large intergenic non-coding RNA-ROR reverses gemcitabine-induced autophagy and apoptosis in breast cancer cells. 724 linc-ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 breast cancer C50 NA qPCR, RIP, in vivo knockdown etc. breast cancer tissues up-regulated linc-ROR was upregulated in breast tumor and ectopic overexpression of linc-ROR in immortalized human mammary epithelial cells induced an epithelial-to-mesenchymal transition (EMT) program. Moreover,linc-ROR enhanced breast cancer cell migration and invasion. Linc-ROR was associated with miRNPs and functioned as a competing endogenous RNA to mi-205. linc-ROR functions as an important regulator of EMT and can promote breast cancer progression and metastasis through regulation of miRNAs. 24922071 2014 LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis. 725 linc-ROR LINC-ROR, ROR, lincRNA-RoR ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 breast cancer C50 NA microarray, qPCR, Western blot etc. breast cancer tissues, cell lines (HEK293T, MCF-7, HS578T, MDA-MB-231) up-regulated lincRNA-RoR was significant upregulated in DCIS and IDC tumor tissues, showing the highest expression in invasive tumor tissues. Overexpression of the long non-coding RNA, lincRNA-RoR, functions as a competitive endogenous RNA sponge in TNBC. Interestingly, lincRNA-RoR is dramatically upregulated in TNBC and in metastatic disease and knockdown restores miR-145 expression. 25253741 2014 lincRNA-RoR and miR-145 Regulate Invasion in Triple-negative Breast Cancer via Targeting ARF6. 726 RP11-169D4.1 RP11-169D4.2 ENSG00000227467 NR_126364 GRCh38_11:72570660-72573229 laryngeal squamous cell cancer C32.3 NA qPCR, Western blot etc. laryngeal squamous cell carcinoma tissues, cell lines (SNU899 and SNU46) down-regulated RP11-169D4.1 expression was markedly decreased in LSCC tissues and cell lines.The overexpression of RP11-169D4.1 inhibited the proliferation,migration and invasion of LSCC cell lines as well as promoted apoptosis.We further verified that miR-205-5p had binding sites with RP11?169D4.1 and that RP11-169D4.1 could regulate the expression of CDH1.Ectopic transfection of RP11-169D4.1 led to a significant reduction in the downstream signaling molecule AKT in LSCC cells. The long non-coding RNA RP11-169D4.1 may serve as a tumor suppressor and a promising therapeutic target in laryngeal cancer,which could inhibit the process of EMT by regulating CDH1. 28534968 2018 Functional significance of the long non-coding RNA RP11-169D4.1 as a metastasis suppressor in laryngeal squamous cell carcinoma by regulating CDH1. 727 RP4 NA NA NA NA colorectal cancer C19.9 NA Western blot, qPCR, in vitro knockdown etc. cell line (SW480) down-regulated Cell proliferation,tumor growth,and early apoptosis in SW480 cells were negatively regulated by lncRNA RP4.Functional experiments indicated that lncRNA RP4 directly upregulated SH3GLB1 expression by acting as a competing endogenous RNA (ceRNA) for miR-7-5p. This interaction led to activation of the autophagy-mediated cell death pathway and de-repression of PI3K and Akt phosphorylation in colorectal cancer cells in vivo. 29531464 2018 Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer. 728 RPPH1 NA ENSG00000277209 NR_002312 GRCh38_14:20343048-20343685 breast cancer C50 NA qPCR etc. cell lines (MCF-7, MDA-MB-231) up-regulated RPPH1 functions as a tumour promoter and plays an important role in advancing tumorigenesis by targeting miR-122 and may serve as a novel and potential therapeutic, diagnostic or prognostic target in breast cancer. 29200969 2017 Inhibition of breast cancer cell proliferation and tumorigenesis by long non-coding RNA RPPH1 down-regulation of miR-122 expression. 729 RSU1P2 RSU1P2 ENSG00000232554 NA GRCh38_10:45099487-45154596 cervical cancer C53 NA qPCR, Western blot, Flow cytometry assay, Cell migration and invasion assay etc. cervical cancer tissues, cell lines (SMMC-7721 and HepG3) up-regulated Here, we found that the lncRNA RSU1P2 is upregulateded in cervical cancer tissues and has a tumour-promoting role. We revealed that RSU1P2 acts as a ceRNA through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. The transcription factor N-myc forms a positive feedback loop with RSU1P2 by in turn activating its expression, thereby enhancing its oncogenic capacity. 27487126 2016 LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells. 730 SIRT1-AS SIRT1-AS NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Northern blot etc. cell line (HCC-9903) up-regulated SIRT1-AS overexpression promoted the proliferation of the human HCC cell lines by upregulating the SIRT1 protein level. The mechanism was that SIRT1-AS bound to SIRT1 mRNA at 3'UTR, masked the miR-29c binding site and stabilized SIRT1 mRNA. 26324025 2015 A novel mutation in SIRT1-AS leading to a decreased risk of HCC 731 SKP2 SKP2, FBL1, FBXL1, FLB1, p45 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 732 SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 non small cell lung cancer C34 M8046/3 qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP NSCLC cell lines (H358, H1299, A549, and SK-MES-1), bronchial epithelial cell line (HBE) up-regulated SNHG1 directly bound to microRNA (miRNA)-145-5p,isolating miR-145-5p from its target gene MTDH.Inhibition of SNHG1 suppressed NSCLC cell viability, proliferation,migration, and invasion in vitro, but its effect was rescued by miR-145-5p inhibition. These results demonstrate that SNHG1 contributes to NSCLC progression by modulating the miR-145-5p/ MTDH axis, and it could potentially be a therapeutic target as well as a diagnostic marker. 29466052 2018 Long noncoding RNA SNHG1 promotes non-small cell lung cancer progression by up-regulating MTDH via sponging miR-145-5p. 733 SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 hepatocellular carcinoma C22.0 M8170/3 qPCR, Cell transfection, Luciferase reporter assay, Cell proliferation assay, ISH etc. HCC tissues, cell lines (HepG2, L02) up-regulated The expression level of lncRNA SNHG1 was remarkably upregulated in HCC tissues and cell lines compared with normal tissues and cell lines. High expression of lncRNA SNHG1 contributed to the downregulation of miR-195 in HepG2 cells. Also, lncRNA SNHG1 exacerbated HCC cell proliferation, invasion, and migration in vitro through the inhibition of miR-195. 27932778 2016 Expression of Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 1 (SNHG1) Exacerbates Hepatocellular Carcinoma Through Suppressing miR-195. 734 SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 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/β-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/β-catenin signaling pathway. 735 SNHG1 SNHG1, LINC00057, NCRNA00057, U22HG, UHG, lncRNA16 ENSG00000255717 NR_003098 GRCh38_11:62851988-62855914 prostate cancer C61.9 NA qPCR, Western blot, Luciferase Reporter Assays prostate cancer tissues, cell lines (PC3, DU145, LNCap, RWPE-1 and HEK293T) up-regulated In this study,we demonstrated that a lncRNA, Small Nucleolar RNA Host Gene 1 (SNHG1), as a ceRNA for miR-199a-3p, played a critical role in prostate cancer cell proliferation. We found that SNHG1 was aberrantly up-regulated in prostate carcinoma tissues; while, miR-199a-3p was abnormally down-regulated. 28400279 2017 SNHG1 lncRNA negatively regulates miR-199a-3p to enhance CDK7 expression and promote cell proliferation in prostate cancer 736 SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 lung adenocarcinoma C34 M8140/3 qPCR lung adenocarcinoma tissues up-regulated while the expression level of SNHG12 was up-regulated in LAD tissues. lncRNA SNHG12 competed for several miRNAs, 28793054 2017 Revealing potential long non-coding RNA biomarkers in lung adenocarcinoma using long non-coding RNA-mediated competitive endogenous RNA network 737 SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 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-κB 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. 738 SNHG12 SNHG12, ASLNC04080, C1orf79, LINC00100, NCRNA00100, PNAS-123 ENSG00000197989 NR_024127 GRCh38_1:28578538-28582983 gastric cancer C16 NA qPCR, RIP, Luciferase reporter assay gastric cancer tissues, cell lines (SGC-7901, BGC823) up-regulated The expression of lncRNA SNHG12 was positively linked with the proliferative ability of BGC-823. RIP experiment confirmed the binding abilities of lncRNA SNHG12,microRNA-199a/b-5p and Argo2. 29565487 2018 LncRNA SNHG12 regulated the proliferation of gastric carcinoma cell BGC-823 by targeting microRNA-199a/b-5p. 739 SNHG14 NA ENSG00000224078 NR_146177 GRCh38_15:24978583-25419462 clear cell renal cell carcinoma C64.9 M8005/0 qPCR, Luciferase reporter assay, Western blot, RIP cell lines (A-498, 786-O,Caki-2, Caki-1, HK-2) up-regulated SNHG14 was significantly up-regulated in ccRCC cell lines.the transcription factor SP1 can bind to the promoter region of SNHG14, resulting in the overexpression of SNHG14 in ccRCC. enhanced expression of lncRNA SNHG14 promoted cell migration and invasion through promoting N-WASP protein level. SNHG14 functioned as ceRNA to regulate N-WASP expression and cell motility ability via a miR-203-dependent manner.SNHG14 is a critical lncRNA that promotes ccRCC migration and invasion via sponging miR-203 and elevating N-WASP. 29312804 2017 SP1-induced up-regulation of lncRNA SNHG14 as a ceRNA promotes migration and invasion of clear cell renal cell carcinoma by regulating N-WASP. 740 SNHG14 NA ENSG00000224078 NR_146177 GRCh38_15:24978583-25419462 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay etc. gastric cancer tissues, cell lines (BGC-823, SGC-7901, and HGC-27) up-regulated LncRNA SNHG14 was markedly up-regulated in gastric cancer tissues and cells.Knockdown of SNHG14 significantly inhibited SGC-7901 cell viability,migration,invasion,and promoted cell apoptosis.In addition, miR-145 was negatively regulated by SNHG14 and the effects of SNHG14 knockdown on cell viability, apoptosis, migration, invasion, and the expression of apoptosis-related proteins and EMT-markers were reversed by inhibition of miR-145 at the same time. Furthermore, SOX9 was verified as a functional target of miR-145, and miR-145 regulated tumor malignant behaviors through regulating SOX9. Besides, knockdown of SNHG14 inhibited the expression of p-PI3K, p-AKT, and p-mTOR and promoted PTEN expression, where miR-145 inhibition had opposite effects. Moreover, the activated PI3?K/AKT/mTOR pathway caused by miR-145 inhibition was counteracted after knockdown of SOX9. 29667771 2018 Long non-coding RNA SNHG14 contributes to gastric cancer development through targeting miR-145/SOX9 axis. 741 SNHG14 NA ENSG00000224078 NR_146177 GRCh38_15:24978583-25419462 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay glioma tissues, glioma cell lines (U251 and U87) down-regulated SNHG14 was found to be downregulated in human glioma tissues and cell lines. there was a negative correlation between SNHG14 expression and miR-92a-3p expression.miR-92a-3p could directly bind to SNHG14. miR-92a-3p was significantly upregulated in glioma and acted as an oncogene in glioma cells by inhibiting Bim. Moreover, mechanistic investigations showed that miR-92a-3p could reverse the tumour suppressive effects induced by SNHG14 in glioma, indicating that SNHG14 may act as an endogenous sponge that competes for binding to miR-92a-3p. 29552296 2018 The long non-coding RNA SNHG14 inhibits cell proliferation and invasion and promotes apoptosis by sponging miR-92a-3p in glioma. 742 SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 esophageal squamous cell cancer NA NA qPCR, Luciferase reporter assay, Western blot, RIP esophageal squamous cell carcinoma tissues, cell lines (eca109, EC9706, TE1, Kyse-30 and Kyse-70) differential expression miR-140-5p could interact with SNHG16 and the level of miR-140-5p was inverse correlated with SNHG16 in ESCC specimens.SNHG16 directly targets miR-140-5p by binding with microRNA binding site harboring in the SNHG16 sequence. SNHG16 could act as an oncogenic lncRNA that promotes tumor progression through acting as an endogenous 'sponge' by competing with miR-140-5p, thereby regulating target ZEB1. 29416674 2017 SNHG16/miR-140-5p axis promotes esophagus cancer cell proliferation, migration and EMT formation through regulating ZEB1. 743 SNHG16 SNHG16, Nbla10727, Nbla12061, ncRAN ENSG00000163597 NR_038108 GRCh38_17:76557766-76565348 breast cancer C50 NA qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. breast cancer tissues, cell lines (MDA-MB-231, MCF-7, MDA-MB-468 and HEK293T) up-regulated Expression levels of SNHG16 were found to be frequently higher in breast cancer tissues than in the paired noncancerous tissues.Gain- and loss-of-function studies proved that SNHG16 significantly promoted breast cancer cell migration. In addition, we identified a positive correlation between SNHG16 and E2F5 in breast cancer tissues. Furthermore,we demonstrated that forced expression of miR-98 could partially abrogate SNHG16-mediated increase of breast cancer cells migration,suggesting that SNHG16 promoted cell migration in a miR-98 dependent manner. 28232182 2017 SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5. 744 SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 ENSG00000203875 NR_003038 GRCh38_6:85660950-85678736 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay etc. gastric cancer tissues, cell lines (SGC-7901 and MGC-803) down-regulated SNHG5 contains a putative miR-32-binding site and that deletion of this site abolishes the responsiveness to miR-32. Suppression of SNHG5 expression by miR-32 was found to be Argonaute (Ago)2-dependent. Immunoprecipitation showed that SNHG5 could be pulled down from the Ago-2 complex with miR-32. 27871067 2017 The lncRNA SNHG5/miR-32 axis regulates gastric cancer cell proliferation and migration by targeting KLF4. 745 SNHG7 SNHG7, NCRNA00061 ENSG00000233016 NR_003672 GRCh38_9:136721366-136728184 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay NSCLC tissues, The lung cancer cell lines (H125, 95D, A549) down-regulated We reported that oncogene SNHG7 predicted a poor clinical outcome and functioned as competitive endogenous RNA (ceRNA) antagonized microRNA-193b (miR-193b) to up-regulate the FAIM2 level in NSCLC 29131440 2017 miR-193b availability is antagonized by LncRNA-SNHG7 for FAIM2-induced tumour progression in non-small cell lung cancer. 746 SOX2OT SOX2-OT, NCRNA00043, SOX2OT ENSG00000242808 NR_004053 GRCh38_3:180989762-181836880 esophageal squamous cell cancer NA NA qPCR etc. human embryonal carcinoma stem cell line (NT-2) down-regulated Compared with mock-transfected cells, overexpression of miR-211 caused a significant down-regulation of both genes. Furthermore, flow-cytometry assay revealed a significant elevation in sub-G1 cell population following ectopic expression of miR-211 in NT-2 cells. Considering the vital role of SOX2OT and SOX2 genes in pluripotency and tumorigenesis, our data suggest an important and inhibitory role for miR-211 in the aforementioned processes. 26862518 2016 Down-Regulatory Effects of miR-211 on Long Non-Coding RNA SOX2OT and SOX2 Genes in Esophageal Squamous Cell Carcinoma 747 SPRY4-IT1 SPRY4-IT1, SPRIGHTLY ENSG00000281881 NR_131221 NA bladder cancer C67 NA qPCR, RNAi, Western blot, Luciferase reporter assay, Cell cycle assay, Cell apoptosis assay etc. bladder cancer tissues, cell lines (EJ, UMUC3, T24T) up-regulated SPRY4-IT1 knockdown induced inhibition of cell proliferation, cell migration and invasion ability,and caused promotion of apoptosis in bladder cancer both in vitro and in vivo.Mechanistically, knockdown of SPRY4-IT1 increased the expression of miR-101-3p and subsequently inhibited the expression of EZH2 at posttranscriptional level. Importantly, SPRY4-IT1 could directly interact with miR-101-3p and down-regulation of miR-101-3p efficiently reversed the suppression of EZH2 induced by SPRY4-IT1 shRNA. Thus, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p, and played an oncogenic role in bladder cancer progression. 27998761 2017 LncRNA SPRY4-IT1 sponges miR-101-3p to promote proliferation and metastasis of bladder cancer cells through up-regulating EZH2. 748 SPRY4-IT1 SPRY4-IT1, SPRIGHTLY ENSG00000281881 NR_131221 NA colorectal cancer C19.9 NA qPCR, Western blot, Luciferase reporter assay etc. colorectal carcinoma tissues, cell lines (LoVo, RKO, SW620 and SW480) up-regulated SPRY4-IT1 was upregulated in human primary colorectal carcinoma tissues.Knockdown of SPRY4-IT1 inhibited colorectal carcinoma cell proliferation,migration,and invasion.Moreover,we confirmed that the expression of epithelial-mesenchymal transition-related genes was modulated through alteration of SPRY4-IT1 expression. SPRY4-IT1 could negatively regulate the expression of miR-101-3p in colorectal carcinoma cells.The bioinformatics prediction revealed putative miR-101-3p binding sites within SPRY4-IT1 transcripts. 28720069 2018 Long non-coding RNA SPRY4-IT1 promotes proliferation and invasion by acting as a ceRNA of miR-101-3p in colorectal cancer cells. 749 TALNEC2 NA ENSG00000163364 NR_040001 GRCh38_2:176629589-176637931 glioma NA M9380/3 qPCR, Western blot etc. cell lines (A172, U87) up-regulated TALNEC2 was highly expressed in GBM with poor prognosis, in GBM specimens derived from short-term survivors and in glioma cells and glioma stem cells.Two of the downregulated miRNAs,miR-21 and miR-191, mediated some of TALNEC2 effects on the stemness and mesenchymal transformation of GSCs. 28423669 2017 The novel long non-coding RNA TALNEC2, regulates tumor cell growth and the stemness and radiation response of glioma stem cells 750 TINCR TINCR, LINC00036, NCRNA00036, PLAC2, onco-lncRNA-16 ENSG00000223573 NA GRCh38_19:5558167-5578349 lung cancer C34 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP etc. cell lines (A549, H322, H460, GLC-82, SPC-A1), lung cancer tumor tissues down-regulated INCR overexpression suppressed proliferation and invasion in lung cancer cells.TINCR was confirmed as a molecular sponge of miR-544a. We further validated that miR-544a facilitated proliferation and invasion, and miR-544a could reverse TINCR-mediated anti-proliferation and anti-invasion effect in lung cancer cells. TINCR acted as a competing endogenous RNA (ceRNA) to sequester miR-544a from its target gene FBXW7. FBXW7 suppressed proliferation and invasion,and FBXW7 knockdown abolished the inhibition of TINCR on proliferation and invasion in lung cancer cells. 29324317 2018 TINCR suppresses proliferation and invasion through regulating miR-544a/FBXW7 axis in lung cancer. 751 TP73-AS1 TP73-AS1, KIAA0495, PDAM ENSG00000227372 NR_033708 GRCh38_1:3735601-3747336 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP glioma tissues, human brain glioma cells (U87, U118, U251, U373 and SHG-44) up-regulated TP73-AS1 was specifically upregulated in brain glioma cell lines and promoted glioma cell growth through targeting miR-124. TP73-AS1 knocking down suppressed human brain glioma cell proliferation, invasion, and metastasis in vitro.The inhibitory effect of TP73-AS1 knocking down on glioma cell proliferation and invasion could partly be restored by miR-124 inhibition.In addition, miR-124-dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) regulation was required in TP73-AS1-induced brain glioma cell growth. 29412778 2018 The Long Noncoding RNA TP73-AS1 Interacted with miR-124 to Modulate Glioma Growth by Targeting Inhibitor of Apoptosis-Stimulating Protein of p53. 752 treRNA TRERNA1, LINC00651, treRNA ENSG00000231265 NR_051976 GRCh38_20:50040716-50041504 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc. cell lines (HepG2, Huh7) up-regulated We further examined the expression profile of treRNA and miR-190a in 24 pairs of HCC tissues and adjacent normal tissues. miR-190a exhibited a significantly low expression in HCC tissues compared to adjacent normal tissues. Meanwhile, an elevated expression of treRNA was observed in HCC tissue compared to adjacent normal tissue. 26608035 2015 miR-190a inhibits epithelial-mesenchymal transition of hepatoma cells via targeting the long non-coding RNA treRNA. 753 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 gallbladder cancer C23.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. GBC tissues, cell lines (EH-GB1, GBC-SD, NOZ, SGC-996) up-regulated TUG1 expression was significantly overexpressed in GBC tissues.Functionally, this study demonstrated that knockdown of TUG1 significantly inhibited GBC cell proliferation, metastasis.Mechanically, we found that TUG1 is upregulated by TGF-β1, and knockdown of TUG1 inhibited GBC cell EMT.Furthermore, we identified that miR-300, which has been reported as a suppressor in other types of cancer, is negatively regulated by TUG1 28178615 2017 Long non-coding RNA TUG1 promotes cell proliferation and metastasis by negatively regulating miR-300 in gallbladder carcinoma. 754 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 hepatoblastoma C22.0 M8970/3 qPCR, RNAi, Western blot etc. hepatoblastoma tissues, cell lines (HepG2, HuH-6, and SMMC-7221) up-regulated We show that TUG1 is significantly upregulated in human hepatoblastoma specimens and metastatic hepatoblastoma cell lines. TUG1 knockdown inhibits tumor growth and angiogenesis in vivo, and decreases hepatoblastoma cell viability, proliferation, migration, and invasion in vitro. TUG1, miR-34a-5p, and VEGFA constitutes to a regulatory network, and participates in regulating hepatoblastoma cell function, tumor progression, and tumor angiogenesis. 27362796 2016 Targeting long non-coding RNA-TUG1 inhibits tumor growth and angiogenesis in hepatoblastoma. 755 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 glioblastoma NA M9440/3 qPCR, RNAi etc. glioblastoma tissues, cell lines (U251 MG, U87MG) up-regulated Here we demonstrated that TUG1 was up-expressed in human glioblastoma tissues and glioblastoma cell lines. Knockdown of TUG1 remarkably suppressed tumor-induced endothelial cell proliferation, migration and tube formation as well as reducing spheroid-based angiogenesis ability in vitro, which are the critical steps for tumor angiogenesis. Overall, the results demonstrated that TUG1 enhances tumor-induced angiogenesis and VEGF expression through inhibiting miR-299. 27345398 2016 Long non-coding RNA taurine upregulated 1 enhances tumor-induced angiogenesis through inhibiting microRNA-299 in human glioblastoma. 756 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 gastric cancer C16 NA qPCR, RNAi, Luciferase reporter assay, Cell proliferation assay etc. cell lines (BGC-823 and SGC-7901) up-regulated TUG1 was significantly overexpressed and miR-145-5p was dramatically downregulated in GC cell lines.TUG1 knockdown strikingly inhibited cell proliferation and invasion in vitro and markedly suppressed tumor growth in vivo. Furthermore, TUG1 could directly bind to miR-145-5p and repress miR-145-5p expression.TUG1 overexpression significantly relieved the inhibition on GC cell proliferation and invasion in vitro and tumor growth in vivo, mediated by miR-145-5p overexpression. 27983921 2017 Long Noncoding RNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation and Invasion in Gastric Cancer via Negatively Modulating miRNA-145-5p. 757 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 breast cancer C50 NA qPCR, Western blot, Luciferase reporter assay, Flow cytometry assay, MTT assay etc. breast cancer tissues, cell lines (BT474, MCF-7, MDA-MB-231, and T47D) up-regulated Higher expression of TUG1 was observed in breast cancer tissues and cell lines than in the corresponding controls. TUG1 knockdown reduced proliferation, suppressed cell cycle progression, and promoted apoptosis of MCF-7 cells. The dual luciferase reporter assay showed that TUG1 could negatively regulate the expression of miR-9. MiR-9 inhibition abrogated the effect of TUG1 knockdown on the proliferation, cell cycle progression, and apoptosis of MCF-7 cells. TUG1 positively regulated the expression of MTHFD2 in breast cancer cells. 28053623 2016 LncRNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation by Inhibiting MicroRNA-9 in MCF-7 Cells. 758 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 osteosarcoma NA M9180/3 qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc. cell lines (U2OS, Saos-2, MG63, and MNNG/HOS) up-regulated TUG1 knockdown inhibited cell proliferation and colony formation, and induced G0/G1 cell cycle arrest and apoptosis in vitro, and suppressed tumor growth in vivo. Besides, we found that TUG1 acted as an endogenous sponge to directly bind to miR-9-5p and downregulated miR-9-5p expression. Moreover, TUG1 overturned the effect of miR-9-5p on the proliferation, colony formation, cell cycle arrest, and apoptosis in osteosarcoma cells. 27658774 2016 Long non-coding RNA TUG1 contributes to tumorigenesis of human osteosarcoma by sponging miR-9-5p and regulating POU2F1 expression. 759 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay etc. Gastric carcinoma tissues, cell lines (GES-1, Bgastric cancer-823, Mgastric cancer-803, Sgastric cancer-7901, MKN28) up-regulated downregulation of miR-381 by lncRNA-TUG1 promoted the metastasis of GC cells by inhibiting SOX4. 28927144 2017 MiR-381 inhibits migration and invasion in human gastric carcinoma through downregulatedting SOX4 760 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 gastric cancer C16 NA qPCR, RNAi, Western blot etc. gastric cancer tissues, cell line (SGC-7901) up-regulated The expression level of lncRNA-TUG1 in GC tissue was significant higher than that in para-C tissue and the high expression level of lncRNA-TUG1 in GC tissue was significantly correlated with tumor lymph nodes metastasis and advance TNM phasing. The transferring and invading capacity of SGC-7901 cells was highly inhibited after being transfected by lncRNA-TUG1 specific siRNA. The results of qRT-PCR and western-blot proved that the expression of microRNA-144 was significantly boosted and the expression level of c-Met mRNA and protein was inhibited after lncRNA-TUG1 was silenced. 27261864 2016 Inhibition of long non-coding RNA TUG1 on gastric cancer cell transference and invasion through regulating and controlling the expression of miR-144/c-Met axis. 761 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 glioma NA M9380/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. glioma tissues, cell lines (U251, SHG-44) up-regulated TUG1 expression was confirmed to be upregulated in glioma tissues, and showed an inverse correlation with downregulated miR-26a. TUG1 could negatively regulate the expression of miR-26a in glioma cells. Further experiments demonstrated the positive regulation of TUG1 on the miR-26a target, PTEN, wherein TUG1 could inhibit the negative regulation of miR-26a on PTEN by binding its 3'UTR. Additionally, the expression of PTEN was also upregulated in glioma tissues, showing a positive or negative correlation with TUG1 or miR-26a, respectively. 27363339 2016 Long non-coding RNA TUG1 acts as a miR-26a sponge in human glioma cells. 762 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 glioma NA M9380/3 qPCR, Lentiviral infection, Western blot, RIP, ChIP etc. glioma tissues, cell lines (hCMEC/D3, astrocytes, brain vascular pericytes) up-regulated LncRNA TUG1 (taurine upregulated gene 1) was highly expressed in glioma vascular endothelial cells from glioma tissues. It also upregulated in glioma co-cultured endothelial cells (GEC) from BTB model in vitro. Knockdown of TUG1 increased BTB permeability, and meanwhile down-regulated the expression of the tight junction proteins ZO-1, occludin, and claudin-5. TUG1 increased BTB permeability via binding to miR-144 and then reducing EC tight junction protein expression by targeting HSF2. 26078353 2015 The long noncoding RNA TUG1 regulates blood-tumor barrier permeability by targeting miR-144. 763 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 osteosarcoma NA M9180/3 RT-qPCR, Western blot, Luciferase reporter assay, in vitro knockdown human OS tissues, Human OS cell lines (U2OS, MG-63, Saos-2, and 143B) up-regulated TUG1 was highly expressed in human OS tissues,OS cell lines,and primary OS cells.TUG1 knockdown hindered proliferation and induced apoptosis in human OS cell lines and primary OS cells.Moreover, TUG1 inhibited miR-132-3p expression by direct interaction,and introduction of miR-132-3p inhibitor partly abrogated the effect of TUG1 knockdown on the proliferation and apoptosis of OS cells.Furthermore, SOX4 was validated as a target of miR-132-3p.Further functional analyses revealed that miR-132-3p inhibited proliferation and induced apoptosis of OS cells, while this effect was greatly abated following SOX4 overexpression.Moreover, TUG1 knockdown suppressed proliferation and promoted apoptosis by upregulating miR-132-3p and downregulating SOX4 in primary OS cells. 29436190 2018 Long Non-Coding RNA TUG1 Promotes Proliferation and Inhibits Apoptosis of Osteosarcoma Cells by Sponging miR-132-3p and Upregulating SOX4 Expression. 764 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 bladder cancer C67 NA qRT-PCR, Luciferase reporter assay, in vitro knockdown BC tissues, BC cell lines (T24, 5637, UMUC-2 and EJ) up-regulated TUG1 was upregulated and microRNA-29c(miR-29c) was downregulated in BC tissues and cell lines.Furthermore, TUG1 knockdown markedly increased the expression of miR-29c in vitro.On the contrary, overexpression of TUG1 remarkably decreased the expression of miR-29c.Transfection with plasmids containing mutant TUG1 has no effect on the expression of miR-29c. There were direct interactions between miR-29c and the binding sites of TUG1.In addition,the inhibitory effects of small interfering RNA specific for TUG1 on BC cell proliferation,migration and invasion were reversed by downregulation of miR-29c. 29321088 2018 Upregulation of long non-coding RNA TUG1 promotes bladder cancer cell 5 proliferation, migration and invasion by inhibiting miR-29c. 765 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 osteosarcoma NA M9180/3 qPCR, RNAi, Western blot, Luciferase reporter assay etc. osteosarcoma tissues, cell lines (MG-63, U2OS and MNNG/HOS) up-regulated TUG1 was elevated and correlated with a poor prognosis in osteosarcoma patients. Decreased TUG1 could remarkably inhibit osteosarcoma cell migration and invasion. Furthermore, the results of a real-time quantitative PCR showed that TUG1 and miR-335-5p could affect each other's expression. respectively. Finally, we affirmed that TUG1 affected ROCK1 expression and ROCK1-mediated migration/invasion by working as a competitive endogenous RNA (ceRNA) via miR-335-5p. 28205334 2017 Long non-coding RNA TUG1 promotes migration and invasion by acting as a ceRNA of miR-335-5p in osteosarcoma cells. 766 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 bladder cancer C67 NA qPCR, Western blot, MIT bladder cancer tissues, cell lines (T24 and BIU-87) up-regulated The levels of TUG1 and ZEB2 were significantly increased in bladder cancer tissues and cells. Moreover, ZEB2 was verified as a direct target of miR-142 and miR-142 could specially bind to TUG1. 28503069 2017 Downregulation of long noncoding RNA TUG1 inhibits proliferation and induces apoptosis through the TUG1/miR-142/ZEB2 axis in bladder cancer cells 767 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 osteosarcoma NA M9180/3 qPCR, Luciferase Reporter Assays, RIP Osteosarcoma tissues, cell lines (MG63 and U2-OS) down-regulated TUG1 was overexpressed and miR-153 was downregulated in osteosarcoma tissues and cell lines. Moreover, TUG1 was confirmed to be a miR-153 sponge. 28411362 2017 Knockdown of Long Noncoding RNA TUG1 Inhibits the Proliferation and Cellular Invasion of Osteosarcoma Cells By Sponging MiR-153 768 TUNAR TUNAR, HI-LNC78, LINC00617, TUNA ENSG00000250366 NR_038861 GRCh38_14:95876392-95925571 glioma NA M9380/3 qPCR, Western blot, luciferase reporter assay etc. cell lines (SHG44, U251, GL15, U87) down-regulated TUNAR was confirmed to positively regulate miR-200a,and knockdown of miR-200a reversed TUNAR-induced inhibitory effects on glioma cells. Further, Rac1 was negatively regulated by miR-200a.Rac1 overexpression abolished miR-200a overexpression-induced inhibition of viability,migration, and invasion, as well as increase of apoptosis.Besides,Rac1 knockdown inhibited glioma by inactivating the Wnt/β-catenin and NF-κB signal pathways.TUNAR played an anti-cancer role in glioma cells by upregulating miR-200a and inhibiting Rac1,thereby might represent a potential therapeutic target for the treatment of human glioma. 29540255 2018 Long non-coding RNA TUNAR represses growth, migration and invasion of human glioma cells through regulating miR-200a and Rac1. 769 TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 ENSG00000243197 NR_015391 GRCh38_3:116709235-116723581 glioma NA M9380/3 qPCR, RIP, Luciferase reporter assay, RNA pull-down assay, Cell proliferation assay etc. glioma tissues, cell lines (U251, U87 and HEK 293T) down-regulated TUSC7 was poorly expressed in tissues and cell lines of glioma, and the lower expression was correlated with glioma of the worse histological grade. Moreover, TUSC7 is a prognostic biomarker of glioma patients. Up-regulation of TUSC7 suppressed cellular proliferation and invasion of glioma cells, and accelerated cellular apoptosis. TUSC7 inhibited the proliferation, migration and invasion of glioma cells and promoted cellular apoptosis largely bypassing miR-23b. 27766072 2016 Long Non-coding RNA TUSC7, a Target of miR-23b, Plays Tumor-Suppressing Roles in Human Gliomas. 770 TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 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. 771 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 papillomavirus-mediated cervical cancer C53 NA RNA-seq etc. CSCC tissues up-regulated UCA1 was upregulated and interacted with hsa-miR-206, hsa-miR-3158-3p, hsa-miR-3158-5p, hsa-miR-486-3p, hsa-miR-135a-5p and hsa-miR-135b-5p 28970820 2017 Identification of Novel Long Non-coding and Circular RNAs in Human Papillomavirus-Mediated Cervical Cancer 772 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 esophageal cancer C15 NA qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. EC tissues, cell lines (EC9706 and KYSE) up-regulated UCA1 was significantly upregulated in EC tissues and associated with poor prognosis. Overexpression of UCA1 promoted the proliferation of EC cells, while silence of UCA1 inhibited EC cells growth. Furthermore, we found that Sox4 was a direct target gene of UCA1. UCA1 regulated Sox4 expression through functioning as a competing endogenous RNA (ceRNA). UCA1 directly interacted with miR-204 and decreased the binding of miR-204 to Sox4 3'UTR, which suppressed the degradation of Sox4 mRNA by miR-204. 27667646 2016 lncRNA-UCA1 enhances cell proliferation through functioning as a ceRNA of Sox4 in esophageal cancer. 773 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 lung cancer C34 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RNAi Cell lines (H520, SKMES1) up-regulated UCA1 down-regulation inhibited cell proliferation and migration in both SKMES-1 and H520 lung cancer cells.Then we demonstrated that repressed UCA1 promoted the miR-193a expression and miR-193a could bind to the predicted binding site of UCA1.We then dissected the role of miR-193a in lung cancer and proved the anti-tumor role of miR-193a.Furthermore,miR-193a displayed its role in lung cancer via modulating the HMGB1 expression.In addition,over-expression of HMGB1 could restore the UCA1 knockdown induced repression of cell proliferation and migration. 29355524 2018 Long non-coding RNA UCA1 promotes lung cancer cell proliferation and migration via microRNA-193a/HMGB1 axis. 774 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 melanoma NA M8720/3 qPCR, RNAi, Western blot, RIP, Cell proliferation assay etc. melanoma tissues, cell lines (A375 and SK-MEL-2) up-regulated In our experiments, UCA1 expression was discovered to be upregulated in melanoma tissues and cells, while the depletion of UCA1 led to the inhibition of cell proliferation, invasion and cell cycle arrest. To further our understanding of the mechanisms of UCA1, a system of experiments was built. We found that miR-507 could directly bind to UCA1 at the miRNA recognition site, and that there was a negative correlation between miR-507 and UCA1. Additionally, FOXM1 is a target of miR-507 and can be downregulated by either miR-507 overexpression or UCA1 depletion. Downregulated FOXM1 was analogous to the depletion of UCA1 and the overexpression of miR-507. 27389544 2016 LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanoma. 775 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 glioma NA M9380/3 qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc. glioma tissues, cell lines (U373MG, T98MG, SWO38, U251 and SHG44) up-regulated Upregulation of lncRNA-UCA1 in glioma tissues and cell lines could promote glioma cell proliferation and migration through interaction with miR-182, and knockdown of UCA1 inhibited the proliferation and migration of human glioma cell. In addition, miR-182 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) was required in the regulation of UCA1 induced glioma cell proliferation. 28137422 2017 The lncRNA UCA1 interacts with miR-182 to modulate glioma proliferation and migration by targeting iASPP. 776 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 non small cell lung cancer C34 M8046/3 qPCR, Western blot, RIP, Luciferase reporter assay etc. NSCLC tissues, cell lines (A549, H1299, H446, H460, NCIH1650, BEAS-2B) up-regulated UCA1 overexpression enhanced, whereas UCA1 silencing impaired the proliferation and colony formation of NSCLC cells. Moreover, mechanistic investigations showed that UCA1 upregulated the expression of miR-193a-3p target gene ERBB4 through competitively 'spongeing' miR-193a-3p. Overall, we concluded that UCA1 functions as an oncogene in NSCLC, acting mechanistically by upregulating ERBB4 in part through 'spongeing' miR-193a-3p 26655272 2015 LncRNA-UCA1 exerts oncogenic functions in non-small cell lung cancer by targeting miR-193a-3p 777 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 liver cancer C22.0 NA qPCR, Western blot, in vitro knockdown cell line (MHCC97, MG63, hFOB1.19, OS-732), neuroblastoma tissues up-regulated Knockdown of UCA1 reduced cell viability, inhibited migration and invasion, and promoted cell apoptosis.However,the effect of UCA1 knockdown on cell growth and migration was blocked by miR-301a overexpression,whose expression was regulated by UCA1. We also found that miR-301a positively regulated the CXCR4 expression.CXCR4 inhibition reversed the effect of miR-301a overexpression on cell growth and migration.Moreover,miR-301a activated the Wnt/?-catenin and NF-B pathways via regulating CXCR4. 29523218 2018 Knockdown of urothelial carcinoma associated 1 suppressed cell growth and migration through regulating miR-301a and CXCR4 in osteosarcoma MHCC97 cells. 778 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 cervical cancer C53 NA qPCR, Luciferase reporter assay, in vitro knockdown etc. cell lines (SIBCB), cervical cancer tissues up-regulated Interference of lncRNA UCA1 inhibited cell proliferation,migration,invasion,and viability. Results of the luciferase reporter assay revealed a binding site between lncRNA UCA1 and miR-206. Knockdown of lncRNA UCA1 could directly upregulate miR-206 expression.VEGF downregulation was also observed after knockdown of lncRNA UCA1. 29523226 2018 Downregulation of lncRNA UCA1 inhibits proliferation and invasion of cervical cancer cells through miR-206 expression. 779 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 pancreatic cancer C25 NA qPCR, RNAi, Northern blot, Luciferase reporter assay, Flow cytometry assay etc. pancreatic cancer tissues, cell lines (SW1990, BxPC-3, MiaPaCa-2, PANC-1, CAPAN-1) up-regulated UCA1 was overexpressed in PC tissues and cell lines. The proliferation of PC cells was inhibited after UCA1 was suppressed by a lentiviral vector. Cell apoptosis rate was largely promoted by down-regulating UCA1. Luciferase activity assay further comfirmed the targeting relationship between UCA1 and miR-135a. Moreover, miRNA-135a reversed the effect of UCA1 on cell apoptosis rate and cell viability in SW1990 cells. The migration and invasion capacity of PC cells suppressed by UCA1 siRNA was then enhanced by miR-135a inhibitor. 28315290 2017 UCA1 Regulates the Growth and Metastasis of Pancreatic Cancer By Sponging MiR-135a. 780 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 breast cancer C50 NA qPCR, Western blot etc. cell lines (MDA-MB-231, T47D and MCF7) up-regulated In breast cancer cells,IMP1 interacts with UCA1 via the "ACACCC" motifs within UCA1 and destabilizes UCA1 through the recruitment of CCR4-NOT1 deadenylase complex.Meanwhile,binding of IMP1 prevents the association of miR-122-5p with UCA1,thereby shifting the availability of miR-122-5p from UCA1 to the target mRNAs and reducing the UCA1-mediated cell invasion.Accordingly, either IMP1 silencing or UCA1 overexpression resulted in reduced levels of free miR-122-5p within the cytoplasm, affecting miR-122-5p in regulating its target mRNAs.Our study provides initial evidence that interaction between IMP1 and UCA1 enhances UCA1 decay and competes for miR-122-5p binding,leading to the liberation of miR-122-5p activity and the reduction of cell invasiveness. 29669595 2018 IMP1 regulates UCA1-mediated cell invasion through facilitating UCA1 decay and decreasing the sponge effect of UCA1 for miR-122-5p. 781 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell proliferation assay etc. HCC tissues, cell lines (MHCC97L, Huh7, MHCC97H and SK-hep1) up-regulated UCA1 was markedly upregulated in HCC tissues. Furthermore, gain-of-function and loss-of-function analysis showed that UCA1 knockdown inhibited HCC cells proliferation and invasion in vitro and xenograft tumour growth in vivo. Moreover, UCA1 overexpression promoted cell epithelial-mesenchymal transition (EMT) in HCC via effectively sponging to miR-203 and thereby activating the expression of transcription factor Snail2. 28271214 2017 Long non-coding RNA UCA1 regulates the expression of Snail2 by miR-203 to promote hepatocellular carcinoma progression. 782 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 bladder cancer C67 NA qPCR, RNAi, Western blot etc. bladder cancer cell lines up-regulated In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. 24890811 2014 Long non-coding RNA UCA1 promotes glycolysis by upregulating hexokinase 2 through the mTOR-STAT3/microRNA143 pathway. 783 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 bladder cancer C67 NA qPCR, RNAi, Western blot etc. bladder cancer tissues up-regulated Here, we report that downregulated hsa-miR-1 and upregulated lncRNA urothelial cancer associated 1 (UCA1) were inversely expressed in bladder cancer. Hsa-miR-1 decreased the expression of UCA1 in bladder cancer cells in an Ago2-slicer-dependent manner. The binding site between UCA1 and hsa-miR-1 was confirmed. Overexpression of hsa-miR-1 inhibited bladder cancer cell growth, induced apoptosis, and decreased cell motility. hsamiR-1 to play tumor suppressive roles via downregulating lncRNA UCA1 in bladder cancer, which may have potential therapeutic significance. 25015192 2014 Hsa-miR-1 downregulates long non-coding RNA urothelial cancer associated 1 in bladder cancer. 784 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 breast cancer C50 NA microarray, qPCR, RNAi, ISH etc. breast cancer tissues, cell lines (MDA-MB-231) up-regulated UC1 was significantly upregulated, while miR-143 was significantly downregulated in the tumor tissues than in the adjacent normal tissues. There are direct interactions between miR-143 and the miRNA recognition sites of UCA1. UCA1 is present in Ago2-containing RNA-induced silencing complex (RISC), through association with miR-143. Through downregulating miR-143, UCA1 can modulate breast cancer cell growth and apoptosis 26439035 2015 Long noncoding RNA UCA1 modulates breast cancer cell growth and apoptosis through decreasing tumor suppressive miR-143 785 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 bladder cancer C67 NA qPCR, Western blot, RIP bladder cancer tissues, cell lines (5637, UMUC2) up-regulated UCA1 enhances mitochondrial function in bladder cancer cells.These data suggest that UCA1 enhanced mitochondrial function and cell viability through the UCA1/miR-195/ARL2 axis in vitro and in vivo. 29130995 2017 LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway 786 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 bladder cancer C67 NA qPCR, Western blot, Luciferase reporter assay etc. bladder cancer tissues, cell lines (5637, T24, UMUC2) up-regulated Here, we demonstrated that overexpression of lncRNA-UCA1 could induce epithelial to mesenchymal transition (EMT) and increase the migratory and invasive abilities of bladder cancer cells. Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1). 26544536 2015 Long noncoding RNA UCA1 promotes bladder cancer cell migration and invasion via hsa-miR-145/ ZEB1/2 /FSCN1 pathway. 787 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 bladder cancer C67 NA qPCR, Western blot, Luciferase reporter assay etc. bladder cancer tissues, cell lines (UMUC2, 5637) up-regulated Real-time reverse transcriptase-polymerase chain reaction demonstrated that the RNA level of urothelial carcinoma-associated 1 and GLS2 was positively correlated in bladder cancer tissues and cell lines. Furthermore, luciferase reporter assays indicated that there was a miR-16 binding site in urothelial carcinoma-associated 1, and it showed appreciable levels of sponge effects on miR-16 as readouts in a dose-dependent manner. 26373319 2015 Long non-coding RNA UCA1 promotes glutamine metabolism by targeting miR-16 in human bladder cancer. 788 ucoo2kmd.1 NA NA NA NA colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. cell lines (HCT116, SW480) up-regulated We found that lncRNA-uc002kmd.1 expression was usually highly expressed in carcinoma compared with the tissue adjacent to the carcinoma. Through a series of experiments, the results showed that lncRNA-uc002kmd.1 regulates CD44 as a molecular decoy for miR211-3p. Our data indicated that the overexpression of lncRNA-uc002kmd.1 enhanced cell proliferation in CRC 26974151 2016 Long Non-Coding RNA ucoo2kmd.1 Regulates CD44-Dependent Cell Growth by Competing for miR-211-3p in Colorectal Cancer 789 UFC1 UFC1, HSPC155 ENSG00000143222 NA GRCh38_1:161152776-161158856 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, in vitro knockdown etc. HCC tissues, cell lines (BEL-7402, SK-Hep1, Huh7, MHCC-97H) up-regulated Levels of the lincRNA-UFC1 were increased in HCC tissues compared with controls, and associated with tumor size, Barcelona Clinic Liver Cancer stage, and patient outcomes. Transgenic expression of the lincRNA-UFC1 in HCC cells promoted their proliferation and cell-cycle progression and inhibited apoptosis, whereas short hairpin RNA knockdown of lincRNA-UFC1 had opposite effetcs.The lincRNA-UFC1 interacted directly with the messenger RNA (mRNA) stabilizing protein HuR (encoded by ELAVL1) to increase levels of β-catenin mRNA (encoded by CTNNB1) and protein. In contrast, there was a negative correlation between levels of microRNA 34a and lincRNA-UFC1 in HCC tissues microRNA 34a reduced the stability of lincRNA-UFC1. 25449213 2014 The Long Intergenic Noncoding RNA UFC1, A Target of MicroRNA 34a, Interacts With the mRNA Stabilizing Protein HuR to Increase Levels of β-Catenin in HCC Cells. 790 UICLM NA NA NA NA colorectal cancer C19.9 NA qPCR, Western blotting, RIP etc. cell lines (SW620, SW480, LoVo, HT-29, HCT116, DLD-1, RKO) up-regulated lncRNA UICLM (up-regulated in colorectal cancer liver metastasis) was significantly up-regulated in cases of CRC with liver metastasis. Moreover, UICLM expression was higher in CRC tissues than in normal tissues, and UICLM expression was associated with poor patient survival. Knockdown of UICLM inhibited CRC cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and CRC stem cell formation in vitro as well as tumor growth and liver metastasis in vivo. Ectopic expression of UICLM promoted CRC cell proliferation and invasion. Mechanistic investigations revealed that UICLM induced its biological effects by regulating ZEB2, as the oncogenesis facilitated by UICLM was inhibited by ZEB2 depletion. Further study indicated that UICLM acted as a competing endogenous RNA (ceRNA) for miR-215 to regulate ZEB2 expression. 29187907 2017 Long non-coding RNA UICLM promotes colorectal cancer liver metastasis by acting as a ceRNA for microRNA-215 to regulate ZEB2 expression 791 Unigene56159 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Cell migration and invasion assay, MTT assay etc. HCC tissues, cell lines (SMMC-7721 and HepG2) up-regulated We identified a novel lncRNA, lncRNA-Unigene56159, which is highly expressed in HBV-related HCC tissues, and further analysis showed that this lncRNA was induced by HBV in vitro. Functionally, Unigene56159 significantly promoted cell migration/invasion and epithelial-mesenchymal transition (EMT) in HCC. Mechanistically, Unigene56159 could directly bind to miR-140-5p and effectively act as a competing endogenous RNA (ceRNA) for miR-140-5p to de-repress the expression of the target gene Slug. 27597739 2016 Long non-coding RNA Unigene56159 promotes epithelial-mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells. 792 USP16 NA ENSG00000156256 NA GRCh38_21:29024629-29054488 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot cell lines (MHCC97H, MHCC97L, HepG2, SMMC-7721, and LO2) down-regulated Linc-USP16 expression was significantly down-regulated in HCC patient tissues and cell lines. Further functional experiments suggested that Linc-USP16 could directly increase PTEN expression by acting as a competing endogenous RNA (ceRNA) for miR-21 and miR-590-5p. 29179215 2017 Long Non-Coding RNA Linc-USP16 Functions As a Tumour Suppressor in Hepatocellular Carcinoma by Regulating PTEN Expression 793 WT1AS WT1-AS, WIT-1, WIT1, WT1-AS1, WT1AS ENSG00000183242 NR_023920 GRCh38_11:32435518-32458769 colon cancer C18 NA microarray, qPCR, RNA pull-down assay etc. cell line (HCT-117) 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. 794 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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. 795 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 prostate cancer C61.9 NA qPCR, Luciferase reporter assays, Western blot etc. cell lines (PC3, DU145, LNCAP) down-regulated XIST was down-regulated in prostate cancer specimens and cell lines. Low expression of XIST was correlated with poor prognosis and advanced tumor stage in prostate cancer patients.XIST negatively regulates the expression of miR-23a and subsequently promotes RKIP expression at post-transcriptional level. Consequently, we investigated the correlation between XIST and miR-23a, and identified miR-23a as a direct target of XIST. In addition, over-expression of miR-23a efficiently abrogated the up-regulation of RKIP induced by XIST, suggesting that XIST positively regulates the expression of RKIP by competitively binding to miR-23a. Taken together, our study indicated that lncRNA XIST acts as a tumor suppressor in prostate cancer, and this regulatory effect of XIST will shed new light on epigenetic diagnostics and therapeutics in prostate cancer. 29212233 2017 LncRNA XIST acts as a tumor suppressor in prostate cancer through sponging miR-23a to modulate RKIP expression 796 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 glioma NA M9380/3 qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay, Cell migration assay etc. cell lines (hCMEC/D3, U87MG, U118MG, HEK293T) up-regulated lncRNA X-inactive-specific transcript (XIST) was upregulated in endothelial cells that were obtained in a BTB model in vitro. XIST knockdown increased BTB permeability and inhibited glioma angiogenesis. The analysis of the mechanism of action revealed that the reduction of XIST inhibited the expression of the transcription factor forkhead box C1 (FOXC1) and zonula occludens 2 (ZO-2) by upregulating miR-137. FOXC1 decreased BTB permeability by increasing the promoter activity and expression of ZO-1 and occludin, and promoted glioma angiogenesis by increasing the promoter activity and expression of chemokine (C-X-C motif) receptor 7b (CXCR7). 28287613 2017 Knockdown of long non-coding RNA XIST increases blood-tumor barrier permeability and inhibits glioma angiogenesis by targeting miR-137. 797 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 glioma NA M9380/3 qPCR, Luciferase reporter assay etc. cell lines (A172, U251) up-regulated lncRNA XIST expression inversely correlated with miR-429 expression in glioma cells; miR-429 modulated XIST expression by directly targeting the XIST gene sequence.In addition, miR-429 inhibitor restored metastatic and pro-angiogenic ability of gliomas abolished by silencing XIST. 29187887 2017 Long Non-coding RNA XIST Promotes Glioma Tumorigenicity and Angiogenesis by Acting as a Molecular Sponge of miR-429 798 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 gastric cancer C16 NA qPCR, Western blot , RIP, Luciferase reporter assay etc. cell lines (SGC-7901, BGC-823, HGC-27, MKN-28) up-regulated 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. Our fndings suggested that lncRNA XIST may be a candidate prognostic biomarker and a target for new therapies in GC patients. 29212249 2017 Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer 799 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 bladder cancer C67 NA qPCR, Western blot, Luciferase reporter assay bladder cancer tissues, cell lines (TCC-SUP, EJ, SW780 and UM-UC-3) up-regulated XIST and AR were upregulated in bladder cancer tissues and positively correlated. These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation. 28869948 2017 The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR) 800 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. cell lines (QSG-7701, SMMC-7721, Huh-6, Huh-7, HepG2, HCCLM3 and QGY-7703) differential expression we showed that miR-92b was significantly upregulated in tumor tissue and plasma of HCC patients, and its expression level was highly correlated with gender and microvascular invasion. Functionally, miR-92b could promote cell proliferation and metastasis of HCC in vitro and in vivo. Mechanistic investigations suggested that Smad7, which exhibited an inverse relationship with miR-92b expression in HCC, was a direct target of miR-92b and could reverse its effects on HCC tumorigenesis. Furthermore, long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and miR-92b could directly interact with and repress each other, and XIST could inhibit HCC cell proliferation and metastasis by targeting miR-92b 27100897 2016 MicroRNA-92b promotes hepatocellular carcinoma progression by targeting Smad7 and is mediated by long non-coding RNA XIST 801 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 nasopharyngeal cancer C11 NA qPCR, Western blot etc. nasopharyngeal carcinoma tissues, cell lines (CNE1, CNE2, SUNE-1 and C666-1) up-regulated XIST expression was significantly upregulated in NPC tissues and cell lines.Knockdown of XIST inhibited NPC cell proliferation and invasion and induced apoptosis in vitro,as well as suppressed NPC tumor growth in vivo.Further analysis revealed that XIST and miR-491-5p interact with and repress each other.XIST may function as an endogenous miR-491-5p sponge to regulate the target gene of miR-491-5p. 29219216 2018 Knockdown of long non-coding RNA XIST suppresses nasopharyngeal carcinoma progression by activating miR-491-5p. 802 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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. 803 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 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. 804 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 breast cancer C50 NA qPCR, Western blot, Luciferase reporter assay etc. breast cancer tissues, cell lines (MCF-7, ZR-75-1, HCC-1937, MDA-MB-231, MDA-MB-468 and MDA-MB-453) up-regulated XIST was significantly down-regulated in breast cancer tissues and cell lines. Further functional analysis indicated that overexpression of XIST remarkably inhibited breast cancer cell growth, migration, and invasion.The results of luciferase reporter assays verified that miR-155 was a direct target of XIST in breast cancer.Moreover,caudal-type homeobox 1 (CDX1) was identified as a direct target of miR-155 and miR-155/CDX1 rescued the effects of XIST in breast cancer cells.Taken together,XIST is down-regulated in breast cancer and suppresses breast cancer cell growth, migration, and invasion via the miR-155/CDX1 axis. 29550489 2018 Long non-coding RNA XIST inhibited breast cancer cell growth, migration, and invasion via miR-155/CDX1 axis. 805 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc. HCC tissues, cell lines (HepG2, Hep3B, PLC, Huh7, smmc7721 and L02) up-regulated XIST expression was significantly increased in hepatocellular carcinoma tissues and cell lines. XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to hepatocellular carcinoma cell growth. In addition, we revealed that there was reciprocal repression between XIST and miR-139-5p. PDK1 was identified as a direct target of miR-139-5p. 28231734 2017 Long non-coding RNA XIST promotes cell growth by regulating miR-139-5p/PDK1/AKT axis in hepatocellular carcinoma. 806 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. hepatocellular carcinoma tissues, cell lines (HCCLM3, HepG2, Hep3B, SMMC-7721, and Huh7) differential expression MiR-181a had multiple binding sites with the long non-coding RNA (lncRNA) XIST. The regulation of miR-181a on PTEN was mediated by lncRNA XIST. The proliferation and invasion of cells with siXIST were significantly enhanced compared with those of control cells, while knockdown of miR-181a abolished the enhancing effects. 28388883 2017 Long non-coding RNA XIST regulates PTEN expression by sponging miR-181a and promotes hepatocellular carcinoma progression 807 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase Reporter Assays osteosarcoma tissues, cell lines (U2OS, Saos-2, MG63, and MNNG/HOS) up-regulated XIST expression was significantly increased in osteosarcoma tissues and cell lines by LncRNA Profiler and qRT-PCR.The competing relationship between XIST and miR-320b was confirmed by Luciferase report assay. 28409547 2017 Long Non-Coding RNA XIST Promotes Osteosarcoma Progression by Targeting Ras-Related Protein RAP2B via miR-320b 808 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 colorectal cancer C19.9 NA qPCR, Western blot etc. colorectal cancer tissues, cell lines (LOVO, HCT116, SW620, SW480 and HT29) up-regulated The expression level of XIST was significantly increased in both CRC tissues sample and CRC cells.XIST promoted CRC cell proliferation by affecting the cell cycle.In addition,XIST and miR-132-3p were inhibited by each other reciprocally. 28730777 2017 Long non-coding RNA XIST functions as an oncogene in human colorectal cancer by targeting miR-132-3p 809 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 non small cell lung cancer C34 M8046/3 qPCR, Western blot, in vitro knockdown, RNAi, RIP etc. cell lines (A549, H226), NSCLC tissues up-regulated lncRNA XIST and ZEB2 mRNA in metastatic NSCLC tissues.Knockdown of lncRNA XIST inhibited ZEB2 expression,and repressed TGF-β-induced EMT and NSCLC cell migration and invasion. Being in consistent with the in vitro findings, the in vivo experiment of metastasis showed that knockdown of lncRNA XIST inhibited pulmonary metastasis of NSCLC cells in mice. In addition, knockdown of ZEB2 expression can inhibit TGF-β-induced EMT and NSCLC cell migration and invasion. Mechanistically, lncRNA XIST and ZEB2 were targets of miR-367 and miR-141. Furthermore, both miR-367 and miR-141 expression can be upregulated by knockdown of lncRNA XIST. Taken together, our study reveals that lncRNA XIST can promote TGF-β-induced EMT and cell invasion and metastasis by regulating miR-367/miR-141-ZEB2 axis in NSCLC. 29339211 2018 Long non-coding RNA XIST promotes TGF-β-induced epithelial-mesenchymal transition by regulating miR-367/141-ZEB2 axis in non-small-cell lung cancer. 810 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay, RIP etc. non-small cell lung cancer tissues, cell line (A549, H450, 95D, H1299, SPC-A-1 and H522) up-regulated XIST was substantially upregulated and miR-137 was aberrantly downregulated in NSCLC tissues and cells. XIST was identified to function as a competitive endogenous RNA (ceRNA) for miR-137 to promote NSCLC cell viability and invasion. Additionally, our results suggested that miR-137 targeted the 3'UTR of paxillin (PXN) to suppress NSCLC cell viability and invasion. Meanwhile, miR-137 was negatively correlated with PXN expression while XIST was positively correlated with PXN expression.More importantly, XIST positively regulated PXN levels by sponging miR-137 in vitro and in vivo. 29337100 2018 Knockdown of long non-coding RNA XIST inhibits cell viability and invasion by regulating miR-137/PXN axis in non-small cell lung cancer. 811 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 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 (NL9980, NCI-H1299, NCI-H460, SPC-A-1, and A549) up-regulated The expression levels of XIST were significantly elevated. Knockdown of XIST significantly inhibited the cell proliferation, migration and invasion, and promoted cell apoptosis. Furthermore, XIST knockdown elevated the expression of E-cadherin, and suppressed the expression of Bcl-2. We further identified reciprocal repression between XIST and miR-449a, which eventually influenced the expression of Bcl-2: XIST functioned as a miRNA sponge of miR-449a, which was a negative regulator of Bcl-2. 28248928 2017 The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer. 812 XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 non small cell lung cancer C34 M8046/3 qPCR, Western blot, RNAi, Luciferase reporter assay non-small cell lung cancer tissue, cell lines (A549, H1299, SK-MES-1, Calu-3) up-regulated XIST was upregulated in NSCLC cell lines and tissues. Functionally, XIST knockdown inhibited cancer cell proliferation and invasion, and induced apoptosis in vitro, and suppressed subcutaneous tumor growth in vivo.Mechanistic investigations revealed a reciprocal repressive interaction between XIST and miR-186-5p. 28448993 2017 The Long Non-Coding RNA XIST Controls Non-Small Cell Lung Cancer Proliferation and Invasion by Modulating miR-186-5p 813 XLOC_008466 NA NA NA NA non small cell lung cancer C34 M8046/3 qPCR, Western blot, RIP, Luciferase reporter assay etc. non-small cell lung cancer tissues, cell lines (A549, H460) up-regulated Up-regulation of XLOC_008466 in NSCLC patients was related to lymph node metastasis and the TNM stage.Experiments on mechanisms revealed that XLOC_008466 functioned as a ceRNA, directly binding to miR-874, and could affect cell proliferation, apoptosis and invasion through regulation of miR-874 expression as well as by increasing matrix metalloproteinase 2 (MMP2) and X-linked inhibitor of apoptosis (XIAP) expression 28501870 2017 Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874 814 ZEB1 NA ENSG00000148516 NA GRCh38_10:31318495-31529814 pancreatic cancer C25 NA Microarray, qPCR, Western blot etc. cell lines (HEK-293T, PANC-1 and SW-1991) up-regulated MiR-205-5p was low-expressed while ZEB1 and ADPGK-AS1 were high-expressed in PC tissues and cells compared with the normal.Dual-luciferase reporter gene assay proved that ADPGK-AS1 could directly target miR-205-5p and miR-205-5p could directly target ZEB1 3'UTR. The expression of MiR-205-5p was negatively correlated with proliferation,migration and invasion, and positively correlated with apoptosis rate of PC cells, while ZEB1 and ADPGK-AS1 had an inversed effect. Further in vitro and in vivo investigation indicated that epithelial-mesenchymal transition (EMT) could be restrained by miR-205-5p through targeting ZEB1. ADPGK-AS1 strongly promoted the tumorigenesis via downregulating miR-205-5p expression and induced the EMT process in vivo. ADPGK-AS1 inhibited miR-205-5p and therefore promoted PC progression through activating ZEB1-induced EMT. 29667486 2018 LncRNA ADPGK-AS1 promotes pancreatic cancer progression through activating ZEB2-mediated epithelial-mesenchymal transition. 815 ZEB1-AS1 ZEB2-AS1, ZEB2-AS, ZEB2AS, ZEB2NAT ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 colorectal cancer C19.9 NA qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown CRC tissues, CRC cell lines (SW480, DLD-1, HCT116, SW620, and HT29) up-regulated ZEB1-AS1 was upregulated in CRC tissues and cells.MiR-101 was downregulated in CRC tissues and negatively correlated with ZEB1-AS1 and ZEB1 expression levels in CRC. Functional experiments showed that, consistent with ZEB1-AS1 depletion,miR-101 overexpression and ZEB1 depletion inhibited the proliferation and migration of CRC cells. Overexpression of miR-101 partially abolished the effects of ZEB1-AS1 on the proliferation and migration of these cells. Moreover, combined ZEB1-AS1 depletion and miR-101 overexpression significantly inhibited cell proliferation and migration of the CRC cells. Hence, ZEB1-AS1 functioned as a molecular sponge for miR-101 and relieved the inhibition of ZEB1 caused by miR-101. 29511455 2018 Interplay between long noncoding RNA ZEB1-AS1 and miR-101/ZEB1 axis regulates proliferation and migration of colorectal cancer cells. 816 ZEB1-AS1 ZEB2-AS1, ZEB2-AS, ZEB2AS, ZEB2NAT ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 osteosarcoma NA M9180/3 qPCR, RNAi, Western blot, Northern blot, RIP, Luciferase reporter assay, Cell proliferation assay etc. osteosarcoma tissues, cell lines (HOS and Saos-2) up-regulated ZEB1-AS1 functions as a molecular sponge for miR-200s and relieves the inhibition of ZEB1 caused by miR-200s. ZEB1-AS1 and miR-200s reciprocally negatively regulate each other.MiR-200s are downregulated in osteosarcoma tissues,and negatively correlated with ZEB1-AS1 and ZEB1 expression levels in osteosarcoma. Functional experiments showed that consistent with ZEB1-AS1 depletion,miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration.Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration.Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. 28075045 2017 Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration. 817 ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 ENSG00000177410 NR_003604 GRCh38_20:49278178-49295738 osteosarcoma NA M9180/3 qPCR, Luciferase reporter assays, RIP etc. cell lines (U2OS, Saos-2, HOS, MG-63) up-regulated Furthermore,the up-regulated expression of ZFAS1 was closely related to poor prognosis. In vitro, loss-of-function experiments showed that ZFAS1 knockdown significantly suppressed the proliferation, induced cycle arrest at G0/G1 phase and enhance apoptosis. In vivo, ZFAS1 knockdown inhibited the tumor growth. Bioinformatics online programs predicted that ZFAS1 sponge miR-486 at 3’-UTR with complementary binding sites, which was validated using luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Rescue experiments confirmed that miR-486 could reverse the functions of ZFAS1 on osteosarcoma genesis. In conclusion, our results demonstrate that ZFAS1 act as competing endogenous RNA (ceRNA) for miR- 486, and act as oncogene in osteosarcoma tumorigenesis, and discover the functional regulatory pathway of ZFAS1 sponging miR-486. 29262629 2017 Long non-coding RNA ZFAS1 sponges miR-486 to promote osteosarcoma cells progression and metastasis in vitro and vivo 818 ZFAS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 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. 819 ZNFX1-AS1 ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 NA NA NA 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.