LncRNA name Synonyms geneid ensg_name refseq_id position cancer type ICD-0-3 ICD-0-3 methods sample regulated function description pubmed id year title drug MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 lung cancer C34 NA qRT-PCR, Western blot lung cancer tissues, lung cancer cell lines (A549, H1703 and H292) down-regulated lncRNA MEG3 showed a low expression in chemotherapy-sensitive lung cancer tissues, and overexpression of lncRNA MEG3 attenuated autophagy level, thus increasing the sensitivity of vincristine in chemotherapy of lung cancer. 29509250 2018 LncRNA MEG3 promotes the sensitivity of vincristine by inhibiting autophagy in lung cancer chemotherapy. Vincristine TP73-AS1 TP73-AS1, KIAA0495, PDAM 57212 ENSG00000227372 NR_033708 GRCh38_1:3735601-3747336 breast cancer C50 NA qPCR, Luciferase reporter assay, Western blot breast cancer tissues, cell lines (Hs578Bst, BT474, MDA-MB-231, T47D, MCF-7, and MDA-MB-453) up-regulated TP73-AS1 was specifically upregulated in BC tissues and BC cell lines and was correlated to a poorer prognosis in patients with BC. TP73-AS1 could regulate miR-200a through direct targeting. Moreover, TP73-AS1 might compete with TFAM for miR-200a binding thus to promote TFAM expression.TP73-AS1 promoted BC cell proliferation through acting as a competing endogenous RNA (ceRNA) by sponging miR-200a. High TP73-AS1 expression in BC was related with poorer clinicopathological parameters and shorter overall survival. 28639399 2017 TP73-AS1 promotes breast cancer cell proliferation through miR-200a-mediated TFAM inhibition. TZM GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA microarray, qPCR etc. breast cancer tissues, cell line (SKBR-3) down-regulated Expression of the lncRNA GAS5 was decreased in SKBR-3/Tr cells and in breast cancer tissue from trastuzumab-treated patients. Inhibition of GAS5 promoted SKBR-3 cell proliferation, and GAS5 knockdown partially reversed lapatinib-induced inhibition of SKBR-3/Tr cell proliferation. GAS5 suppresses cancer proliferation by acting as a molecular sponge for miR-21, leading to the de-repression of phosphatase and tensin homologs (PTEN), the endogenous target of miR-21. Moreover, mTOR activation associated with reduced GAS5 expression was required to suppress PTEN. 27034004 2016 Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer trastuzumab SNHG14 NA 104472715 ENSG00000224078 NR_146177 GRCh38_15:24978583-25419462 breast cancer C64.9 M8005/0 qRT-PCR ect. breast cancer cell lines ( SKBR-3 and BT474) up-regulated lncRNA?SNHG14 may promote the effect of trastuzumab by targeting the apoptosis regulator Bcl?2 (Bcl?2)/apoptosis regulator BAX (Bax) signaling pathway. Furthermore, the expression level of serum exosomal lncRNA?SNHG14 was upregulated in patients who exhibited resistance to trastuzumab, compared with patients exhibiting a response. 30015837 2018 Exosome-mediated transfer of lncRNA?SNHG14 promotes trastuzumab chemoresistance in breast cancer. trastuzumab UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 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. Trastuzumab HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 pancreatic cancer C25 NA qPCR etc. cell lines (MiaPaCa-2, BxPC3, Suit2 and PANC-1) down-regulated We observed that TRAIL-resistant pancreatic cancer cells had higher levels of HOTAIR expression, whereas TRAIL-sensitive pancreatic cancer cells had lower HOTAIR levels. Overexpressing HOTAIR in TRAIL-sensitive cells attenuated TRAIL-induced apoptosis, and shRNA-mediated HOTAIR knockdown in TRAIL-resistant PANC-1 cells sensitized them to TRAIL-induced apoptosis. These results support a causative effect of HOTAIR on TRAIL sensitivity. Mechanistically, we found that increased HOTAIR expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increased DR5 expression. We further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the DR5 gene. Taken together, these results demonstrate that high HOTAIR levels increase the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via epigenetic regulation of DR5 expression. 28476883 2017 The long non-coding RNA HOTAIR enhances pancreatic cancer resistance to TNF-related apoptosis-inducing ligand. TRAIL CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP TRAIL-resistant hepatocellular carcinoma cell lines (HepG2R and Bel-7402R) up-regulated CASC2, a well-established tumor suppressive long non-coding RNA, could serve as a Sponge of miR-24 and miR-221, thus modulating TRAIL-induced tumor cell apoptosis TRAIL resistance of hepatocellular carcinoma. Taken together, we demonstrated a CASC2/miR-24/miR-221 axis, which can affect the TRAIL resistance of hepatocellular carcinoma through regulating caspase 3/8; through acting as a Sponge of miR-24 and miR-221, CASC2 may contribute to improving hepatocellular carcinoma TRAIL resistance, and finally promoting the treatment efficiency of TRAIL-based therapies. 29476051 2018 CASC2/miR-24/miR-221 modulates the TRAIL resistance of hepatocellular carcinoma cell through caspase-8/caspase-3. TNF Related Apoptosis Inducing Ligand (TRAIL) HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colon cancer C18 NA microarray, qPCR, RNAi, ChIP, Luciferase reporter assay etc. cell lines (HT-29, DLD1, MCF10a, HCC1954) up-regulated Here, we investigated the role of Hotair in the scenario of epithelial-to-mesenchymal transition (EMT) and in the arising and maintenance of cancer stem cells (CSCs). We found that treatment with TGF-B1 resulted in increased Hotair expression and triggered the EMT program. Interestingly, ablation of Hotair expression by siRNA prevented the EMT program stimulated by TGF-B1, and also the colony-forming capacity of colon and breast cancer cells. Furthermore, we observed that the colon CSC subpopulation (CD133(+)/CD44(+)) presents much higher levels of Hotair when compared with the non-stem cell subpopulation. 24022994 2013 Brief report: The lincRNA Hotair is required for epithelial-to-mesenchymal transition and stemness maintenance of cancer cell lines. TGF-b1 PRNCR1 PRNCR1, CARLo-3, PCAT8 101867536 ENSG00000282961 NR_109833 GRCh38_8:127079874-127092600 glioblastoma multiforme NA M9440/3 qPCR etc. GBM tissues, serum down-regulated Firstly, RT-qPCR was performed to verify the 10 lncRNAs using 90 GBM tissues from patients showing response to TMZ and 90 from patients showing no response. Among these, four lncRNAs (MALAT1, LOC100506474, MEG3 and PRNCR1) were found significantly dysregulated in responding tissues compared with non-responding tissues. 28187000 2017 MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression. Temozolomide, TMZ CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 glioma NA M9380/3 qPCR, Luciferase reporter assay, Western blot glioma tissues, cell lines (U257 and U87) down-regulated CASC2 is downregulated in gliomas, resulting in increased miR-193a-5p level and a decrease in mTOR expression, which further induces protective autophagy, leading to TMZ resistance. Inhibition of autophagy helps to increase the efficacy of TMZ. 29136760 2017 Upregulation of CASC2 sensitized glioma to temozolomide cytotoxicity through autophagy inhibition by sponging miR-193a-5p and regulating mTOR expression. temozolomide(TMZ) MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioblastoma multiforme NA M9440/3 qRT-PCR, in vitro knockdown, RNAi GBM cell lines (U87, T98G and LN-18, U251) up-regulated Importantly, our nanocomplex is able to target CSCs that are considered to be the prime culprits in therapeutic resistance and recurrence of GBM. Attenuation of MALAT1 by RNA interference significantly lowered the growth, motility and stemness of GBM cells. In addition, silencing of MALAT1 clearly improved the sensitivity of GBM cells to chemotherapeutic agents including the current first-line therapy of GBM [temozolomide (TMZ)]. In animal models of GBM, tumor involution with a modest but statistically significant survival benefit was achieved with concurrent treatment of TMZ and nanocomplex-mediated silencing of MALAT1.Expressions of both OCT4 and NANOG, transcription factors known to maintain pluripotency and self-renewal of embryonic stem cells, were significantly reduced (34.2% and 20.2%, respectively) after scL-siMAL treatment. 29202181 2018 Targeted nanocomplex carrying siRNA against MALAT1 sensitizes glioblastoma to temozolomide. temozolomide H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioma NA M9380/3 qPCR, RNAi, Western blot etc. glioma tissues, cell lines (U87, U251) up-regulated Taken together, these findings suggest that H19 plays an important role in the development of TMZ resistance, and may represent a novel therapeutic target for TMZ-resistant gliomas. Importantly, expression of H19 variant 1 was significantly higher in TMZ-resistant tumor tissues than in TMZ-sensitive tumor tissues. 27366087 2016 Knockdown of long noncoding RNA H19 sensitizes human glioma cells to temozolomide therapy Temozolomide MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioblastoma NA M9440/3 qPCR, Western blot cell lines (U251, U87) up-regulated The expression of MALAT1 was upregulated in the U251/TMZ and U87/TMZ cell lines compared to that in U251 and U87 cell lines, respectively. MALAT1 decreased the sensitivity of resistant glioma cell lines to TMZ by regulating ZEB1. 28668966 2017 Long Non-Coding RNA MALAT1 Decreases the Sensitivity of Resistant Glioblastoma Cell Lines to Temozolomide Temozolomide MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 glioma NA M9380/3 qPCR, 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 temozolomide RP11-838N2.4 NA NA NA NA GRCh38_18:3466250-3478978 glioblastoma NA M9440/3 qPCR, Western blot, RIP etc. glioblastoma tissues, cell lines (U87, U251) down-regulated We found that the level of the lncRNA RP11-838N2.4 was lower in TMZ-resistant GBM cells (U87TR, U251TR) compared to the parental, non-resistant GBM cells (U87, U251).In GBM patients, the decreased level of lncRNA RP11-838N2.4 correlated with higher risk of GBM relapse, as well as shorter postoperative survival times.Moreover, lncRNA RP11-838N2.4 acts as an endogenous sponge, suppressing the function of miR-10a through conserved sequences and increasing the expression of EphA8 that enhanced the rate of cell apoptosis, thereby intensified sensitivity of GBM cells to TMZ 27270310 2016 Long noncoding RNA RP11-838N2.4 enhances the cytotoxic effects of temozolomide by inhibiting the functions of miR-10a in glioblastoma cell lines temolozomide HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, RIP, ChIP, ISH etc. breast cancer tissues, cell lines (MCF7, T47D) up-regulated In this study, we report that HOTAIR (HOX antisense intergenic RNA) is upregulated in tamoxifen-resistant breast cancer tissues compared to their primary counterparts. Mechanistically, HOTAIR is a direct target of ER-mediated transcriptional repression and is thus restored upon the blockade of ER signaling, either by hormone deprivation or by tamoxifen treatment. Interestingly, this elevated HOTAIR increases ER protein level and thus enhances ER occupancy on the chromatin and potentiates its downstream gene regulation. 26364613 2015 LncRNA HOTAIR enhances ER signaling and confers tamoxifen resistance in breast cancer. tamoxifen LINC00894-002 NA 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 ERa.Knocking down LINC00894-002 downregulates expression of miR-200a-3p and miR-200b-3p, upregulates the expression of TGF-B2 and ZEB1,and finally contributes to TamR.Herein, we report the first case of an inhibitory lncRNA against TamR through the miR-200-TGF-B2-ZEB1 signaling pathway. 29738694 2018 Downregulation of LINC00894-002 Contributes to Tamoxifen Resistance by Enhancing the TGF-B Signaling Pathway. tamoxifen linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 breast cancer C50 NA qPCR, Western blot, RIP etc. cell line MCF-7 up-regulated linc-RoR functions as an onco-lncRNA to promote estrogen-independent growth of ER+ breast cancer. Under estrogen deprivation, linc-RoR causes the upregulation of phosphorylated MAPK/ERK pathway which in turn activates ER signaling. Knockout of linc-RoR abrogates estrogen deprivation-induced ERK activation as well as ER phosphorylation, whereas re-expression of linc-RoR restores all above phenotypes. Moreover, we show that the ERK-specific phosphatase Dual Specificity Phosphatase 7 (DUSP7), also known as MKP-X, is involved in linc-RoR KOinduced repression of MAPK/ERK signaling. Interestingly, linc-RoR KO increases the protein stability of DUSP7, resulting in repression of ERK phosphorylation. Clinical data analysis reveal that DUSP7 expression is lower in ER+ breast cancer samples than that in ER- breast cancer. Moreover, downregulation of DUSP7 expression is associated with poor patient survival. 29041978 2017 Linc-RoR promotes MAPK/ERK signaling and confers estrogen-independent growth of breast cancer tamoxifen linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 breast cancer C50 NA qPCR, Western blot etc. breast cancer tissues, cell lines (MCF7, BT474, MDA-MB-435, and MDA-MB-231) differential expression These results implied that downregulated long non-coding RNA ROR suppressed BT474 cell proliferation, invasion, and migration and reversed the effect of Tamoxifen on the BT474 cells. These results indicate that inhibition of long non-coding RNA ROR reverses resistance to Tamoxifen by inducing autophagy in breast cancer. 28635401 2017 Inhibition of long non-coding RNA ROR reverses resistance to Tamoxifen by inducing autophagy in breast cancer Tamoxifen PTENP1 PTENP1, PTEN-rs, PTEN2, PTENpg1, PTH2, psiPTEN 11191 ENSG00000237984 NA GRCh38_9:33673504-33677499 breast cancer C50 NA qPCR, Western blot etc. cell line (MCF7, 293T) down-regulated LncRNA PTENP1 can inhibit the proliferation and migration of breast cancer cells via the AKT and MAPK signaling pathways.Studies show that lncRNA PTENP1 can also regulate the expression of PTEN through the method in ceRNA hypothesis, thus affecting the progression of tumor cells. 29085464 2017 Long non-coding RNA PTENP1 inhibits proliferation and migration of breast cancer cells via AKT and MAPK signaling pathways tamoxifen UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 cholangiocarcinoma NA M810/3 qPCR, Western blot etc. CCA tissues up-regulated For the part of functional assays, knockdown of UCA1 could attenuate CCA cell growth both in vitro and in vivo. Besides, UCA1 facilitates apoptosis via Bcl-2/caspase-3 pathway. In addition, UCA1 regulates migration and invasion potential of CCA cells by affecting EMT. Furthermore, AKT/GSK-3B axis was activated to upregulate CCND1 expression due to overexpression of UCA1 in CCA. To summary, UCA1 might be a potentially useful prognostic biomarker and therapeutic target for CCA. 29221199 2017 Long non-coding RNA UCA1 indicates an unfavorable prognosis and promotes tumorigenesis via regulating AKT/GSK-3B signaling pathway in cholangiocarcinoma tamoxifen HOXA13 HOXA13, HOX1, HOX1J NA ENSG00000106031 NA GRCh38_7:27193503-27200106 hepatocellular carcinoma C22.0 M8170/3 qPCR, microarray hepatocellular carcinoma tissues up-regulated patients with HOXA13-positive HCC had worse overall survival than those with HOXA13-negative HCC. HOXA13 and HOTTIP were expressed in the same neoplastic hepatocyte populations.Stable overexpression of HOXA13 in liver cancer cell lines resulted in increased colony formation on soft agar and migration potential as well as reduced sensitivity to sorafenib in vitro. 29035381 2017 High expression of HOXA13 correlates with poorly differentiated hepatocellular carcinomas and modulates sorafenib response in in vitro models. sorafenib MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR etc. cell lines (MNNG/HOS) up-regulated MALAT1 induces pro-angiogenic effects, and demonstrate that the underlying mechanism involves a MALAT1/mechanistic target of rapamycin (mTOR)/hypoxia inducible factor-1a (HIF-1a) loop. With the help of chemically-modified small interfering RNAs targeting MALAT1 (siMALAT1), we confirm that siMALAT could provide a potential strategy to block the abnormally active OS-induced pro-angiogenic effect, and ultimately successfully suppress progression of OS tumours. 29209144 2017 Targeting the long noncoding RNA MALAT1 blocks the pro-angiogenic effects of osteosarcoma and suppresses tumour growth siMALAT1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 bladder cancer C67 NA Western blot, qPCR, ChIP cell lines (T24, UM-UC-3) up-regulated Silibinin was found to significantly decrease the expression levels of oncogenic HOTAIR and ZFAS 29190895 2017 Silibinin suppresses bladder cancer through down-regulation of actin cytoskeleton and PI3K/Akt signaling pathways Silibinin uc.57 NA 642394 ENSG00000205696 NR_033387 GRCh38_10:1526637-1556984 breast cancer C50 NA qPCR, Western blot, RIP etc. breast cancer tissues, cell line (MCF-7, MCF-7R) down-regulated uc.57 binds to BCL11A. Uc.57 overexpression downregulated BCL11A and reduced tamoxifen resistance in MCF-7R cells both in vitro and in vivo. 29179465 2017 Shikonin reduces tamoxifen resistance through long non-coding RNA uc.57 Shikonin, tamoxifen PEG10 PEG10, EDR, HB-1, MEF3L, Mar2, Mart2, RGAG3, RTL2, SIRH1 NA ENSG00000242265 NA GRCh38_7:94656325-94669695 diffuse large B-cell lymphoma NA M9680/3 qPCR, RNAi etc. DLBCL tissues, cell lines (OCI-LY-3, OCI-LY-7, OCI-LY-10 etc.) up-regulated We first found that the expression of PEG10 was upregulated in DLBCL tumorous tissues and that cell lines compared with the normal. Moreover, we illustrated that PEG10 was significantly correlated with B symptoms, IPI score, CHOP-like treatment and rituximab. 25864113 2015 Upregulation of long noncoding RNA PEG10 associates with poor prognosis in diffuse large B cell lymphoma with facilitating tumorigenicity. rituximab H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 acute promyelocytic leukemia NA M9866/3 qPCR etc. cell lines (NB4, APL, NB4-LR1 and NB4-LR1SFD) up-regulated We showed both in retinoid-treated cell lines and in APL patient cells an inverse relationship between the expression of H19 and the expression and activity of hTERT. Exploring the mechanistic link between H19 and hTERT regulation, we showed that H19 is able to impede telomerase function by disruption of the hTERT-hTR interaction. 29703210 2018 Telomerase regulation by the long non-coding RNA H19 in human acute promyelocytic leukemia cells. retinoids lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 102800311 NA NA NA prostate cancer C61.9 NA qPCR, Western blot cell lines (DU145 and LNCaP) down-regulated lincRNA-p21 silencing in DU145 and LNCaP cells induced up-regulation of PKM2 and activation of glycolysis, which could be reversed by PKM2 knockdown or rapamycin treatment.the proliferation and tumorigenesis of lincRNA-p21-silenced prostate cancer cells were significantly inhibited after knocking down PKM2. 3-bromopyruvate (3-Brpa) or rapamycin treatment largely decreased the tumour burden. PKM2 expression was inversely correlated with the lincRNA-p21 level and the survival of prostate cancer patients. 28994148 2017 LincRNA-p21 suppresses development of human prostate cancer through inhibition of PKM2. rapamycin,3-bromopyruvate (3-Brpa) lncRNA-LET NPTN-IT1, lncRNA-LET 101241892 ENSG00000281183 NR_103844 GRCh38_15:73567012-73569294 non small cell lung cancer C34 M8046/3 qPCR, Western blot NSCLC tissues, cell lines (A549, 95D, NCI-H292, and NCI-H1975, HBE) down-regulated Decreased lncRNA-LET expression was strongly associated with advanced tumor stages and poorer overall survival of NSCLC patients.overexpression of lncRNA-LET in NSCLC H292 cells significantly suppressed cell proliferation, migration and invasion, and promoted cell cycle arrest and apoptosis.lncRNA-LET overexpression significantly reduced the expression of Notch1 intracellular Domain (NICD1) in H292 cells while knockdown of lncRNA-LET increased NICD1 expression in H1975 cells. 29416684 2017 Downregulation of long non-coding RNA LET predicts poor prognosis and increases Notch signaling in non-small cell lung cancer. puromycin UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 ovarian cancer C56.9 NA qPCR, western blot etc. cell lines (SKOV3 and HeyA-8) up-regulated Collectively, our study elaborated a novel UCA1/miR-129/ABCB1 regulatory axis underlying PTX resistance of OC cells, providing a potential therapeutic target for OC. 29777711 2018 UCA1 confers paclitaxel resistance to ovarian cancer through miR-129/ABCB1 axis PTX HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, Western blot etc. cell lines (HeLa, Caski and C33A) up-regulated Propofol significantly decreased the cell viability and increased the cell apoptosis in Hela, Caski and C-33A cells, while HOTAIR overexpression promoted cell viability and inhibits cell apoptosis. mTOR/p70S6K protein expression levels were also markedly reduced by propofol but the effects were reversed with pcDNA-HOTAIR. In vivo, propofol inhibited the tumor size but had no inhibition effect in HOTAIR overexpression group 26523512 2016 Propofol promotes cell apoptosis via inhibiting HOTAIR mediated mTOR pathway in cervical cancer Propofol lncAGER AGER-1 NA ENSG00000204305 NA GRCh38_6:32180968-32184324 lung cancer C34 NA qRT-PCR, western blotting, Luciferase reporter assay lung cancer tissues, lung cancer cell lines (PC9, L78, A549, GLC-82, SBC-5, 95D, NCI-H460, NCI-H292 and NCI- H1395) down-regulated LncAGER expression was moderately correlated with AGER expression underlying a mechanism that lncAGER upregulates AGER by competitively binding to miRNA-185. LncAGER was significantly down-regulated in 76.4% of lung cancer tissues compared to adjacent normal tissues due to promoter hypermethylation. Over-expression of the lncRNA resulted in significant decreases in proliferation rate, migration ability,colony formation efficiency of lung cancer cells and tumor growth in nude mice. 29068471 2017 Long non-coding RNA AGER-1 functionally upregulates the innate immunity gene AGER and approximates its anti-tumor effect in lung cancer. programmed death 1 (PD-1)/programmed death ligand 1 (PD-1/PD-L1) HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 prostate cancer C61.9 NA qPCR, Western blot etc. cell lines differential expression Conversely, exogenously expressed HOTAIR resisted the PPI-inhibited MUC1 protein expression, and excessive expression of MUC1 antagonized the PPI-inhibited cell growth. 29807357 2018 Crosstalk of NF-kB/P65 and LncRNA HOTAIR-Mediated Repression of MUC1 Expression Contribute to Synergistic Inhibition of Castration-Resistant Prostate Cancer by Polyphyllin 1-Enzalutamide Combination Treatment Polyphyllin 1-Enzalutamide HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, RNAi, Luciferase reporter assay cell lines (KURAMOCHI, A2780p, A2780_CR5) differential expression Treatment of HOTAIR-overexpressing ovarian and breast cancer cell lines with PNAs decreased invasion and increased chemotherapy sensitivity. 28420874 2017 Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer platinum LINC00857 LINC00857 439990 ENSG00000237523 NR_038464 GRCh38_10:80207710-80219657 bladder cancer C67 NA qPCR etc. cell lines (UM‐UC‐3 (ATCC: CRL‐1749) and T24 (ATCC: HTB‐4)) differential expression Furthermore, LINC00857 knockdown sensitized UM-UC-3 and T24 bladder cancer cells to cisplatin, via the negative regulation of the LMAN1 gene. Our data indicate that LINC00857 plays an important role in the regulation of response to platinum-based chemotherapy. 29856124 2018 LINC00857 expression predicts and mediates the response to platinum-based chemotherapy in muscle-invasive bladder cancer platinum PCGEM1 PCGEM1, LINC00071, NCRNA00071, PCAT9 64002 ENSG00000227418 NR_002769 GRCh38_2:192749845-192776899 prostate cancer C61.9 NA qPCR etc. cell lines (PC-3, DU145 etc.) up-regulated We demonstrated for the first time that cholesterols upregulated the expression of PCGEM1 even in androgen-insensitive prostate cancer cell lines. Phytosterol inhibition of PCGEM1 and cell growth and the overexpression of caveolin-1, suggests that poor disease prognosis anchors on the ability of caveolin-1 to regulate downstream oncogene(s) and apoptosis genes. 19186008 2009 Differential effects of cholesterol and phytosterols on cell proliferation, apoptosis and expression of a prostate specific gene in prostate cancer cell lines. phytosterols ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 lung adenocarcinoma C34 M8140/3 qPCR, Western blot etc. LAD tissues, cell line A549/Taxol up-regulated Our results showed that ANRIL functioning as a potential oncogene was up-regulated in LAD, and promoted the acquisition of chemo-resistance in paclitaxel partly through the mitochondrial pathway by modulating the expression of apoptosis-related protein cleaved-PARP and Bcl-2. 28402932 2017 The long noncoding RNA ANRIL acts as an oncogene and contributes to paclitaxel resistance of lung adenocarcinoma A549 cells paclitaxel CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 nasopharyngeal cancer C11.9 NA qPCR, western blot, luciferase reporter assay, MIT nasopharynx cancer tissues, cell lines (CNE1 and CNE2) differential expression Our findings revealed that the upregulated CCAT1 results in significantly enhancing paclitaxel resistance in nasopharyngeal cancer cells. Bioinformatics analysis and luciferase reporter assay indicated that the upregulated CCAT1 sponges miR-181a in NPC cells. Taken together, lncRNA CCAT1 regulates the sensitivity of paclitaxel in NPC cells via miR-181a/CPEB2 axis. 28358263 2017 LncRNA CCAT1 modulates the sensitivity of paclitaxel in nasopharynx cancers cells via miR-181a/CPEB2 axis paclitaxel HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 lung adenocarcinoma C34 M8140/3 qPCR, Western blot lung adenocarcinom tissue, cell lines (16HBE, A549, A549/PA) up-regulated HOTTIP was overexpressed in lung adenocarcinoma and significantly increased in the treatment-insensitive group.Overexpression of HOTTIP, proliferation ability of A549 and drug resistance of A549/PA was significantly enhanced.HOTTIP can promote the progression of lung adenocarcinoma, and the formation of lung adenocarcinoma resistance regulated by the protein kinase B (AKT) signaling pathway. 29272003 2017 Overexpression of HOTTIP promotes proliferation and drug resistance of lung adenocarcinoma by regulating AKT signaling pathway. Paclitaxel NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 ovarian cancer C56.9 NA qPCR, luciferase reporter assay, Western blot etc. cell lines (SKOV3, HeyA-8) up-regulated NEAT1 was upregulated, and miR-194 was downregulated in PTX-resistant ovarian cancer tissues and cells.Functionally, NEAT1 knockdown enhanced cell sensitivity to PTX via promoting PTX-induced apoptosis in vitro. NEAT1 was identifed as a molecular sponge of miR-194 to upregulate ZEB1 expression. Mechanistically, NEAT1-knockdown-induced PTX sensitivity was mediated by miR-194/ZEB1 axis.Moreover, NEAT1 knockdown improved PTX sensitivity of ovarian cancer in vivo. 29180871 2017 lncrna NEAT1 contributes to paclitaxel resistance of ovarian cancer cells by regulating ZeB1 expression via mir-194 paclitaxel PCAT7 PCAT7, PCAN-R2 101928099 ENSG00000231806 NR_121566 GRCh38_9:94555054-94603990 non small cell lung cancer C34 M8046/3 qPCR, Luciferase reporter assay, Western blot NSCLC tissues, cell lines (SUNE-1, CNE-1, HNE-1, CNE-2, C666-1 and HONE-1) up-regulated Overexpression of PCAT7 resulted in the promotion of tumor cell proliferation,inhibition of cells apoptosis, facilitation of cells metastasis, and formation of EMT phenotype, while PCAT7 expression deletion remarkably prohibited cell proliferation, accelerated their apoptosis, weakened metastasis, and reversed EMT to MET.PCAT7 participates in tumor progression in NSCLC by inhibiting miR-134-5p.higher PCAT7 expression implied a worse survival rate in NPC patients. 29275424 2017 Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC). paclitaxel MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 colorectal cancer C19.9 NA RT-qPCR, Western blot, in vitro knockdown CRC cell lines (HT29, SW480) up-regulated lncRNA MALAT1 was significantly upregulated in the oxymatrine resistant cells (P<0.01), while knockdown of MALAT1 partially reversed the EMT phenotype in HT29 resistant cells.Furthermore, oxymatrine treatment suppressed the migration and invasion ability of CRC cells, however, this effect was significantly reversed by overexpression of MALAT1. Finally, we investigated the clinical role of MALAT1 and found that high lncRNA MALAT1 expression level is associated with poor prognosis in CRC patients receiving oxymatrine treatment(P<0.01). 29328404 2018 Chronic oxymatrine treatment induces resistance and epithelial mesenchymal transition through targeting the long non-coding RNA MALAT1 in colorectal cancer oxymatrine CASC11 CASC11, CARLo-7, LINC00990, TCONS_00014535 100270680 ENSG00000249375 NR_117101 GRCh38_8:127730194-127733967 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated The results showed that the expression levels of lncRNA ENST00000438347, ENST00000518376, ENST00000502804, and NR_073454 were significantly higher in HCC specimens than those in corresponding adjacent non-tumorous tissues. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. oxaliplatin ENST00000460497 RPL9P20, RPL9_7_879 NA NA NA GRCh38_8:17150203-17150909 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. oxaliplatin ENST00000502804 CXCL1P1, CXCL1P, GRO1P, GROP, MGSAP, SCYB1P NA ENSG00000250339 NA GRCh38_4:73944011-73944324 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated The results showed that the expression levels of lncRNA ENST00000438347, ENST00000518376, ENST00000502804, and NR_073455 were significantly higher in HCC specimens than those in corresponding adjacent non-tumorous tissues. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. oxaliplatin LOC389641 RP11-1149O23.3, LOC389641 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. oxaliplatin NEST00000480069 NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. oxaliplatin NR_073453 LINC00601 101101772 ENSG00000235180 NR_073453 GRCh38_10:126413869-126421879 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. oxaliplatin NR_073453 LINC00601 101101772 ENSG00000235180 NR_073453 GRCh38_10:126413869-126421879 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated The results showed that the expression levels of lncRNA ENST00000438347, ENST00000518376, ENST00000502804, and NR_073456 were significantly higher in HCC specimens than those in corresponding adjacent non-tumorous tissues. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. oxaliplatin PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 gastric cancer C16 NA Microarray, qRT-PCR, RIP GC tissues, normal gastric tissues, Gastric cancer cell lines (SNU-484, SNU-520, SNU-620, SNU-638, SNU-668, AGS, NCI-N87, SNU-1, SNU-5, KATO) up-regulated Upregulated PANDAR in GC patients was positively correlated with increased tumour size, advanced TNM classification and a poor survival rate in GC patients. As a target, the CDKN1A gene was successfully downregulated by PANDAR. PANDAR controlled the transcription of the CDKN1A gene by competitively binding with p53 protein. In combination with a p53 activator (nutlin3), the knockout of PANDAR by CRISPR/Cas9 technology synergistically inhibited GC tumour growth in vivo.upregulated HOTAIR inhibits the expression of p53 by enhancing the p53 promoter histone H3 lysine 27 trimethylation (H3K27me3), and the overexpression of PANDAR increases the stability of the p53 protein in response to DNA damage. 29416011 2018 Long noncoding RNA PANDAR blocks CDKN1A gene transcription by competitive interaction with p53 protein in gastric cancer. oxaliplatin X15675 ERV9-1, pTR2 NA NA NA NA breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. oestrogen LINC00460 NR_034119 728192 ENSG00000233532 NR_034119 GRCh38_13:106374477-106384315 esophageal squamous cell cancer NA NA qPCR etc. ESCC tissues, cell lines (EC109, KYSE150, KYSE450) up-regulated linc00460 was overexpressed in the majority of tumor tissues and ESCC cell lines. Linc00460 expression was positively correlated with ESCC TNM stage, lymph node metastasis and predicted poor prognosis. In vitro experiments showed that linc00460 depletion suppressed ESCC cell growth through regulating cell proliferation and cell cycle; in additional, linc00460 depletion accelerated ESCC cell apoptosis. We further revealed that linc00460 overexpression was manipulated by transcriptional co-activator CBP/P300 through histone acetylation. Given the high expression and important biological functions of linc00460, we suggest that linc00460 work as an oncogene and might be a valuable prognostic biomarker for ESCC diagnosis and treatment. 28939763 2017 A novel long noncoding RNA linc00460 upregulated by CBP/P300 promotes carcinogenesis in Esophageal Squamous Cell Carcinoma MTX H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA qPCR, Cell transfection, Western blot etc. cell lines (HT-29 and HT-29 resistant cell) up-regulated LncRNA H19 was found to be significantly upregulated in this resistant cell line. Further investigation showed that H19 knockdown sensitized the MTX resistance in HT-29-R cells while its overexpression improved the MTX resistance in the parental cells, suggesting that H19 mediate MTX resistance. The Wnt/B-catenin signaling was activated in HT-29-R cells, and H19 knockdown suppressed this signaling in the parental cells. 27919747 2017 H19 mediates methotrexate resistance in colorectal cancer through activating Wnt/B-catenin pathway. methotrexate MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 cervical cancer C53 NA qPCR, Western blot etc. cell lines (SiHa and HeLa) down-regulated Real-time PCR and Western blotting were used to measure the gene and protein expression, respectively, of microRNA (miRNA) miR-142-3p, long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript-1 (MALAT1), and high-mobility group AT-hook 2 (HMGA2). We found that metformin could suppress cervical cancer migration and invasion. During the process of tumor metastasis, miR-142-3p was significantly upregulated, whereas lncRNA MATAL1 and HMGA2 were suppressed by metformin. The binding site that allow the direct interaction between miR-142-3p and MALAT1 were located in the 3' untranslated region (3' UTR) of lncRNA MATAL1 and HMGA2 at base pairs (bp) 4452-5255, while that between miR-142-3p and HMGA2 was located at bp 1562-2521 of HMGA2. 29704494 2018 Metformin, a first-line drug for type 2 diabetes mellitus, disrupts the MALAT1/miR-142-3p sponge to decrease invasion and migration in cervical cancer cells. metformin DSCAM-AS1 DSCAM-AS1, M41 100506492 ENSG00000235123 NR_038896 GRCh38_21:40383083-40385358 breast cancer C50 NA RNA-seq, qRT-PCR, Western blot, in vitro knockdown, RNAi cell lines (MCF-7, ZR-75.1, T-47D) up-regulated By the analysis of H3K27ac enrichment in hormone-deprived MCF-7 cells, we defined a set of Super Enhancers (SEs) occupied by apoERa, including one mapped in proximity of the DSCAM-AS1 lncRNA gene.This represents a paradigm of apoERa activity since its expression is largely unaffected by estrogenic treatment,despite the fact that E2 increases ERa binding on DSCAM-AS1 promoter. We validated the enrichment of apoERa, p300, GATA3, FoxM1 and CTCF at both DSCAM-AS1 TSS and at its associated SE by ChIP-qPCR. Furthermore, by analyzing MCF-7 ChIA-PET data and by 3C assays, we confirmed long range chromatin interaction between the SE and the DSCAM-AS1 TSS. Interestingly, CTCF and p300 binding showed an enrichment in hormone-depleted medium and in the presence of ERa, elucidating the dynamics of the estrogen-independent regulation of DSCAM-AS1 expression.The most significant down-regulated lncRNAs were RP11-68L18.1, MIR9-3HG, and LINC01016, whereas NKILA, AC144831.1, and LINC00657 were the most significant up-regulated lncRNAs 29462945 2018 Luminal lncRNAs Regulation by ERa-Controlled Enhancers in a Ligand-Independent Manner in Breast Cancer Cells. MCF-7 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioma NA M9380/3 qRT-PCR, Western blot, in vitro knockdown glioma cell lines U-251 and M059J up-regulated that the expression of H19 was significantly increased in U-251TMZ and M059JTMZ cells. Knockdown of H19 expression using specific shRNA in U-251TMZ and M059JTMZ led to decreased half maximal inhibitory concentration (IC50) values for TMZ and increased cell apoptosis rates, indicating that the silencing of H19 decreased chemoresistance of glioma cells to TMZ.the reduced expression of H19 down-regulated the expression of B-Catenin and its downstream targets c-myc and Survivin in TMZ-treated glioma cells. Activation of Wnt/B-Catenin pathway by Licl treatment promoted EMT and enhanced chemoresistance to TMZ compared with TMZ+H19 shRNA group. 29391808 2018 The silencing of LncRNA-H19 decreases chemoresistance of human glioma cells to temozolomide by suppressing epithelial-mesenchymal transition via the Wnt/B-Catenin pathway. Licl SNHG5 SNHG5, C6orf160, LINC00044, NCRNA00044, U50HG, bA33E24.2 387066 ENSG00000203875 NR_003038 GRCh38_6:85660950-85678736 chronic myeloid leukemia NA M9863/3 qPCR, Western blot etc. cell line (K562) up-regulated SNHG5 and ABCC2 expressions were up-regulated in the isolated peripheral blood cells of the CML patients when compared with healthy controls, and SNHG5 expression levels was positively correlated with ABCC2 in CML patients.In vitro studies showed that the expressions of SNHG5 and ABCC2 were up-regulated in imatinib resistant cells (K562-R) when compared to K562 cells. Overexpression of SNHG5 suppressed the expression of miR-205-5p and the expression of SNHG5 was negatively correlated with the miR-205-5p expression in CML patients. In addition, ABCC2 was predicted as a downstream target of miR-205-5p, and overexpression of miR-205-5p suppressed the expression of ABCC2 in K562-R cells.overexpression of SNHG5 in K562 cells increased imatinib resistance and knock-down of SNHG5 reduced the imatinib resistance in K562-R cells. Further experiments showed that SNHG5 promotes imatinib resistance through regulating ABCC2. Taken together, SNHG5 promotes imatinib resistance in CML via acting as a competing endogenous RNA against miR-205-5p. 28861326 2017 LncRNA SNHG5 regulates imatinib resistance in chronic myeloid leukemia via acting as a CeRNA against MiR-205-5p. imatinib CCDC26 CCDC26, RAM 137196 ENSG00000229140 NR_130917 GRCh38_8:128634199-129683679 gastrointestinal stromal tumor C16 M8936/0 qRT-PCR, Western blot, in vitro knockdown GIST cell lines (GIST-882 and GIST-T1) differential expression We found that human GIST-882 cells with lower CCDC26 expression were less sensitive to imatinib compared with GIST-T1 cells with higher CCDC26 expression. CCDC26 expression decreased in a time-dependent manner in the presence of imatinib. Moreover, small interfering RNA (siRNA) knockdown of CCDC26 increased GIST cell sensitivity to imatinib. The RNA pull-down experiment showed that CCDC26 can interact with c-KIT and that CCDC26 knockdown can upregulate c-KIT expression. We also found that inhibiting c-KIT induced resistance to imatinib. 29423012 2018 CCDC26 knockdown enhances resistance of gastrointestinal stromal tumor cells to imatinib by interacting with c-KIT. imatinib SUMO1P3 NA NA ENSG00000235082 NA GRCh38_1:160317403-160317706 breast cancer C50 NA qPCR, Luciferase reporter assay breast cancer tissues, cell lines (MCF-10A, MCF7, MDA-MB-231, MDA-MB-468, and SKBR-3) up-regulated high levels of SUMO1P3 expression associated significantly with tumor progression and poor survival of breast cancer patients.knockdown of SUMO1P3 suppressed proliferation, migration, and invasion of breast cancer cells. SUMO1P3 binds to miR-320a,which has been identified as a tumor suppressor in various cancers, including breast cancer. the tumor-promoting effects of SUMO1P3 in breast cancer are partly mediated by negative regulation of miR-320a. 29312511 2017 The long non-coding RNA SUMO1P3 facilitates breast cancer progression by negatively regulating miR-320a. imatinib lncTCF7 WSPAR, LncTCF7, TCONS_00009511, NR_033449 6932 ENSG00000081059 NA GRCh38_5:134114711-134151865 glioma NA M9380/3 qPCR, in vitro knockdown glioma tissues up-regulated lncTCF7 was significantly associated with WHO grade and tumour size.patients with high lncTCF7 expression levels exhibited markedly worse overall survival prognoses. knockdown of lncTCF7 significantly inhibited glioma cell migration, proliferation and tumorigenicity in vitro and in vivo. hypoxia induced lncTCF7 expression in an autocrine manner through IL-6 in glioma. 29234033 2017 lncTCF7 is a negative prognostic factor, and knockdown of lncTCF7 inhibits migration, proliferation and tumorigenicity in glioma. IL-6 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 prostate cancer C61.9 NA RNA-seq, qPCR, ChIP etc. prostate cancer tissues, cell lines (LnCaP, PC3) up-regulated Among putatively ERa-regulated intergenic long non-coding RNAs (lncRNAs), we identified nuclear enriched abundant transcript 1 (NEAT1) as the most significantly overexpressed lncRNA in prostate cancer. Prostate cancer cells expressing high levels of NEAT1 were recalcitrant to androgen or AR antagonists. NEAT1 drives oncogenic growth by altering the epigenetic landscape of target gene promoters to favour transcription. 25415230 2014 The oestrogen receptor alpha-regulated lncRNA NEAT1 is a critical modulator of prostate cancer. ICI and 4OHT ROR1-AS1 NA 101927034 ENSG00000223949 NR_110665 GRCh38_1:64094442-64171297 mantle cell lymphoma NA M9673/3 qPCR, RNAi cell lines (Mino, Granta, JVM2 and Z138) up-regulated Results showed that overexpression of ROR1-AS1 lncRNA promoted growth of MCL cells while decreased sensitivity to the treatment with drugs ibrutinib and dexamethasone. ROR-AS1 overexpression also decreased the mRNA expression of P16 (P = 0.21), and SOX11 (p = 0.017), without much effect on P53, ATM and P14 mRNA. 29113297 2017 Long non-coding RNA profile in mantle cell lymphoma identifies a functional lncRNA ROR1-AS1 associated with EZH2/PRC2 complex ibrutinib H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA Microarray, qPCR, Western blot cell lines (MDA-MB-231, MDA-MB-468 and MCF7) differential expression Microarray data derived from Huaier-treated breast cancer cells identified H19 as a potential target. Huaier extract reduced the expression of H19. Collectively, the data demonstrate that Huaier extract reduces viability and induces apoptosis in breast cancer cells via H19-miR-675-5p-CBL axis regulation. 29145193 2017 Huaier Extract Inhibits Breast Cancer Progression Through a LncRNA-H19/MiR-675-5p Pathway Huaier PCGEM1 PCGEM1, LINC00071, NCRNA00071, PCAT9 64002 ENSG00000227418 NR_002769 GRCh38_2:192749845-192776899 prostate cancer C61.9 NA qPCR, Flow cytometry assay etc. cell lines (LNCaP, DU145 and PC3) down-regulated In our settings, LNCaP and DU145 treated cells had reduced PCGEM1 gene expression. We found that γ-oryzanol decreases cell viability and culture biomass by apoptosis and/or necrosis death in androgen unresponsive (PC3 and DU145) and responsive (LNCaP) cell lines, and signals through pERK1/2 in LNCaP and DU145 cells. γ-oryzanol also appears to block cell cycle progression at the G2/M in PC3 and LNCaP cells and at G0/G1 in DU145 cells. These effects were accompanied by a down regulation in the expression of the cav-1 in both androgen unresponsive cell lines and PCGEM1 gene in DU145 and LNCaP cells. 25619388 2015 γ-Oryzanol reduces caveolin-1 and PCGEM1 expression, markers of aggressiveness in prostate cancer cell lines. g-oryzanol HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 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. Genistein AB209630 NA NA NA NA GRCh38_9:69248696-69251364 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, Western blot pancreatic ductal adenocarcinoma tissues, cell lines (Panc-1 and BXPC-3) down-regulated increased expression of lncRNA AB209630 could suppress cell proliferation and cell colony formation ability in gemcitabine resistance cells of PDAC. upregulation of lncRNA AB209630 suppressed the PI3K/AKT signaling pathway in gemcitabine resistance cells.lncRNA AB209630 expression was dramatically downregulated in PDAC tissues compared to adjacent normal tissues. Lower PDAC expression predicted a poor prognosis in PDAC patients. lncRNA AB209630 expression associated 184 with poor overall survival time. 29526843 2018 LncRNA AB209630 inhibits gemcitabine resistance cell proliferation by regulating PI3K/AKT signaling in pancreatic ductal adenocarcinoma. gemcitabine ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 bladder urothelial cancer NA M8120/3 qPCR, Western blot, etc. BUC tissues, cell lines (SV-HUC-1, J82, T24) up-regulated LncRNA CDKN2B-AS is high-expressed in BUC and related to low Gemcitabine sensitivity of BUC. CDKN2B-AS inhibited Gemcitabine sensitivity through Wnt signaling pathway in BUC. 29937935 2018 Long non-coding RNA CDKN2B antisense RNA 1 gene inhibits Gemcitabine sensitivity in bladder urothelial carcinoma. Gemcitabine FOXD2-AS1 NA 84793 ENSG00000237424 NR_026878 GRCh38_1:47432133-47434641 bladder cancer C67 NA qPCR, Western blot, Luciferase reporter assay etc. cell line (T24) up-regulated LncRNA FOXD2-AS1 was high-expressed in gemcitabine-resistant bladder cancer cells. In vitro experiments, FOXD2-AS1 knockdown suppressed the 50% inhibitive concentration (IC50) of gemcitabine, drug-resistance related genes (MDR1, MRP2, LRP1) expression,invasion and ABCC3 protein expression in gemcitabine-resistant bladder cancer cells (T24/GEM, 5637/GEM). In vivo of xenograft assay, FOXD2-AS1 knockdown inhibited the tumor growth of bladder cancer cells.Bioinformatics program and validation experiments confirmed that FOXD2-AS1 positively regulated ABCC3 protein through targeting miR-143,acting as a competing endogenous RNA (ceRNA).In summary,the vital roles of FOXD2-AS1/miR-143/ABCC3 axis in gemcitabine resistance of bladder cancer cells, providing a novel therapeutic strategy for bladder cancer. We found that lncRNA FOXD2-AS1 sponged miR-143 to indirectly target ABCC3 protein ex- pression, consisting the FOXD2-AS1/miR-143/ABCC3 axis. 29674277 2018 Long noncoding RNA FOXD2-AS1 accelerates the gemcitabine-resistance of bladder cancer by sponging miR-143. gemcitabine HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 pancreatic cancer C25 NA qPCR etc. Panc-1 cell lines up-regulated HOTAIR knockdown in PANC-1 CSCs treated with or without gemcitabine decreased the cell proliferation, altered the cell cycle progression and induced apoptosis, demonstrating its critical roles in regulating the malignant character of PANC-1 CSCs. In conclusion, the present study demonstrated that HOTAIR may be induced by gemcitabine and acts as a tumor promoter by inhibiting the chemosensitivity, and promoting the self-renewal capacity, proliferation and migration of PANC-1 CSCs, which supports its potential application as a novel therapeutic approach for pancreatic cancer. 29201179 2017 Gemcitabine treatment causes resistance and malignancy of pancreatic cancer stem-like cells via induction of lncRNA HOTAIR gemcitabine PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 pancreatic cancer C25 NA qPCR, Western blot etc. cell line (BxPC3, MiaPaCa2, Panc1, PDAC, BxPC3) up-regulated Here, we report the re-sensitization of chemoresistant PDAC cells by curcumin through the inhibition of the PRC2-PVT1-c-Myc axis. Using gemcitabine-resistant PDAC cell lines, we found that curcumin sensitized chemoresistant cancer cells by inhibiting the expression of the PRC2 subunit EZH2 and its related lncRNA PVT1. Curcumin was also found to prevent the formation of spheroids, a hallmark of CSCs, and to down-regulate several self-renewal driving genes. In addition, we confrmed our in vitro fndings in a xenograft mouse model where curcumin inhibited gemcitabine-resistant tumor growth. Overall, this study indicates clinical relevance for combining curcumin with chemotherapy to overcome chemoresistance in PDAC. 29048549 2017 Curcumin sensitizes pancreatic cancer cells to gemcitabine by attenuating PRC2 subunit EZH2, and the lncRNA PVT1 expression gemcitabine PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 pancreatic cancer C25 NA qPCR etc. cell line (ASPC-1) up-regulated We demonstrated that overexpression of a full length PVT1 cDNA in the antisense orientation reconstituted enhanced sensitivity to Gemcitabine in naive ASPC-1 cells, whereas overexpression of a full length PVT1 cDNA in the sense orientation resulted in decreased sensitivity to Gemcitabine. Our results identified PVT1 as a regulator of Gemcitabine sensitivity in pancreatic cancer cells and validated the genome-wide genetic screening approach for the identification of genetic determinants as well as potential biomarkers for the rational design of Gemcitabine chemotherapies for pancreatic cancer. 21316338 2011 Genome-wide screen identifies PVT1 as a regulator of Gemcitabine sensitivity in human pancreatic cancer cells. Gemcitabine HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, in vitro knockdown, RNAi cell lines (PC9, RPC9) up-regulated HOTAIR silencing resulted in the upregulation of B cell lymphoma 2-associated X protein (Bax), Caspase-3 and transforming growth factor a (TGF-a) and downregulation of EGFR and B cell lymphoma 2 (Bcl-2) levels. HOTAIR normally prevents the activation of Bax/Caspase-3 while inducing TGF-a/EGFR signaling. 29467862 2017 Lentivirus-mediated silencing of HOTAIR lncRNA restores gefitinib sensitivity by activating Bax/Caspase-3 and suppressing TGF-a/EGFR signaling in lung adenocarcinoma. gefitinib EGFR-AS1 NA 100507500 ENSG00000224057 NR_047551 GRCh38_7:55179750-55188934 squamous cell carcinoma NA M8070/3 qPCR etc. cell lines (NCC-NH1, NCC-NH43, NCC-NH73, NCC-NH26, NCC-NH64, NCC-NH119) up-regulated Remarkably, single-copy G>A nucleotide editing in isogenic models conferred a 70-fold increase in sensitivity due to decreased stability of the EGFR-AS1 long noncoding RNA (lncRNA). In the appropriate context, sensitivity could be recapitulated through EGFR-AS1 knockdown in vitro and in vivo, whereas overexpression was sufficient to induce resistance to TKIs. Reduced EGFR-AS1 levels shifted splicing toward EGFR isoform D, leading to ligand-mediated pathway activation. In co-clinical trials involving patients and patient-derived xenograft (PDX) models, tumor shrinkage was most pronounced in the context of the A/A genotype for EGFR-Q787Q, low expression of EGFR-AS1 and high expression of EGFR isoform D. Our study reveals how a ‘silent’ mutation influences the levels of a lncRNA, resulting in noncanonical EGFR addiction, and delineates a new predictive biomarker suite for response to EGFR TKIs. 28920960 2017 Long noncoding RNA EGFR-AS1 mediates epidermal growth factor receptor addiction and modulates treatment response in squamous cell carcinoma gefitinib GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 lung adenocarcinoma C34 M8140/3 qPCR, Western blot etc. lung cancer tissues, cell lines (A549, H1299, H1975, HCC827) down-regulated Our results showed that GAS5 was significantly downregulated in lung adenocarcinoma tissues compared with the paired adjacent non-tumorous tissue samples. Furthermore, lower GAS5 expression levels were associated with larger tumor sizes, poor tumor differentiation, and advanced pathological stages. GAS5 overexpression was inversely correlated with the expression of the EGFR pathway and IGF-1R proteins. 25925741 2015 The long non-coding RNA, GAS5, enhances gefitinib-induced cell death in innate EGFR tyrosine kinase inhibitor-resistant lung adenocarcinoma cells with wide-type EGFR via downregulation of the IGF-1R expression. gefitinib LOC554202 MIR31HG, hsa-lnc-31, LncHIFCAR 554202 ENSG00000171889 NR_027054 GRCh38_9:21455642-21559669 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. cell line (PC9) up-regulated Expression of various lncRNAs differed significantly between the two cell lines, and MIR31HG expression in particular was significantly higher in PC9-R cells. Furthermore, overexpression of MIR31HG lncRNAs may contribute to gefitinib resistance in PC9-R cells through the EGFR/PI3K/AKT pathway, 28529576 2017 Increased MIR31HG lncRNA expression increases gefitinib resistance in non-small cell lung cancer cell lines through the EGFR/PI3K/AKT signaling pathway gefitinib MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 non small cell lung cancer C34 M8046/3 qPCR, Luciferase reporter assay, Western blot, RIP cell lines (A549, H23, H522, H1299, H460, 16HBE and HEK-293T) up-regulated MALAT1 was significantly upregulated in five human NSCLC cells.On the contrary,miR-124 was remarkably downregulated, which indicated a potential negative correlation between miR-124 and MALAT1.MALAT1can act as a competing endogenous lncRNA (ceRNA) to modulate miR-124/STAT3 in NSCLC. MALAT1/miR-124/STAT3 was involved in NSCLC development.MALAT1 can have interactions with estrogen receptor and indicate poor survival of breast cancer. 29215698 2017 The lncRNA MALAT1 contributes to non-small cell lung cancer development via modulating miR-124/STAT3 axis. gefitinib MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT 440823 ENSG00000225783 NR_003491 GRCh38_22:26646428-26676475 lung cancer C34 NA RNA-seq, qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP lung cancer tissues, human lung cancer cell lines (PC9, HCC827, A549, H1870, H1048, and H1299U87) up-regulated LncRNA MIAT expression was associated with tumor size, lymph node metastasis,distant metastasis and TNM stage.Univariate analysis and multivariate analysis revealed that the lncRNA MIAT to be an independent factor for predicating the prognosis of lung cancer patients.Low lncRNA MIAT have longer overall survival time and progression-free survival time than patients with high lncRNA MIAT expression. Moreover, the knockdown of MIAT significantly sensitized PC9 and gefitinib-resistant PC9 cells to gefitinib in vitro and in vivo, and increased the expression of miR-34a and inactivated PI3K/Akt signaling. MIAT interacted with miR-34a and epigenetically controlled the miR-34a expression by hyper-methylating its promotor. MiR-34a promoter methylation status was measured by MSP in tissues and BSP in cells. 29487526 2018 Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a. Gefitinib RHPN1-AS1 RHPN1-AS1, C8orf51 78998 ENSG00000254389 NR_026785 GRCh38_8:143366631-143368548 non small cell lung cancer C69.9 M8720/3 PCR, RNA pull-down assay, Luciferase reporter assay, Western blot analysis NSCLC samples and adjacent non-tumor tissues, The NSCLC cell lines (A549, H1975, H1299, HCC827, PC9) and human bronchial epithelial cells (16HBE) down-regulated RHPN1-AS1 was observed to be downregulated in gefitinib resistant patients and NSCLC cell lines.RHPN1-AS1 was found to positively regulate the expression of TNFSF12 by directly interacting with miR-299-3p.Collectively, RHPN1-AS1 modulates gefitinib resistance through miR-299-3p/TNFSF12 pathway in NSCLC. 30010468 2018 The lncRNA RHPN1-AS1 downregulation promotes gefitinib resistance by targeting miR-299-3p/TNFSF12 pathway in NSCLC. gefitinib ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 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. G418 ERIC ERICD, ERIC, LINC01130, TCONS_00014875 104355217 ENSG00000280303 NA GRCh38_8:140636281-140638283 osteosarcoma NA M9180/3 RNA-seq, qPCR, RNAi, Western blot, ChIP etc. cell lines (U2OS and SAOS-2) up-regulated We show that expression levels of ERIC were elevated upon activation of exogenous E2F1, E2F3 or endogenous E2Fs. Moreover, knockdown of either E2F1 or E2F3 reduced ERIC levels and endogenous E2F1 binds ERIC's promoter. Expression of ERIC was cell cycle regulated and peaked in G1 in an E2F1-dependent manner. Inhibition of ERIC expression increased E2F1-mediated apoptosis, suggesting that E2F1 and ERIC constitute a negative feedback loop that modulates E2F1 activity. Furthermore, ERIC levels were increased following DNA damage by the chemotherapeutic drug Etoposide, and inhibition of ERIC expression enhanced Etoposide -induced apoptosis. 24168400 2013 The long non-coding RNA ERIC is regulated by E2F and modulates the cellular response to DNA damage. Etoposide HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, RNAi, ChIP, Dual-luciferase reporter assay etc. cell line (MCF7) up-regulated Microscopic analysis showed that HOTAIR knockdown has suppressed the growth of MCF7 cells in comparison to the control or scramble-antisense treated cells even at 24 h of post HOTAIR siSENSE transfection. Growth analysis showed that HOTAIR knockdown has suppressed the growth of MCF7 cells significantly in comparison to the control (untreated) or scramble-antisense treated cells. 23375982 2013 Antisense transcript long noncoding RNA (lncRNA) HOTAIR is transcriptionally induced by estradiol. estradiol RP11-838N2.4 NA NA NA NA GRCh38_18:3466250-3478978 non small cell lung cancer C34 M8046/3 Microarray, qPCR, Western blot etc. non small cell lung cancer tissues, serum, cell lines (HCC827 and HCC4006) up-regulated In addition, the serum expression levels of exosomal lncRNA RP11-838N2.4 were upregulated in patients exhibiting resistance to erlotinib treatment. On the whole, exosomal lncRNA RP11-838N2.4 may serve as a therapeutic target for patients with NSCLC. 29845246 2018 Exosome-mediated transfer of lncRNA RP11-838N2.4 promotes erlotinib resistance in non-small cell lung cancer erlotinib HOXA10 NA NA ENSG00000253293 NA GRCh38_7:27170591-27180261 lung adenocarcinoma C34 M8140/3 DNA methylation etc. cell line differential expression competing endogenous RNA network analysis inferred that lncRNA ENSG00000240990 competed with HOXA10 to absorb hsa-let-7a/b/f/g-6p and affected patient prognosis in LUAD. Last but not least, by integrating target information of miRNA we also provided a newperspective for the discovery of potential small molecule drugs. In summary, we systematically analyzed the regulatory role of SCNA lncRNAs. This work may facilitate cancer research and serve as the basis for future efforts to understand the role of SCNA lncRNAs, develop novel biomarkers and improve knowledge of tumor biology. We used strict approach to construct ceRNA network. The approach not only considered the lncRNAs/PCGs that acted as miRNA sponges, but also selected negative miRNA-target interactions. 29069717 2017 Integrated analysis of dosage effect lncRNAs in lung adenocarcinoma based on comprehensive network. Enoxacin and Etoposide, CDF (analogues of curcumin) HOXA11-AS HOXA11-AS, HOXA-AS5, HOXA11-AS1, HOXA11AS, HOXA11S, NCRNA00076 221883 ENSG00000240990 NR_002795 GRCh38_7:27184518-27189293 lung adenocarcinoma C34 M8140/3 DNA methylation etc. cell lines differential expression competing endogenous RNA network analysis inferred that lncRNA ENSG00000240990 competed with HOXA10 to absorb hsa-let-7a/b/f/g-5p and affected patient prognosis in LUAD. Last but not least, by integrating target information of miRNA we also provided a new perspective for the discovery of potential small molecule drugs. Some small molecule drugs, such as Enoxacin and Etoposide, regulated the competitive relations of lncRNA-PCG pairs by influencing the expression of hsa-let-7a/b/f/g-5p, which provided novel clues for LUAD treatment. Therefore, we combined the information that was provided by SM2miR [67] with the module to infer potential small molecule drugs for LUAD treatment. In the ceRNA module, some potential drugs could up-regulate the hsa-let-7a/b/f/g-5p expression and further down-regulate the expression of related lncRNAs/PCGs and contribute to the treatment of LUAD ((Figure10)). 29069717 2017 Integrated analysis of dosage effect lncRNAs in lung adenocarcinoma based on comprehensive network. Enoxacin and Etoposide, CDF (analogues of curcumin) NR_026685 PDIK1L, CLIK1L, STK35L2 NA NA NA NA non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) up-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. EGFR-TKIs- ENST00000507437 RNPS1P1 NA ENSG00000250896 NA GRCh38_4:11371975-11372892 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) up-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. EGFR-TKIs ENST00000508827 RP11-47I22.2, LOC101927780 NA NA NA GRCh38_14:61556320-61570653 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) up-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. EGFR-TKIs H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) up-regulated Overexpression of H19 and BC200 were observed in gefitinib-resistant lung cancer cell lines (PC9/R, A549, H1299 and H1975). However, in the gefitinib-sensitive cell line (PC9), MALAT1 and HOTAIR were downregulated. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. EGFR-TKIs HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) down-regulated Overexpression of H19 and BC200 were observed in gefitinib-resistant lung cancer cell lines (PC9/R, A549, H1299 and H1975). However, in the gefitinib-sensitive cell line (PC9), MALAT1 and HOTAIR were downregulated. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. EGFR-TKIs ENST00000464359 LINC00635 151658 ENSG00000241469 NR_015414 GRCh38_3:107841303-107878068 lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. cell lines (HCC827 and HCC827-8-1) up-regulated To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance. 27108960 2016 Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray. EGFR-TKI nc886 VTRNA2-1, CBL-3, CBL3, MIR886, MIRN886, VTRNA2, hsa-mir-886, hvg-5, nc886, svtRNA2-1a 100126299 ENSG00000270123 NR_030583 GRCh38_5:136080470-136080597 lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. cell lines (HCC827 and HCC827-8-1) down-regulated To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance. 27108960 2016 Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray. EGFR-TKI NONHSAG031748 NA NA NA NA NA lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. cell lines (HCC827 and HCC827-8-1) up-regulated To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance. 27108960 2016 Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray. EGFR TKIs NONHSAT082241 NA NA NA NA NA lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. cell lines (HCC827 and HCC827-8-1) down-regulated To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance. 27108960 2016 Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray. EGFR TKIs NONHSAT107900 NA NA NA NA NA lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. cell lines (HCC827 and HCC827-8-1) up-regulated To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance. 27108960 2016 Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray. EGFR TKIs HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioblastoma NA M9440/3 CHIP-PCR etc. GBM cell lines (U87, U87vIII), breast cancer cell line (MCF-7) up-regulated The level of HOTAIR expression in GBM was higher than in other low grade gliomas and normal brain tissues. NLK (Nemo-like kinase), a negative regulator of the B-catenin pathway, was negatively correlated with HOTAIR expression. When the B-catenin pathway was inhibited, GBM cells became susceptible to cell cycle arrest and inhibition of invasion. Introduction of the HOTAIR 5' domain in human glioma-derived astrocytoma induced B-catenin. An intracranial animal model was used to confirm that HOTAIR depletion inhibited GBM cell migration/invasion. In the orthotopic model, HOTAIR was required for GBM formation in vivo. 25823657 2015 HOTAIR is a therapeutic target in glioblastoma. DZNEP linc-POU3F3 POU3F3, BRN1, OTF8, brain-1, oct-8 NA ENSG00000198914 NA GRCh38_2:104855511-104858574 colon cancer C18 NA qPCR cell lines (HCT-116, HT-29) differential expression RNA secretion into the bloodstream; we have shown for the first time that the treatment of HCT-116 and HT-29 colon cancer cells with two anti-cancer agents (doxycycline or 3, 3'-diindolylmethane) results in profound changes in the intracellular content of several lnc RNAs 29116072 2017 Treatment with anti-cancer agents results in profound changes in lncRNA expression in colon cancer cells doxycycline and diindolylmethane H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA Microarray, qPCR, Western blot, RNAi etc. cell line (MCF-7, MCF-7/Dox400, MCF-7/Dox800, MCF-7/Dox1600) up-regulated we demonstrated that MDR1 and MRP4 were major effectors of H19-regulated Dox resistance in breast cancer cells as MDR1 and MRP4 expression was markedly elevated in Dox-resistant cells while dramatically reduced when H19 was knocked down. Moreover, we found that CUL4A, an ubiquitin ligase component, was a critical factor bridging H19 lncRNA to MDR1 expression, and a high tumor CUL4A expression was associated with low survival in breast cancer patients treated with chemotherapy. A similar trend was observed in ER-positive breast cancer patients treated with chemotherapy although it was not statistically significant in overall survival due to a small sample size 29190892 2017 LncRNA H19 is a major mediator of doxorubicin chemoresistance in breast cancer cells through a cullin4A-MDR1 pathway. Doxorubicin (Dox) and cisplatin (CDDP) PCGEM1 PCGEM1, LINC00071, NCRNA00071, PCAT9 64002 ENSG00000227418 NR_002769 GRCh38_2:192749845-192776899 prostate cancer C61.9 NA Northern blot etc. cell line (LNCaP) up-regulated This data suggests that overexpression of PCGEM1 attenuated the induction of apoptosis in LNCaP cells. This study provides new insights into cell biologic functions and novel features of an ncRNA. Further, these data unravel biological mechanisms of cell growth/cell survival-associated functions of this ncRNA in a widely used prostate cancer cell culture model. 16569192 2006 Regulation of apoptosis by a prostate-specific and prostate cancer-associated noncoding gene, PCGEM1. doxorubicin (DOX) CTA NA 105375847 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 doxorubicin DLEU2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 10301 ENSG00000176124 NR_002605 GRCh38_13:50082171-50723236 gastric cancer C16 NA qPCR, Western blot, RIP gastric cancer tissues, cell lines (AGS, SGC7901, MGC803, BGC823,GES-1) up-regulated DLEU1 was observably intensified in GC tissues and cell lines. And highly expressed DLEU1 was relevant to tumor size, advanced stage of pathology and lymph node metastasis in GC patients. Silenced DLEU1 obviously suppressed proliferation via leading to the cell cycle arrest and inducing cell apoptosis of GC.DLEU1 could recruit LSD1(lysine specific demethylase 1) to the promoter regions of KLF2 and then suppressed its transcription. the oncogenic function mediated by DLEU1 in GC was partly by regulating KLF2.highly expressed DLEU1 means a poorer survival ability for GC patients. 29282356 2017 Long non-coding RNA DLEU1 predicts poor prognosis of gastric cancer and contributes to cell proliferation by epigenetically suppressing KLF2. doxorubicin ENST00000457390 RP11-14N7.2, LOC100996732 NA NA NA GRCh38_1:144245027-144245821 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin ENST00000476909 LINC00856 NA NA NA GRCh38_10:78267410-78280213 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin ENST00000553559 SNHG10, C14orf62, LINC00063, NCRNA00063 283596 ENSG00000247092 NR_001459 GRCh38_14:95532914-95534872 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) up-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin ENST00000565617 KB-1460A1.5 NA NA NA GRCh38_8:101166805-101169629 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin ENST00000568031 RP11-863P13.3 NA NA NA GRCh38_16:88177298-88178610 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) up-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin ENST00000576810 RP11-462G12.1, LOC102724927 NA NA NA GRCh38_16:3947609-3950444 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 400550 ENSG00000268388 NR_033925 GRCh38_16:86474529-86509099 osteosarcoma NA M9180/3 qPCR, Western blot etc. osteosarcoma tissues, cell lines (MG63, SaoS2 and HOS) down-regulated FENDRR expression was down-regulated in the doxorubicin-resistant OS cell lines and tissues and negatively correlated to the poor prognosis of OS patients. Together, our study demonstrated that lncRNA FENDRR may act as an inhibitory molecule of doxorubicin-resistance through down-regulating the expression of ABCB1 and ABCC1 genes in osteosarcoma cells. 29069754 2017 LncRNA FENDRR sensitizes doxorubicin-resistance of osteosarcoma cells through down-regulating ABCB1 and ABCC1 doxorubicin FENDRR FENDRR, FOXF1-AS1, TCONS_00024240, lincFOXF1, onco-lncRNA-21 NA NA NA NA osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin FOXC2-AS1 FOXC2-AS1, ODRUL 103752587 ENSG00000260944 NR_125795 GRCh38_16:86565145-86567761 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) up-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin FOXC2-AS1 FOXC2-AS1, ODRUL 103752587 ENSG00000260944 NR_125795 GRCh38_16:86565145-86567761 osteosarcoma NA M9180/3 qPCR, RNAi, Western blot, RNA-FISH etc. osteosarcoma tissues, cell lines (MG63, SaoS2 and HOS) up-regulated FOXC2-AS1 and its antisense transcript FOXC2 are positively up-regulated in doxorubicin-resistant osteosarcoma cell lines and tissues, correlate with poor prognosis and promote doxorubicin resistance in osteosarcoma cells in vitro and in vivo. LncRNA FOXC2-AS1 may promote doxorubicin resistance in OS by increasing the expression of transcription factor FOXC2, further facilitating ABCB1 expression. 28323030 2017 Antisense lncRNA FOXC2-AS1 promotes doxorubicin resistance in osteosarcoma by increasing the expression of FOXC2. doxorubicin FOXC2-AS1 FOXC2-AS1, ODRUL 103752587 ENSG00000260944 NR_125795 GRCh38_16:86565145-86567761 osteosarcoma NA M9180/3 qPCR, microarray, Western blot, Luciferase reporter assay etc. cell lines (SaoS2, HOS, U2-OS, MG63, 143B) up-regulated ODRUL is upregulated in OS tissues and cell lines and correlates with poor prognosis. A microarray screen combined with online database analysis showed that miR-3182 is upregulated and MMP2 is downregulated in sh-ODRUL-expressing MG63 cells and that miR-3182 harbors potential binding sites for ODRUL and the 30 UTR of MMP2 mRNA. In addition, miR-3182 expression and function are inversely correlated with ODRUL expression in vitro and in vivo. A luciferase reporter assay demonstrated that ODRUL could directly interact with miR-3182 and upregulate MMP2 expression via its competing endogenous RNA activity on miR-3182 at the posttranscriptional level. 28750740 2017 LncRNA ODRUL Contributes to Osteosarcoma Progression through the miR-3182/MMP2 Axis doxorubicin FOXC2-AS1 FOXC2-AS1, ODRUL 103752587 ENSG00000260944 NR_125795 GRCh38_16:86565145-86567761 osteosarcoma NA M9180/3 microarray, qPCR, RNAi, Western blot etc. cell lines (MG-63, SaoS2, U-2OS) up-regulated lncRNA ODRUL was higher in different doxorubicin-resistant OS cell lines and lower in different doxorubicin-sensitive OS cell lines. Moreover, we showed that lncRNA ODRUL was increased in specimens of OS patients with a poor chemoresponse and lung metastasis. We further demonstrated that lncRNA ODRUL inhibition could inhibit OS cell proliferation, migration, and partly reversed doxorubicin resistance in vitro. In addition, we found that the expression of classical drug resistance-related ATP-binding cassette, subfamily B, member 1 (ABCB1) gene was decreased after the lncRNA ODRUL knockdown. Thus, we concluded that lncRNA ODRUL may act as a pro-doxorubicin-resistant molecule through inducing the expression of the classical multidrug resistance-related ABCB1 gene in osteosarcoma cells. 26408180 2015 A long non-coding RNA contributes to doxorubicin resistance of osteosarcoma. doxorubicin GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 bladder cancer C67 NA qPCR, RNAi, Western blot etc. BTCC tissues, cell lines (T24, J82) down-regulated In this study, we found that GAS5 low-expressed in BTCC tissues and cells, and its low expression level had positive correlation with higher pathological grades of BTCC. Moreover, GAS5 was a prognostic biomarker of disease free survival for BTCC patients. GAS5 over-expression could inhibit cell proliferation of BTCC J82 and T24 cells significantly. The IC50 to doxorubicin in T24/DOX cells (resistance to doxorubicin) presented a conspicuous depression, GAS5 enhancement reduced the chemotherapy resistance to doxorubicin. GAS5 over-expression promoted apoptosis induced by doxorubicin in T24/DOX cells, and depressed the expression of anti-apoptosis protein Bcl-2. 27878359 2017 Long noncoding RNA GAS5 inhibits malignant proliferation and chemotherapy resistance to doxorubicin in bladder transitional cell carcinoma. doxorubicin H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 hepatocellular carcinoma C22.0 M8170/3 MSP-PCR, Northern blot etc. cell lines (HepG2, R-HepG2, Hep3B) up-regulated Overexpression of multi-drug resistance 1 (MDR1) gene and its protein product P-glycoprotein, accompanied with a decrease in doxorubicin accumulation level, was observed in doxorubicin-resistant R-HepG2 cells, a subline derived by selection of human hepatocellular carcinoma HepG2 cells with doxorubicin. In addition, Northern-blot analysis revealed an eight fold upregulation of the imprinted H19 mRNA in R-HepG2 cells. H19 knockdown by transfection with antisense H19 oligonucleotides suppressed the MDR1/P-glycoprotein expression, increased the cellular doxorubicin accumulation level and sensitized doxorubicin toxicity in both HepG2 parent cells and R-HepG2 cells. 17297456 2007 Riboregulator H19 induction of MDR1-associated drug resistance in human hepatocellular carcinoma cells. doxorubicin HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 bladder cancer C67 NA qPCR, RNAi, Western blot etc. cell lines (TCC, T24 and J82) up-regulated HOTAIR was up-regulated in bladder transitional cell carcinoma (TCC) tissues and cell lines compared with normal bladder transitional cell (NBTC) tissues and bladder epithelial immortalized SV-HUC-1 cells, and its expression level had positive correlation with histological grades of TCC. In T24 and J82 cells, HOTAIR over-expression promoted cell proliferation and inhibited chemosensitivity to doxorubicin and cell apoptosis induced by doxorubicin; silence of HOTAIR showed opposite regulative effects. 26781446 2016 Long noncoding RNA HOTAIR is a prognostic biomarker and inhibits chemosensitivity to doxorubicin in bladder transitional cell carcinoma. doxorubicin LINP1 NA 108570035 ENSG00000223784 NR_138480 GRCh38_10:6737382-6739026 breast cancer C50 NA qPCR, Western blot breast cancer tissues, Human breast cancer cells (MDA-MB-231, MDA-MB-468 and MCF7) up-regulated LINP1 knockdown mitigated breast cancer cell growth by inducing G1-phase cell cycle arrest and apoptosis. LINP1 also promoted breast cancer cell metastasis and influenced the expression of epithelial-mesenchymal transition-related markers. We identified p53 as a regulator of LINP1, and LINP1 overexpression could restore the metastatic effects of p53. Furthermore, LINP1 was upregulated in doxorubicin- and 5-fluorouracil-resistant cells and induced chemoresistance. We also observed that LINP1 enrichment played a critical functional role in chemoresistance by inhibiting chemotherapeutics-induced apoptosis. Moreover, LINP1 in tumors was associated with lower overall survival and disease-free survival. 29293402 2018 Long noncoding RNA LINP1 acts as an oncogene and promotes chemoresistance in breast cancer. doxorubicin MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 osteosarcoma NA M9180/3 qPCR, Western blot, Luciferase reporter assay etc. 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. doxorubicin NR_033878 LINC00944 387895 ENSG00000256128 NR_033878 GRCh38_12:126752164-126761045 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) up-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin NR_040001 LINC01116, TALNEC2 375295 ENSG00000163364 NR_040001 GRCh38_2:176629589-176637931 osteosarcoma NA M9180/3 microarray, qPCR, MTT assay etc. cell line (MG63/DXR) down-regulated The results showed that lncRNA ENST00000563280, uc021pbg.1, ENST00000568031, ENST00000545508, uc010lgv.1, ENST00000553559 and uc003txt.3 were up-regulated and that NR-036444, ENST00000440570, ENST00000476909, NR_040001, ENST00000457390, uc002sts.4, ENST00000576810 and ENST00000565617 were down-regulated in the doxorubicin-resistant MG63/DXR cells compared with their parental MG63 cell controls. 26464619 2015 Long noncoding RNA expression profiles of the doxorubicin-resistant human osteosarcoma cell line MG63/DXR and its parental cell line MG63 as ascertained by microarray analysis. doxorubicin SOX2OTV7 NA NA NA NA NA osteosarcoma NA M9180/3 qPCR, Western blot, in vitro knockdown cell lines (U2OS and SaoS2, U-87 MG ) down-regulated EGCG targeting LncRNA SOX2OT variant 7 produced synergistic effects with Doxorubicin on osteosarcoma cell growth inhibition. On the one hand, EGCG could reduce the Doxorubicin-induced pro-survival autophagy through decreasing SOX2OT variant 7 to improve the growth inhibition of Doxorubicin. On the other hand, EGCG could partially inactivate Notch3/DLL3 signaling cascade targeting SOX2OT variant 7 to reduce the stemness then abated drug-resistance of osteosarcoma cells. 29475441 2018 SOX2OT variant 7 contributes to the synergistic interaction between EGCG and Doxorubicin to kill osteosarcoma via autophagy and stemness inhibition. DOX CASC2 CASC2, C10orf5 255082 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. docetaxel LINC00707 NA 100507127 ENSG00000238266 NR_038291 GRCh38_10:6779598-6842906 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, RNAi lung adenocarcinoma tissues, cell lines(SPCA1, A549, H1299, H1975,16HBE) up-regulated The expression level of LINC00707 was clearly upregulated in LAD tissues compared to that in corresponding normal tissues.Its overexpression was related to advanced TNM stage, larger tumor size, lymphatic metastasis, and poor prognosis.LINC00707 knockdown repressed LAD cell proliferation both in vitro and in vivo. This process may involve the inducing of G1 arrest and apoptosis.cell migration was impaired after LINC00707 inhibition.Cdc42 is an important target gene involved in the carcinogenesis of LINC00707.LINC00707 is a noncoding oncogene that exerts important regulatory functions in LAD, suggesting its potential as a biomarker in the prognosis and treatment of LAD.patients expressing higher levels of LINC00707 had poorer disease-free survival and overall survival. 29482190 2018 The Long Intergenic Noncoding RNA 00707 Promotes Lung Adenocarcinoma Cell Proliferation and Migration by Regulating Cdc42. docetaxel linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 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 Docetaxel PCA3 PCA3, DD3, NCRNA00019, PCAT3 50652 ENSG00000225937 NR_015342 GRCh38_9:76691980-76863307 prostate cancer C61.9 NA qPCR etc. prostate cancer tissues up-regulated Upregulation of two new PCA3 isoforms in PCa tissues improves discrimination between PCa and BPH. The functional relevance of this specificity is now of particular interest given PCA3's overlapping association with a second gene BMCC1, a regulator of Rho signalling. Upregulation of PCA3 and BMCC1 in PCa has potential for improved diagnosis. 19319183 2009 New genomic structure for prostate cancer specific gene PCA3 within BMCC1: implications for prostate cancer detection and progression. dihydrotestosterone NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 multiple myeloma C42.1 M9732/3 qPCR, Luciferase reporter assay, Western blot cell lines (RPMI8226, JJN-3, U266, ANBL6, OPM-2, MM1S, and MM1R) up-regulated upregulation of NEAT1 was tightly linked to poor prognosis. knockdown of NEAT1, the DEX-induced sensitivity was enhanced in the resistant cells.Meanwhile, overexpression of NEAT1 increased the DEX-induced resistance in the sensitive cells.the NEAT1/miR-193a/MCL1 pathway is closely associated with the development of DEX resistance in myeloma cells,and knockdown of NEAT1 can significantly improve DEX sensitivity in MM.Patientswith elevatedNEAT1 expression showed reduced survival times compared with patients with low levels of NEAT1 expression. 29205703 2017 LncRNA NEAT1 promotes dexamethasone resistance in multiple myeloma by targeting miR-193a/MCL1 pathway. dexamethasone HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, Western blot etc. cell line (MCF10A) up-regulated The level of HOTAIR significantly increases in a time-dependent manner during chronic breast carcinogenesis. Dp treatment down-regulates HOTAIR expression in breast carcinogenesis and breast cancer cells. Furthermore, Dp administration inhibits the growth of xenografted breast tumors in athymic mice, and decreases HOTAIR in vivo. Further studies showed that Dp represses Akt activation, promotes IRF1 expression and increases IRF1 binding to the HOTAIR promoter. Silence of IRF1 expression via transfecting cells with IRF1 siRNAs significantly reduced the effects of Dp on HOTAIR, resulting in decreased cytotoxic effects of Dp on breast cancer cells. 27388461 2016 Delphinidin-3-glucoside suppresses breast carcinogenesis by inactivating the Akt/HOTAIR signaling pathway. Delphinidin-3-glucoside GAS6-AS2 NA NA ENSG00000272695 NA NA acute myeloid leukemia NA M9861/3 qPCR etc. cell lines (MOLM14, K562, HEK293, HL60) up-regulated Transcriptional activation of the GAS6-AS2 lncRNA, identified in our analysis, leads to hyperactivation of the GAS6/TAM pathway, a resistance mechanism in multiple cancers including AML. 29677511 2018 An Integrated Genome-wide CRISPRa Approach to Functionalize lncRNAs in Drug Resistance. cytarabine HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 renal cell carcinoma C64.9 NA qPCR, Cell migration assay etc. cell lines (769-p, 769-p-vector, 769-p-HOTAIR, 786-0 and kert-3) up-regulated Comparison of the 5 cell lines indicated a correlation between HOTAIR mRNA expression and cell migration. In particular, the migration of 769-P-HOTAIR cells was significantly higher than that of 769-P-vector cells. Curcumin at 2.5-10 μM had no evident toxicity against RCC cells, but inhibited cell migration in a concentration-dependent manner. 24935377 2014 Influence of curcumin on HOTAIR-mediated migration of human renal cell carcinoma cells. curcumin PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. CRC tissues, cell lines (DLD-1, SW620, and HCT116) up-regulated Expression of PANDAR was increased in curcumin-treated CRC cells. Furthermore, silencing PANDAR in curcumin-treated cells increased apoptosis and greatly attenuated senescence possibly by stimulating the expression of PUMA. 28176943 2017 Silence of long noncoding RNA PANDAR switches low-dose curcumin-induced senescence to apoptosis in colorectal cancer cells. curcumin HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 laryngeal squamous cell cancer C32.3 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. LSCC tissues, cell lines (Hep-2, AMC-HN8) up-regulated HOTAIR and EZH2 were over-expressed in LSCC tissue. The higher expression was significantly related to T phase, pathological grades, and risk of lymphatic metastasis of LSCC. Suppressing HOTAIR expression stimulated EZH2 expressing, promoted the proliferation of AMC-HN8 cells, and increased the sensitivity to cis-platinum of the LSCC cells. 27542077 2016 The role of long non-coding RNA HOTAIR in the progression and development of laryngeal squamous cell carcinoma interacting with EZH2. cis-platinum HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 gastric cancer C16 NA qPCR, drugs sensitivity Plasma, gastric adenocarcinoma cell lines (MGC-803 and MKN-45) up-regulated HULC was highly expressed in the plasma and tissues of the GC patients compared with controls, with HULC high expression indicating lower survival rate. HULC knockdown enhanced cisplatin-induced apoptosis in GC cells.We observed that HULC knockdown in both MGC-803 and MKN-45 cells significantly decreased the IC50 values of CDDP, ADR, and 5-FU 28356873 2016 Silencing of LncRNA HULC Enhances Chemotherapy Induced Apoptosis in Human Gastric Cancer Cisplatin,Adriamycin,5-FU CCAL NA NA NA NA NA ovarian cancer C56.9 NA qPCR etc. cell line (A2780 and SW-2) up-regulated We carried out the lncRNA sequencing of the ovarian cancer cell line A2780 and the paxitaxel resistant cell line A2780/PTX which is also cross resistant to the cisplatin and epirubicin. Through integrating the published data with the cisplatin resistant lncRNAs in ovarian cancer cell line or ovarian cancer patients, 5 up-regulated and 21 down-regulated lncRNAs are considered as the multidrug-resistant lncRNAs. By real-time PCR analysis, we confirmed the 5 up-regulated and 4 down-regulated multidrug resistant lncRNAs were similarly changed in both the multidrug resistant ovarian cancer cell lines and the multidrug resistant colon cancer cell lines. Furthermore, we conducted the lncRNA-mRNA co-expression network to predict the potential multidrug resistant lncRNAs' targets. Interestingly, the multidrug resistant genes ABCB1, ABCB4, ABCC3, and ABCG2 are all co-expressed with lncRNA CTD-2589M5.4. 29219179 2018 Multidrug resistant lncRNA profile in chemotherapeutic sensitive and resistant ovarian cancer cells. cisplatin, epirubicin CTD-2589M5.4 NA NA NA NA NA ovarian cancer C56.9 NA qPCR etc. cell line (A2780 and SW-6) up-regulated We carried out the lncRNA sequencing of the ovarian cancer cell line A2780 and the paxitaxel resistant cell line A2784/PTX which is also cross resistant to the cisplatin and epirubicin. Through integrating the published data with the cisplatin resistant. 29219179 2018 Multidrug resistant lncRNA profile in chemotherapeutic sensitive and resistant ovarian cancer cells. cisplatin, epirubicin OIP5-AS1 OIP5-AS1, cyrano, linc-OIP5 729082 ENSG00000247556 NR_026757 GRCh38_15:41283990-41309737 ovarian cancer C56.9 NA qPCR etc. cell line (A2780 and SW-5) down-regulated We carried out the lncRNA sequencing of the ovarian cancer cell line A2780 and the paxitaxel resistant cell line A2783/PTX which is also cross resistant to the cisplatin and epirubicin. Through integrating the published data with the cisplatin resistant. 29219179 2018 Multidrug resistant lncRNA profile in chemotherapeutic sensitive and resistant ovarian cancer cells. cisplatin, epirubicin TP53TG1 TP53TG1, LINC00096, NCRNA00096, P53TG1, P53TG1-D, TP53AP1 11257 ENSG00000182165 NR_015381 GRCh38_7:87325225-87345515 ovarian cancer C56.9 NA qPCR etc. cell line (A2780 and SW-3) down-regulated We carried out the lncRNA sequencing of the ovarian cancer cell line A2780 and the paxitaxel resistant cell line A2781/PTX which is also cross resistant to the cisplatin and epirubicin. Through integrating the published data with the cisplatin resistant. 29219179 2018 Multidrug resistant lncRNA profile in chemotherapeutic sensitive and resistant ovarian cancer cells. cisplatin, epirubicin MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 melanoma NA M8720/3 qPCR etc. melanoma tissues, cell lines (A375, WM35, SK-MEL-5, and SK-MEL-2) differential expression The level of MEG3 was significantly associated with poor prognosis. MEG3 could bind to miR-499-5p and CYLD mRNA contained a binding site of miR-499-5p. Importantly, overexpression of MEG3 suppressed the growth of xenograft tumor and improved chemotherapy sensitivity of A375 cells to cisplatin and 5-FU treatment. 29808164 2018 lncRNA-MEG3 Suppresses the Proliferation and Invasion of Melanoma by Regulating CYLD Expression Mediated by Sponging miR-499-5p cisplatin and 5-FU CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 non small cell lung cancer C34 M8046/3 qPCR, Luciferase reporter assay, Western blot, RIP cell lines (BEAS-2B, A549, H1299, A549/DDP) up-regulated CCAT1 and SOX4 were up-regulated, and miR-130a-3p was down-regulated in DDP-resistant NSCLC cells.CCAT1 directly interacted with miR-130a-3p and negatively regulated miR-130a-3p expression. CCAT1 contributed to DDP resistance of A549/DDP cells by down-regulating miR-130a-3p. CCAT1/miR-130a-3p axis enhanced DDP resistance of NSCLC cells by targeting SOX4, providing potential targets to overcome DDP resistance and improve efficacy of chemotherapy for patients with NSCLC. 29020498 2017 LncRNA CCAT1/miR-130a-3p axis increases cisplatin resistance in non-small-cell lung cancer cell line by targeting SOX4. cisplatin (DDP) HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP GC tissues, GC cell lines (SGC7901 and MGC803) up-regulated HOTAIR was over-expressed in GC tissues and GC cell lines, while miR-34a was low-expressed. HOTAIR directly bound to miR-34a. MiR-34a expression was significantly increased in si-HOTAIR-transfected cells. Anti-miR-34a reversed the effect of si-HOTAIR on the DDP resistance, apoptosis-related genes, PI3K/Akt and Wnt/B-catenin signaling pathways in DDP-resistant GC cells, indicating that the effects of HOTAIR are dependent on miR-34a. 29080815 2017 Knockdown of long non-coding RNA HOTAIR inhibits cisplatin resistance of gastric cancer cells through inhibiting the PI3K/Akt and Wnt/B-catenin signaling pathways by up-regulating miR-34a. cisplatin (DDP) UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 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. cisplatin (CDDP) ENST00000466677 WDR86-AS1 100131176 ENSG00000243836 NR_034012 GRCh38_7:151409271-151412101 lung squamous cell carcinoma C34 M8070/3 microarray, qPCR etc. LSCC tissues up-regulated Five lncRNAs (ENST00000584612, ENST00000579363, NR_038200, ENST00000466677 and ENST00000562112) were randomly selected to validate the microarray consistency by using qPCR. The results demonstrated that lncRNA ENST00000584612 and ENST00000579363 were downregulated and that NR_038200, ENST00000466677 and ENST00000562112 were upregulated in the PR samples compared with PD samples. 25250788 2014 Long noncoding RNAs expression patterns associated with chemo response to cisplatin based chemotherapy in lung squamous cell carcinoma patients. Cisplatin ENST00000562112 NAPSB, NAP1L, NAP2, NAPB, NAPSBP 256236 ENSG00000131401 NA GRCh8_19:50333796-50344767 lung squamous cell carcinoma C34 M8070/3 microarray, qPCR etc. LSCC tissues up-regulated Five lncRNAs (ENST00000584612, ENST00000579363, NR_038200, ENST00000466677 and ENST00000562112) were randomly selected to validate the microarray consistency by using qPCR. The results demonstrated that lncRNA ENST00000584612 and ENST00000579363 were downregulated and that NR_038200, ENST00000466677 and ENST00000562112 were upregulated in the PR samples compared with PD samples. 25250788 2014 Long noncoding RNAs expression patterns associated with chemo response to cisplatin based chemotherapy in lung squamous cell carcinoma patients. Cisplatin ENST00000579363 KRT17P4 NA ENSG00000205312 NA GRCh38_17:16847635-16852777 lung squamous cell carcinoma C34 M8070/3 microarray, qPCR etc. LSCC tissues down-regulated Five lncRNAs (ENST00000584612, ENST00000579363, NR_038200, ENST00000466677 and ENST00000562112) were randomly selected to validate the microarray consistency by using qPCR. The results demonstrated that lncRNA ENST00000584612 and ENST00000579363 were downregulated and that NR_038200, ENST00000466677 and ENST00000562112 were upregulated in the PR samples compared with PD samples. 25250788 2014 Long noncoding RNAs expression patterns associated with chemo response to cisplatin based chemotherapy in lung squamous cell carcinoma patients. Cisplatin ENST00000584612 NA NA NA NA NA lung squamous cell carcinoma C34 M8070/3 microarray, qPCR etc. LSCC tissues down-regulated Five lncRNAs (ENST00000584612, ENST00000579363, NR_038200, ENST00000466677 and ENST00000562112) were randomly selected to validate the microarray consistency by using qPCR. The results demonstrated that lncRNA ENST00000584612 and ENST00000579363 were downregulated and that NR_038200, ENST00000466677 and ENST00000562112 were upregulated in the PR samples compared with PD samples. 25250788 2014 Long noncoding RNAs expression patterns associated with chemo response to cisplatin based chemotherapy in lung squamous cell carcinoma patients. Cisplatin H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 ovarian cancer C56.9 NA RNA-seq, qPCR, Western blot etc. cell lines (A2780, A2780-DR) up-regulated We verified that different H19 expression levels in HGSC tissues showed strong correlation with cancer recurrence. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. Quantitative proteomics analysis indicated that six NRF2-targeted proteins, including NQO1, GSR, G6PD, GCLC, GCLM and GSTP1 involved in the glutathione metabolism pathway, were reduced in H19-knockdown cells. Furthermore, H19-knockdown cells were markedly more sensitive to hydrogen-peroxide treatment and exhibited lower glutathione levels. 27193186 2016 The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer. Cisplatin HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot etc. lung adenocarcinoma tissues, cell lines (A549/DDP, SPC-A1 etc.) up-regulated In this study, we show that HOTAIR expression was significantly upregulated in cisplatin-resistant A549/DDP cells compared with in parental A549 cells. Knockdown of HOTAIR by RNA interference could resensitize the responses of A549/DDP cells to cisplatin both in vitro and in vivo. In contrast, overexpression of HOTAIR could decrease the sensitivity of A549 and SPC-A1 cells to cisplatin. 24155936 2013 The long noncoding RNA HOTAIR contributes to cisplatin resistance of human lung adenocarcinoma cells via downregualtion of p21(WAF1/CIP1) expression. Cisplatin LINC00857 LINC00857 439990 ENSG00000237523 NR_038464 GRCh38_10:80207710-80219657 ovarian cancer C56.9 NA microarray, qPCR etc. cell lines (A2780, CP70, SKOV3, and SKOV3/DDP) down-regulated The lncRNA microarray analysis and qPCR identified seven lncRNAs that were significantly downregulated. 28128423 2017 Long non-coding RNA ENST00000457645 reverses cisplatin resistance in CP70 ovarian cancer cells. cisplatin NR_038200 MRLN, LINC00948, Linc-RAM, M1, MLN, MUSER1 NA NA NA NA lung squamous cell carcinoma C34 M8070/3 microarray, qPCR etc. LSCC tissues up-regulated Five lncRNAs (ENST00000584612, ENST00000579363, NR_038200, ENST00000466677 and ENST00000562112) were randomly selected to validate the microarray consistency by using qPCR. The results demonstrated that lncRNA ENST00000584612 and ENST00000579363 were downregulated and that NR_038200, ENST00000466677 and ENST00000562112 were upregulated in the PR samples compared with PD samples. 25250788 2014 Long noncoding RNAs expression patterns associated with chemo response to cisplatin based chemotherapy in lung squamous cell carcinoma patients. cisplatin NR_038435 HOXD-AS2 100506783 ENSG00000237380 NR_038435 GRCh38_2:176121611-176137098 ovarian cancer C56.9 NA microarray, qPCR etc. cell lines (A2780, CP70, SKOV3, and SKOV3/DDP) down-regulated The lncRNA microarray analysis and qPCR identified seven lncRNAs that were significantly downregulated. 28128423 2017 Long non-coding RNA ENST00000457645 reverses cisplatin resistance in CP70 ovarian cancer cells. cisplatin UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 lung adenocarcinoma C34 M8140/3 Microarray, qPCR cell lines (A549, NCI-H1299, A549/DDP) differential expression We found that 1,543 lncRNAs and 1,713 mRNAs were differentially expressed in A549/DDP cell and A549 cell, hinting that many lncRNAs were irregular from cisplatin resistance in LAD. UCA1 was the aberrantly expressed lncRNA and can significantly reduce the IC50 of cisplatin in A549/DDP cell after knockdown, while it can increase the IC50 of cisplatin after UCA1 was overexpressed in NCI-H1299. 29279851 2017 Aberrant Long Noncoding RNAs Expression Profiles Affect Cisplatin Resistance in Lung Adenocarcinoma Cisplatin AK001796 MIR4435-2HG, AGD2, AK001796, LINC00978, MIR4435-1HG, MIR4435-2HG 541471 ENSG00000172965 NR_015395 GRCh38_2:111036776-111523376 non small cell lung cancer NA NA qPCR, Western blot etc. cell lines (A549) down-regulated The knockdown of AK001796 by small interfering RNA reduced cellular cisplatin resistance and cell viability, and resulted in cell-cycle arrest, with a marked increase in the proportion of A549/DDP cells in the G0/G1 phase. By contrast, the knockdown of AK001796 increased the number of apoptotic cancer cells during cisplatin treatment. It was also shown that the knockdown of AK001796 positively induced the expression of cell apoptosis-associated factors, CCNC and BIRC5, and suppressed the expression of cell cycle-associated factors, CDK1 and GTSE5. Taken together, these fndings indicated that lncRNA AK001796 increased the resistance of NSCLC cells to cisplatin through regulating cell apoptosis and cell proliferation, and thus provides an attractive therapeutic target for NSCLC. 29067469 2017 Long non-coding RNA AK001796 contributes to cisplatin resistance of non-small cell lung cancer cisplatin ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 oral squamous cancer C06.9 M8070/3 qPCR, Western blot, etc. cell lines (OSCC3, SCC4, HSC3, CAL27) down-regulated lncRNA ANRIL expression was signifcantly down-regulated in si-ANRIL-transfected HSC3, OSCC3 and SCC4 cells when compared with control cells.Down-regulated expression of lncRNA ANRIL inhibits OSCC cell proliferation and induces cell apoptosis in vitro. lncRNA ANRIL was involved in OSCC cell proliferation and sensitivity to cisplatin. 29176691 2017 Midkine derived from cancer associated fibroblasts promotes cisplatin-resistance via upregulation of the expression of lncRNA ANRIL in tumour cells cisplatin ASAP1-IT1 ASAP1-IT1, ASAP1-IT, ASAP1IT, ASAP1IT1, DDEF1IT1, HSPC054, NCRNA00050 29065 NA NR_002765 NA non small cell lung cancer C34 M8046/3 Western blot lung cancer tissues, cell lines (A549, H1299, H460, SPCA-1 and SK-MES-1,HBE) up-regulated interference on ASAP1-IT1 expression could inhibit the proliferation of NSCLC cells.the interference on ASAP1-IT1 expression could block the migration and invasion ability of NSCLC cells. ASAP1-IT1 could regulate the biological behaviors of NSCLC cells through phosphatase and tensin homolog deleted on chromosome ten (PTEN)/serine-threonine kinase (AKT) pathway. 29364481 2018 Long non-coding RNA ASAP1-IT1 promotes cell proliferation, invasion and metastasis through the PTEN/AKT signaling axis in non-small cell lung cancer. cisplatin CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 cervical cancer C53 NA qPCR, Western blot, Luciferase Reporter Assays cervical cancer tissues, cell lines (SiHa, Me180, HCE1, HeLa and CaSki) down-regulated In this study, CASC2 expression was down-regulated in cervical cancer tissues, and was related to a shorter survival time and poore clinicopathologic features. Taken together, these observations suggest CASC2 up-regulates PTEN as a ceRNA of miR-21 and plays an important role in cervical cancer sensitivity to DDP and may serve as a potential target for cancer diagnosis and treatment. 28495512 2017 Modulation of CASC2/miR-21/PTEN pathway sensitizes cervical cancer to cisplatin cisplatin ENST00000457645 NA NA NA NA NA ovarian cancer C56.9 NA microarray, qPCR, Cell transfection, Western blot etc. cell lines (A2780, CP70, SKOV3, and SKOV3/DDP) down-regulated The lncRNA microarray analysis and qPCR identified seven lncRNAs that were significantly downregulated. Transfection of lncRNA ENST00000457645 into CP70 cells markedly inhibited viability and migration ability, and significantly increased expression of apoptotic proteins such as Bax and cleaved caspase-3. lncRNA ENST00000457645 negatively affects the viability and migration of cisplatin-resistant CP70 ovarian cancer cells. 28128423 2017 Long non-coding RNA ENST00000457645 reverses cisplatin resistance in CP70 ovarian cancer cells. cisplatin ENST00000458468 NA NA NA NA NA ovarian cancer C56.9 NA microarray, qPCR etc. cell lines (A2780, CP70, SKOV3, and SKOV3/DDP) down-regulated The lncRNA microarray analysis and qPCR identified seven lncRNAs that were significantly downregulated. 28128423 2017 Long non-coding RNA ENST00000457645 reverses cisplatin resistance in CP70 ovarian cancer cells. cisplatin GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay etc. NSCLC tissues, cell lines (H1650, H1299, H1975, A549 etc.) down-regulated NSCLC tissues had a substantially lower expression of GAS5 than adjacent normal tissues. The NSCLC tissues from patients with progressive disease (PD) had even lower GAS5 expression. 27338051 2016 GAS5 modulated autophagy is a mechanism modulating cisplatin sensitivity in NSCLC cells. cisplatin H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 ovarian cancer C56.9 NA RT-PCR, Western blot, in vitro knockdown Human epithelial ovarian cancer cell lines (A2780 S and A2780/CP) up-regulated H19 knockdown by siRNA induced apoptosis and sensitized the A2780/CP cells to cisplatin-induced cytotoxicity. These data indicated that VPA negatively regulates the expression of H19 in ovarian cancer cells, which subsequently leads to apoptosis induction, cell proliferation inhibition, and overwhelming to cisplatin resistance. The implication of H19→EZH2→p21/PTEN pathway by VPA treatment suggests that we could repurpose an old drug, valproic acid, as an effective drug for treatment of ovarian cancer in the future. 29468525 2018 Valproic Acid Promotes Apoptosis and Cisplatin Sensitivity Through Downregulation of H19 Noncoding RNA in Ovarian A2780 Cells. cisplatin H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 gastric cancer C16 NA qPCR, Western blot, Luciferase reporter assay gastric cancer tissue, cell lines (SGC-7901, SGC-7901/DDP) up-regulated In our study H19 and miR-675 were increased in gastric cancer cell lines and tissues. In addition, qRT-PCR revealed that H19 and miR-675 were overexpressed and FADD was decreased in SGC-7901/DDP, suggesting H19/miR-675 expression may be associated with cisplatin resistance 28848149 2017 Long Noncoding RNA H19/miR-675 Axis Promotes Gastric Cancer via FADD/Caspase 8/Caspase 3 Signaling Pathway cisplatin HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 endometrial cancer NA M8380/3 qPCR, Western blot, RNAi, etc. endometrial cancer cell line down-regulated Autophagy activity was significantly boosted in cisplatin-resistant Ishikawa cells, a human endometrial cancer cell line, compared with that in parental Ishikawa cells. After analyzing the overall long noncoding RNA (lncRNA) profiling, a meaningful lncRNA, HOTAIR, was identified.It was downregulated simultaneously in cisplatin-resistant Ishikawa cells and parental Ishikawa cells treated with cisplatin. RNA interference of HOTAIR reduced the proliferation of cisplatin-resistant Ishikawa cells and enhanced the autophagy activity of cisplatin-resistant Ishikawa cells with or without cisplatin treatment, in addition, beclin-1, multidrug resistance (MDR), and P-glycoprotein (P-gp) were mediated by lncRNA HOTAIR. 28721581 2017 Autophagy regulated by lncRNA HOTAIR contributes to the cisplatin-induced resistance in endometrial cancer cells cisplatin HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot, 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. cisplatin HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 non small cell lung cancer C34 M8046/3 qPCR, Cell transfection, Western blot etc. NSCLC tissues up-regulated HOTAIR expression in tissues of drug-resistant NSCLC patients was higher than that of non-drug-resistant patients. HOTAIR expression was elevated in cisplatin-resistant cell strains (A549/CDDP), and reducing HOTAIR expression increased the sensitivity of A549/CDDP cells to cisplatin. In addition, overexpression of HOTAIR in A549 cells increased resistance to cisplatin. Tumor sphere formation assays showed that the volume of spheres formed by cell strains expressing elevated levels of HOTAIR was greater than that of cell strains with low expression. Western blot experiments showed that elevated expression of HOTAIR upregulated tumor stem cell-related biomarkers and HOTAIR expression was directly related to Klf4 expression. 28066612 2017 Elevated HOTAIR expression associated with cisplatin resistance in non-small cell lung cancer patients. cisplatin HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, RNAi etc. cell line (SKOV-3) up-regulated The results indicated that the expression level of HOTAIR was higher in epithelial ovarian cancer tissues than the level in the benign ovarian tissues. The expression level was also higher in late-stage malignant ovarian tumors compared with the level in early-stage tumors. Levels of HOTAIR were also higher in the SKOV-3CDDP/R cisplatin-resistant ovarian carcinoma cell line than in the SKOV-3 cisplatin-sensitive cell line. The knockdown of HOTAIR using siRNAs with transfection reagent suppressed cell proliferation, reduced the invasion ability of the cells. 25824616 2015 HOTAIR is a potential target for the treatment of cisplatin-resistant ovarian cancer. cisplatin HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot cell line (Huh7) up-regulated knockdown of HOTAIR expression in HCC Huh7 cells resulted in decreased cell proliferation and increased chemosensitivity to cisplatin.expression levels of ATP binding cassette subfamily B member 1 (ABCB1) mRNA and protein were decreased in Huh7 cells upon HOTAIR-knockdown. In addition, HOTAIR-knockdown reduced the levels of phosphorylated signal transducer and activator of transcription 3(STAT3), and inhibition of STAT3 phosphorylation reduced HOTAIR-mediated ABCB1 expression.knockdown of HOTAIR in Huh7 cells decreased STAT3 activity and ABCB1 expression, and increased chemosensitivity to cisplatin. 29250186 2017 Knockdown of long non-coding RNA HOTAIR sensitizes hepatocellular carcinoma cell to cisplatin by suppressing the STAT3/ABCB1 signaling pathway. cisplatin HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 cervical cancer C53 NA qPCR, Western blot, Dual luciferase reporter assay, etc. cervical cancer tissues, cell lines (CaSki, HeLa) up-regulated downregulation of HOXD-AS1 suppressed chemoresistance of cisplatin-resistant CC cells. we confirmed that HOXD-AS1 can act as a ceRNA to upregulate ZEB1 through miR-130a-3p. HOXD-AS1 enhanced chemoresistance of cisplatin-resistant CC cells through modulating miR-130a-3p/ZEB1 axis 29896986 2018 HOXD-AS1 exerts oncogenic functions and promotes chemoresistance in cisplatin-resistant cervical cancer cells. cisplatin LINC00261 LINC00261, ALIEN, C20orf56, DEANR1, HCCDR1, NCRNA00261, onco-lncRNA-17 140828 ENSG00000259974 NR_001558 GRCh38_20:22547671-22578642 colon cancer C18 NA qPCR, Western blot colon cancer tissues, cell lines (HCT116, HCT8, HT29, SW480, FHC) down-regulated LINC00261 overexpression might relieve cisplatin resistance of colon cancer cells via promoting cell apoptosis, and inhibiting cell viability,migration, and invasion.LINC00261 might down-regulate nuclear B-catenin through restraining B-catenin from cytoplasm into nuclei or it could also promote B-catenin degradation and inhibit activation of Wnt pathway.LINC00261 reduced cisplatin resistance of colon cancer in vivo and enhanced the anti-colon cancer effect of cisplatin through reducing tumor volume and weight.Overexpression of LINC00261 in SW480/DDP cells inhibited the survival rate. 29267503 2017 Long non-coding RNA LINC00261 sensitizes human colon cancer cells to cisplatin therapy. cisplatin MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 lung cancer C34 NA qPCR, Luciferase reporter assay, Western blot, RIP lung cancer tissues, cell lines (A549, H1299, H469, SPC-A1 and A549/DDP, NHBE) up-regulated Lung cancer patients with high MALAT1 levels were associated with cisplatin resistance and low overall survival.MALAT1 knockdown in lung cancer cells resulted in miR-101-3p upregulation and increased cisplatin sensitivity.miR-101-3p decreased myeloid cell leukemia 1(MCL1) expression by binding to the 3'-untranslated region (3'-UTR) of its mRNA. MALAT1/miR-101-3p/MCL1 signaling underlies cisplatin resistance in lung cancer. 29484127 2017 MALAT1/miR-101-3p/MCL1 axis mediates cisplatin resistance in lung cancer. cisplatin MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 non small cell lung cancer C34 M8046/3 qPCR, Western blot, luciferase reporter assay, RIP etc. cell lines (A549, H1299) down-regulated MEG3 was downregulated in DDP-resistant NSCLC cells. Overexpression of MEG3 enhanced DDP sensitivity of NSCLC cells in vitro. MEG3 directly interacted with miR-21-5p and suppressed its expression. miR-21-5p signifcantly abolished the effects of MEG3 on DDP resistance via modulating cell proliferation and apoptosis. SOX7 was identifed as a direct target of miR-21-5p and MEG3 positively regulated SOX7 expression by suppressing miR-21-5p. Moreover, MEG3 knockdown-induced pro-proliferative and anti-apoptotic effects were reversed in DDP-resistant NSCLC cells by upregulating SOX7. Furthermore, upregulation of MEG3 induced sensitivity of NSCLC cells to DDP in vivo. 29123412 2017 lncrna Meg3 enhances cisplatin sensitivity in non-small cell lung cancer by regulating mir-21-5p/sOX7 axis cisplatin MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 glioma NA M9380/3 qPCR, western blot U87 cell line down-regulated The results demonstrated that MEG3 expression levels were increased in U87 cells following cisplatin treatment.Decreased MEG3-induced autophagy improved the chemosensitivity of U87 cells to cisplatin. 28677749 2017 Long non-coding RNA MEG3 contributes to cisplatin-induced apoptosis via inhibition of autophagy in human glioma cells. cisplatin MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 bladder cancer C67 NA qPCR, Western blot, Flow cytometry, etc. bladder cancer tissues, cell lines (T24, 5637) down-regulated MEG3 overexpression sensitized BC cells to the chemotherapy drug cisplatin (DDP).MEG3 and p53 could stimulate the expression of each other in BC cells, indicating a potential positive feedback loop of MEG3 and p53.Our data showed that the BC cells overexpressing MEG3 displayed weaker migration and invasion ability than the control cells. 29940769 2018 Up-regulation of LncRNA MEG3 inhibits cell migration and invasion and enhances cisplatin chemosensitivity of bladder cancer cells cisplatin NAG7 LINC00312, ERR-10, ERR10, LMCD1DN, LOH3CR2A, NAG-7, NAG7, NCRNA00312 29931 NA NR_024065 NA ovarian cancer C56.9 NA qPCR, Western blot, Flow cytometry, etc. ovarian cancer tissues, cell lines (SKOV3, SKOV3/DDP) down-regulated Linc00312 enhanced the sensitivity of SKOV3/DDP cells to cisplatin by promoting cell apoptosis via the Bcl-2/Caspase-3 signaling pathway. 29952351 2018 Long non-coding RNA Linc00312 modulates the sensitivity of ovarian cancer to cisplatin via the Bcl-2/Caspase-3 signaling pathway. cisplatin NMR NA 100505887 ENSG00000228750 NR_104620 GRCh38_1:6724637-6730012 esophageal squamous cell cancer NA NA in vitro knockdown esophageal squamous cell carcinoma tissues down-regulated We identified a novel NSUN2 methylated lncRNA (NMR), which was significantly upregulated in esophageal squamous cell carcinoma (ESCC), functioned as a key regulator of ESCC tumor metastasis and drug resistance. Upregulation of NMR correlated with tumor metastasis and indicated poor overall survival in ESCC patients. Functionally, NMR could promote tumor cell migration and invasion, inhibit cisplatin-induced apoptosis and increase drug resistance in ESCC cells. Mechanistically, transcription of NMR could be upregulated by NF-kB activation after IL-1B and TNF-a treatment. NMR was methylated by NSUN2 and might competitively inhibit methylation of potential mRNAs. 29763634 2018 Novel long noncoding RNA NMR promotes tumor progression via NSUN2 and BPTF in esophageal squamous cell carcinoma. cisplatin PCAT-1 LPCAT1, AGPAT10, AGPAT9, AYTL2, LPCAT-1, PFAAP3, lpcat, lysoPAFAT, PCAT-1 100750225 ENSG00000253438 NR_045262 GRCh38_8:126556323-127419050 oesophageal cancer NA M8070/3 qPCR oesophageal cancer tissues, cell lines (KYSE30, KYSE450, and Eca109) up-regulated PCAT-1, showed higher expression in OC tissues, especially higher in secondary OC compared with normal mucosa tissues. Overexpression of PCAT-1 increased the proliferation rate and growth of OC cells. Inhibition of PCAT-1 decreased proliferation and growth of OC cells, and increased cisplatin chemosensitivity. PCAT-1 may potentially serve as a therapeutic target for treating OC.PCAT-1 promotes development of OC and represses the chemoresistance of OC to cisplatin, and silencing of PCAT-1 may be a therapeutic strategy for treating OC.the expression of HOTAIR in oesophageal squamous cell carcinoma was significantly higher than that in adjacent tissues, and it was significantly correlated with the metastasis, high stage, and survival rate of oesophageal carcinoma. 29314203 2017 LncRNA PCAT-1 promotes tumour growth and chemoresistance of oesophageal cancer to cisplatin. cisplatin RAB11B-AS1 NA 100507567 ENSG00000269386 NR_038237 GRCh38_19:8374373-8390685 osteosarcoma NA M9180/3 qPCR, Western blot, etc. osteosarcoma tissues, cell lines (U2OS, Sao-2, MG-63, MNNG/HOS Cl#5[R-1059-D]) down-regulated Here we discovered a novel lncRNA, RAB11B antisense RNA (RAB11B-AS1), which is markedly down-regulated in human osteosarcoma (OS) and associated with OS metastasis and poor prognosis. We find that reduction of RAB11B-AS1 significantly facilitates proliferation, migration and invasiveness and prevents apoptosis of OS cells and results in lower sensitivity to cisplatin in these cells.These data suggest that DNA hyper-methylation in the promoter region of lnc-RAB11B-AS1 might play an important role in down-regulation of lnc-RAB11B-AS1 in osteosarcoma. 29928484 2018 Long non-coding RNA RAB11B-AS1 prevents osteosarcoma development and progression via its natural antisense transcript RAB11B. cisplatin RP11-135L22.1 NA NA NA NA NA ovarian cancer C56.9 NA qRT-PCR, Western blot ovarian cancer tissues, ovarian cancer cell lines (A2780, HEY, HO8910) down-regulated RP11-135L22.1 was lowly expressed in ovarian cancer.RP11-135L22.1 expression was negatively correlated with the treating time and dose of cisplatin. Western blot showed that cisplatin induced autophagy in ovarian cancer cells in a time- and dose-dependent manner. Cisplatin combined with RP11-135L22.1 can reduce autophagy, increase the apoptosis and inhibit its activity of ovarian cancer cells to a certain extent. 29509240 2018 Cisplatin suppresses tumor proliferation by inhibiting autophagy in ovarian cancer via long non-coding RNA RP11-135L22.1. Cisplatin SFTA1P SFTA1P, SFTPF NA ENSG00000225383 NA GRCh38_10:10784437-10794980 lung squamous cell carcinoma C34 M8070/3 qPCR, Western blot etc. cell lines (NCl-H226, SK-MES-1, NCl-H1299, A549, A549-DDP) up-regulated Here, we found that lncRNA SFTA1P (surfactant associated 1, pseudogene), highly expressed in lung, was down-regulated in LSCC tissues and could be induced upon cisplatin treatment in LSCC cells. Elevated SFTA1P induced apoptosis and enhanced the sensitivity to cisplatin of LSCC cells. We further identified that hnRNP-U (heterogeneous nuclear ribonucleoprotein U) was down-regulated in LSCCs and positively correlated with patients’ poor prognosis as well as SFTA1P. Mechanistic studies revealed that SFTA1P could up-regulate hnRNP-U expression. In addition, we identified that hnRNP-U enhanced cisplatin-induced apoptosis through up-regulation of GADD45A, high expression of which was correlated with good prognosis in LSCC patients. 29228625 2017 Long noncoding RNA SFTA1P promoted apoptosis and increased cisplatin chemosensitivity via regulating the hnRNP-U-GADD45A axis in lung squamous cell carcinoma cisplatin TRPM2-AS TRPM2-AS, TRPM2-AS1 101928607 ENSG00000230061 NR_109964 GRCh38_21:44414588-44425272 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. cell lines (DDP, A549) up-regulated A549/DDP cells presented remarkably higher expression of lncRNA TRPM2-AS than paired A549 cells. Moreover, re-sensitization to cisplatin was seen in A549/DDP cells after lncRNA TRPM2-AS knockdown. 28678322 2017 Downregulated long non-coding RNA TRPM2-AS inhibits cisplatin resistance of non-small cell lung cancer cells via activation of p53-p66shc pathway cisplatin UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 tongue squamous cell carcinoma C02 M8070/3 qPCR, Western blot etc. cell lines (CAL27, SCC-9) up-regulated Transient transfection of siRNA was used to knock down UCA1 in human TSCC cell lines CAL 27 and SCC-9, where UCA1 was highly overexpressed compared to normal human tongue tissues. UCA1 knockdown resulted in one magnitude decrease in the half maximal inhibitory concentration (IC50) of cisplatin in CAL 27 and SCC-9 cells, from 8.9 mM and 20.7 mM down to 0.6 mM and 1.7 mM, respectively. 29441929 2017 Knockdown of long noncoding RNA urothelial cancer-associated 1 enhances cisplatin chemosensitivity in tongue squamous cell carcinoma cells cisplatin UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 cervical cancer C53 NA qPCR, Western blot, in vitro knockdown cell line (HeLa) up-regulated This study showed that overexpression of UCA1 confers cisplatin resistance by promoting cancer cell proliferation and inhibiting apoptosis. In addition, knockdown of UCA1 remarkably decreased cisplatin resistance in cervical cancer cells. 28414550 2017 Expression of Long Noncoding RNA Urothelial Cancer Associated 1 Promotes Cisplatin Resistance in Cervical Cancer cisplatin XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 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 cisplatin XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 non small cell lung cancer C34 M8046/3 qPCR, Western blot non-small cell lung cancer tissues up-regulated lncRNA-XIST was overexpressed in NSCLC tumor samples, and knockdown of lncRNA-XIST significantly decreased autophagy by regulation of ATG7.miR-17 was upregulated following knockdown of lncRNA-XIST, and miR-17 mimics decreased the protein levels of ATG7 by directly targeting the 3'-untranslated region of ATG7 mRNA. the expression level of lncRNA-XIST was markedly increased in cisplatin-resistant A549 cells. Knockdown of lncRNA-XIST restored the chemosensitivity of cisplatin-resistant A549-cells to cisplatin, which was reversed by miR-17 inhibitor and overexpression of ATG7. lncRNA-XIST may be a potential marker of poor response to cisplatin chemotherapy in NSCLC patients and the pathway 'lncRNA-XIST/miR-17/autophagy' may be a promising target for patients with chemoresistant NSCLC. 29130102 2017 Knockdown of lncRNA-XIST enhances the chemosensitivity of NSCLC cells via suppression of autophagy. cisplatin SNHG8 SNHG8, LINC00060, NCRNA00060 100093630 ENSG00000269893 NR_003584 GRCh38_4:118278709-118279823 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). chemotherapy MIR100HG MIR100HG, AGD1, linc-NeD125, lncRNA-N2 399959 ENSG00000255248 NR_024430 GRCh38_11:122028327-122556721 colorectal cancer C19.9 NA qPCR etc. cell lines up-regulated MIR100HG, miR-100 and miR-125b overexpression was also observed in cetuximab-resistant colorectal cancer and head and neck squamous cell cancer cell lines and in tumors from colorectal cancer patients that progressed on cetuximab. miR-100 and miR-125b coordinately repressed five Wnt/B-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness. Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG, but this repression is relieved by miR-125b targeting of GATA6. These findings identify a clinically actionable, epigenetic cause of cetuximab resistance. 29035371 2017 lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/B-catenin signaling cetuximab lnc-PTMS-1:4 NA NA NA NA NA gastric cancer C16 NA qPCR etc. cell line (NCI-N88) differential expression a low dose of celecoxib may exert an anti-cancer effect by regulating the cell cycle and apoptosis independent of COX-2 in GC cells. ITGA3 and/or DVL1 co-expressed with lnc-SCD-1:13 and lnc-PTMS-1:4 may be involved in the effects of a low dose of celecoxib on GC. 28789409 2017 Anti-cancer effect of low dose of celecoxib may be associated with lnc-SCD-1:13 and lnc-PTMS-1:3 but not COX-2 in NCI-N88 cells. celecoxib lnc-SCD-1:13 NA NA NA NA NA gastric cancer C16 NA qPCR etc. cell line (NCI-N87) differential expression a low dose of celecoxib may exert an anti-cancer effect by regulating the cell cycle and apoptosis independent of COX-2 in GC cells. ITGA3 and/or DVL1 co-expressed with lnc-SCD-1:13 and lnc-PTMS-1:3 may be involved in the effects of a low dose of celecoxib on GC. 28789408 2017 Anti-cancer effect of low dose of celecoxib may be associated with lnc-SCD-1:13 and lnc-PTMS-1:3 but not COX-2 in NCI-N87 cells. celecoxib TUSC7 TUSC7, LINC00902, LSAMP-AS1, LSAMP-AS3, LSAMPAS3, NCRNA00295 285194 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 CDDP and Taxol MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 ovarian cancer C56.9 NA qPCR, Western blot, RIP etc. ovarian cancer tissues, cell lines (A2780, OVCAR3, COC1, A2780/CDDP, COC1/CDDP and OVCAR3/DDP) down-regulated Our data demonstrated that MALAT1 and Notch1 mRNA were upregulated in ovarian cancer tissues, as well as cisplatin (CDDP)-resistant ovarian cancer cells. A positive correlation between MALAT1 and Notch1 mRNA expression was observed. MALAT1 knockdown significantly attenuated CDDP resistance, and enhanced CDDP-induced apoptosis in CDDP-resistant ovarian cancer cells. MALAT1 knockdown enhanced CDDP-induced apoptosis in vivo, as indicated by upregulation of Bax protein expression and downregulation of Bcl-2 protein expression. Additionally, MALAT1 knockdown inhibited the Notch1 pathway and ABCC1 expression in CDDP-resistant ovarian cancer cells. MALAT1 was demonstrated to interact with Notch1. Notch1 knockdown attenuated CDDP resistance, and downregulated the protein expression of ABCC1 in ovarian cancer cells. 29548748 2018 Knockdown of MALAT1 enhances chemosensitivity of ovarian cancer cells to cisplatin through inhibiting the Notch1 signaling pathway. CDDP PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 ovarian cancer C56.9 NA qPCR, RNAi etc. cell line (3AO) down-regulated Among six up-regulating lncRNAs, we screened out carboplatin-docetaxel-induced lncRNA PVT1 which may be a central downstream target of carboplatin plus docetaxel because expression of PVT1 positively correlates with anticancer action of carboplatin plus docetaxel. Besides, p53 and tissue inhibitor of matrix metalloproteinases-1 (TIMP1) were mediated by lncRNA PVT1, which may explain partially the anticancer activity of lncRNA PVT1. knockdown of lncRNA PVT1 cause a marked reduction in tumor size in a human ovarian cancer xenograft model. 26097562 2015 Carboplatin-docetaxel-induced activity against ovarian cancer is dependent on up-regulated lncRNA PVT1. carboplatin plus docetaxel HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR etc. ovarian cancer tissues up-regulated HOTAIR expression was significantly associated with poor survival in carboplatin-treated patients with adjusted hazard ratios for death of 3.64 in the discovery and 1.63 in the validation set. This effect was not seen in patients who did not receive carboplatin. HOTAIR expression or its surrogate DNAme signature predicted poor outcome in all additional sets of carboplatin-treated ovarian cancer patients while HOTAIR expressors responded preferentially to cisplatin. 26497652 2015 HOTAIR and its surrogate DNA methylation signature indicate carboplatin resistance in ovarian cancer. carboplatin H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 multiple myeloma C42.1 M9732/3 qPCR, Western blot bone marrow tissues, cell lines ( OPM-2, U266, KM3, XG1, JJN3, RPMI, U1996, H929, and MM1S) up-regulated H19 knockdown induced by shRNA transfection significantly inhibited proliferation, viability and colony formation in MM cells, as well as inactivated NF-kB pathway.combination treatment of H19 knockdown and NF-kB suppression (induced by specific inhibitor PDTC) produced synergistically inhibitory effects.patients with high expression of H19 had a lower survival rate.H19 was involved in MM cell growth. The linkage between H19 and NF-kB pathway may provide a novel interpretation for the mechanism of H19's growth regulation in MM. 29273733 2017 Knockdown of long non-coding RNA H19 inhibits multiple myeloma cell growth via NF-kB pathway. bortezomib BDLNR NA NA NA NA NA cervical cancer C53 NA qPCR, Western blot, RIP cervical cancer tissues, cell lines (HeLa, SiHa, ME-180, and Caski,H8) up-regulated BDLNR physically bound to YBX1, recruited YBX1 to PIK3CA promoter, activated PIK3CA expression and PI3K/Akt pathway.BDLNR was upregulated in cervical cancer and associated with poor prognosis of cervical cancer patients. BDLNR mediated the anti-cancer effects of baicalein in cervical cancer via activating PI3K/Akt pathway and BDLNR would be potential therapeutic target for enhancing the anti-cancer effects of baicalein in cervical cancer.upregulated BDLNR expression indicated poor overall survival of cervical cancer patients. 29175387 2017 Baicalein inhibits cervical cancer progression via downregulating long noncoding RNA BDLNR and its downstream PI3K/Akt pathway. Baicalein PAX8-AS1-N NA NA NA NA NA breast cancer C50 NA qPCR, Western blot etc. breast cancer tissue, cell lines (MDA-MB-231 and MCF-7) down-regulated we identified a novel isoform of lncRNA PAX8-AS1 (PAX8-AS1-N), which is activated by baicalein in a dose- and time-dependent manner.PAX8-AS1-N reduced cell viability,inhibited cell-cycle progression,and induced apoptosis of breast cancer cells in vitro.Depletion of PAX8-AS1-N promoted breast xenograft tumor growth in vivo. Furthermore, depletion of PAX8-AS1-N attenuated the suppressive roles of baicalein on cell viability,the apoptosis induced by baicalein, and also the suppressive roles of baicalein on tumor growth in vivo. Mechanistically, PAX8-AS1-N bound to miR-17-5p, and up-regulated miR-17-5p targets,such as PTEN, CDKN1A, and ZBTB4. In addition, PAX8-AS1-N was down-regulated in breast cancer and reduced expression of PAX8-AS1-N indicated poor survival of breast cancer patients. 29693272 2018 Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8-AS1-N. baicalein H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown breast cancer cell lines (MDA-MB-231,MCF-7, SK-BR-3 and HEK293T) up-regulated Furthermore, H19 knockdown decreases PDK1 xpression in hypoxia, and ablation of PDK1 counteracts H19-mediated glycolysis and self-renewal ability in vitro and in vivo.Reprogramming is referred to as the conversion of differentiated cells to a stem-like state. Ectopic expression of four transcription factors (Oct4, Klf4, Sox2 and c-Myc) reprograms various types of somatic cells to induced pluripotent stem cells. Accordingly, H19 and PDK1 expression exhibits strong correlations in primary breast carcinomas. H19 acting as a competitive endogenous RNA sequesters miRNA let-7 to release Hypoxia-inducible factor 1a, leading to an increase in PDK1 expression. Lastly, aspirin markedly attenuates glycolysis and cancer stem-like characteristics by suppressing both H19 and PDK1. 29106390 2017 Glycolysis gatekeeper PDK1 reprograms breast cancer stem cells under hypoxia. aspirin UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 prostate cancer C61.9 NA qPCR, Western blot, RIP, Luciferase reporter assay cell lines (DU145 and LNCaP) up-regulated UCA1 was up-regulated in prostate cancer tissues compared to hyperplastic prostatic tissues,and a higher UCA1 level predicted poor prognosis in PCa patients.Then we determined that the miR-184/Bcl-2 axis might be the downstream signaling pathway of UCA1 upon ART treatment. UCA1 binds to miR-184 through its seed sequences and may function as a sponge for miR-184. 28209917 2017 Artesunate suppresses the viability and mobility of prostate cancer cells through UCA1, the sponge of miR-184 Artesunate lncRNA-PRLB NA NA NA NA NA breast cancer C50 NA Microarray, qPCR, Western blot, RIP etc. breast cancer tissues, cell lines lncRNA-PRLB was upregulated in human breast cancer tissues and breast cancer cell lines.Further evaluation verified that lncRNA-PRLB was positively correlated with the extent of metastasis, and its expression was correlated with shorter survival time of breast cancer patients. We identified microRNA miR-4766-5p as an inhibitory target of lncRNA-PRLB.Both lncRNA-PRLB overexpression and miR-4766-5p knockdown could remarkably enhance cell growth, metastasis, and chemoresistance. We also determined that sirtuin 1 (SIRT1) was an inhibitory target of miR-4766-5p, and that SIRT1 was inhibited by both lncRNA-PRLB knockdown and miR-4766-5p overexpression. The subcellular distribution assay revealed that lncRNA-PRLB is predominately located in the plasma. 29752439 2018 A novel long non-coding RNA-PRLB acts as a tumor promoter through regulating miR-4766-5p/SIRT1 axis in breast cancer. anticancer drugs HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, RNAi etc. gastric cancer tissues, cell lines (MKN7, MKN45, MKN74, NUGC4, AZ521, AGS, KATOIII) up-regulated Expression of both lncRNAs was significantly higher in cancerous tissues than in corresponding normal mucosa, and higher expression of these lncRNAs significantly correlated with peritoneal metastasis in GC patients. In addition, elevated HOTAIR expression emerged both as an independent prognostic and risk factor for peritoneal dissemination. SiRNA knockdown of HOTAIR in GC cells significantly inhibited cell proliferation, migration and invasion, but concurrently enhanced the anoikis rate in transfetced cells. 25280565 2014 Metastasis-associated long non-coding RNA drives gastric cancer development and promotes peritoneal metastasis. anoikis HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 breast cancer C50 NA qPCR, Western blot, in vitro knockdown, RNAi humanbreast cancer cell lines (MCF-7 and MCF-10A) up-regulated Using gain-and-loss-of experiments in vitro and in vivo, we observed the marked upregulation of HOTTIP/HOXA11 in the breast cancer cell line, MCF-7, and the downregulation of HOTTIP or HOXA11, which might inhibit cell proliferation and migration but promote cell apoptosis in breast cancer MCF-7 cells. In addition, by further rescue experiments with HOXA11 overexpression, we uncovered a novel potential regulatory mechanism between HOTTIP and one of its physical HOXA clusters, HOXA11. Hence, HOTTIP may mediate, at least partly, HOXA11 expression involved in cell growth, migration, and apoptosis of breast cancer MCF-7 cells. 29415429 2018 LncRNA HOTTIP-Mediated HOXA11 Expression Promotes Cell Growth, Migration and Inhibits Cell Apoptosis in Breast Cancer. Adriamycin NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 gastric cancer C16 NA qPCR gastric cancer tissues, cell lines (SGC7901, GES-1) up-regulated NEAT1 was up-regulated in GC tissues and cells, especially in in GC adriamycin-resistant cells. NEAT1 silence in SGC7901 cells could inhibit proliferation and invasion ability, and promote cell apoptosis significantly.lncRNA NEAT1 is high-expressed in GC and functions as an oncogene to modulate apoptosis,invasion, proliferation and chemotherapy resistance of GC cells, which might be a novel potential therapeutic target for GC. 28401449 2017 Silence of Long Noncoding RNA NEAT1 Inhibits Malignant Biological Behaviors and Chemotherapy Resistance in Gastric Cancer. adriamycin UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 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-1a-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-1a-dependent glycolysis in HL60 and HL60/ADR cells.Furthermore, 2-deoxy-glucose (2-DG) exposure inhibited HIF-1a-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. adriamycin VELUCT NA NA NA NA NA lung cancer C34 NA RNA-seq, qPCR, RNAi, Northern blot etc. cell lines (NCI-H460, NCI-H1944 and NCI-H1437) differential expression Despite its extremely low abundance, loss-of-function of VELUCT with three independent experimental approaches in three different lung cancer cell lines led to a significant reduction of cell viability. In summary, the extremely low abundant lncRNA VELUCT is essential for regulation of cell viability in several lung cancer cell lines. 28160600 2017 The lncRNA VELUCT strongly regulates viability of lung cancer cells despite its extremely low abundance actinomycin D NR_038990 EHHADH-AS1 339926 ENSG00000223358 NR_038990 GRCh38_3:185162871-185191955 colorectal cancer C19.9 NA microarray, qPCR etc. cell line (HCT116) down-regulated To validate the microarray results, we randomly selected 6 differentially expressed lncRNAs (TCONS_00026506, ENST00000468960, NR_038990, ENST00000575202, ENST00000539009 and ENST00000544591) between CRR-HCT116 and parental HCT116 cells to confirm their expression levels by qPCR. Changes in lncRNA expression are involved in 5-FU-based CRR in CRC cells. 25921151 2015 Microarray Analysis of Long Non-coding RNA Expression Profile Associated with 5-Fluorouracil-Based Chemoradiation Resistance in Colorectal Cancer Cells. 5-FU CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colorectal cancer C19.9 NA qPCR colorectal cancer tissues up-regulated The expression level of lncRNA CCAT2 in CRC tissues was increased significantly compared with adjacent normal tissues or non-cancerous tissues. CCAT2 expression was observed to be progressively increased between tumor-node-metastasis (TNM) stages I and IV. A high level of CCAT2 expression was revealed to be associated with poor cell differentiation, deeper tumor infiltration, lymph node metastasis,distance metastasis, vascular invasion and advanced TNM stage. patients with high levels of CCAT2 expression had shorter disease-free survival and overall survival times.high CCAT2 expression was an independent poor prognostic factor. 29181105 2017 Overexpression of long non-coding RNA colon cancer-associated transcript 2 is associated with advanced tumor progression and poor prognosis in patients with colorectal cancer. 5-FU DGCR5 DGCR5, LINC00037, NCRNA00037 26220 ENSG00000237517 NR_002733 GRCh38_22:18970514-18994628 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR pancreatic ductal adenocarcinoma tumors tissues differential expression Here, we present evidence that shows that the lncRNA DGCR5 is significantly reduced in PDAC tissues as well as in PDAC cell lines and that the downregulation of DGCR5 predicts poor prognosis. Further experiments demonstrated that DGCR5 and miR-320a regulate each other in a reciprocal manner and that DGCR5 reverses the inhibition of PDCD4 by miR-320a, which is involved in the regulation of the PDAC cell phenotype and response to 5-FU. 29207609 2017 Reciprocal regulation of DGCR5 and miR-320a affects the cellular malignant phenotype and 5-FU response in pancreatic ductal adenocarcinoma 5-FU LINC00152 CYTOR, C2orf59, LINC00152, NCRNA00152 112597 ENSG00000222041 NR_024204 GRCh38_2:87454781-87636740 colorectal cancer C19.9 NA qPCR, Western blot etc, cell lines (HCT8, HT29, LoVo, HCT116, SW480, SW620) up-regulated LINC00152 was overexpressed in CRC tissues and negatively related to the survival time of CRC patients. Functional analyses revealed that LINC00152 could promote cell proliferation. LINC00152 could increase the resistance of CRC cells to 5-fluorouracil (5-FU) by suppressing apoptosis. We also discovered that LINC00152 could enhance cell migration and invasion. 29180678 2017 Long non-coding RNA LINC00152 promotes cell proliferation, metastasis, and confers 5-FU resistance in colorectal cancer by inhibiting miR-139-5p 5-FU PRAS NA NA NA NA NA colon cancer C18 NA qPCR etc. cell lines (SNU-C4R, SNU-C5R etc.) down-regulated We selected three lncRNAs, snaR, BACE1AS, and PRAS, and we detected their expression by RT-qPCR using specific primer sets. SnaR and BACE1AS were significantly down-regulated in both resistant cell lines (SNU-C4R and SNU-C5R), whereas PRAS was down-regulated in SNU-C4R cells but not in SNU-C5R cells. Down-regulation of snaR decreased cell death after 5-FU treatment, which indicates that snaR loss decreases in vitro sensitivity to 5-FU. 25078450 2014 A long non-coding RNA snaR contributes to 5-fluorouracil resistance in human colon cancer cells. 5-FU MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 gastric cancer C16 NA qPCR, Western blot etc. cell lines (SGC7901, BGC823) up-regulated Chemoresistant GC cells had higher levels of MALAT1 and increased autophagy compared with parental cells. Silencing of MALAT1 inhibited chemo-induced autophagy, whereas MALAT1 promoted autophagy in gastric cancer cells. Knockdown of MALAT1 sensitized GC cells to chemotherapeutics. MALAT1 acts as a competing endogenous RNA for miR-23b-3p and attenuates the inhibitory effect of miR-23b-3p on ATG12, leading to chemo-induced autophagy and chemoresistance in GC cells. 29162158 2017 Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer 5-fluorouracil (5-FU), VCR and cisplatin (CDDP) HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR gastric cancer tissues, cell lines (BGC-823 and MKN-45) up-regulated lncRNA HOTAIR had an extremely high expression level in GC cells, and predicted poor prognosis in patients.Down-regulation of HOTAIR could promote chemosensitivity, induce apoptosis of GC cells, and significantly inhibit GC cell proliferation, invasion and metastasis in vivo and in vitro. 29236333 2017 Effect and mechanism of lncRNA HOTAIR on occurrence and development of gastric cancer. 5-fluorouracil (5-FU) and Cisplatin NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, Luciferase reporter assay, Western blot breast cancer tissues, cell lines (MCF-10A, MCF-7, MDA-MB-231, T-47-D and ZR-75-1) up-regulated lncRNA NEAT1 was up-regulated in breast cancer cell lines and tissues.NEAT1 promoted invasion through inducing Epithelial-mesenchymal transition (EMT) and NEAT1 played a role in 5-fluorouracil (5-FU) resistance.the EMT-inducer HMGA2 was identified as a down-stream target of miR-211.LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis.breast cancer patients with low levels of NEAT1 expression had better overall survival time than those with high levels. 28720546 2017 The lncRNA NEAT1 facilitates cell growth and invasion via the miR-211/HMGA2 axis in breast cancer. 5-fluorouracil (5-FU) RP11-708H21.4 NA NA NA NA NA colorectal cancer C19.9 NA RNA-seq, qPCR, Western blot etc. colorectal cancer tissues, cell lines (DLD-1, SW-480, HT-29, SW-620, HCT-116 and LOVO) up-regulated Overexpressed RP11-708H21.4 suppresses CRC cell proliferation through inducing G1 arrest. Moreover, up-regulation of RP11-708H21.4 inhibits cell migration and invasion, causes cell apoptosis, and enhances 5-FU sensitivity of CRC cells. 28427191 2017 Down-regulation of long non-coding RNA RP11-708H21.4 is associated with poor prognosis for colorectal cancer and promotes tumorigenesis through regulating AKT/mTOR pathway 5-Fluorouracil (5-FU) GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 pancreatic cancer C25 NA qPCR, Western blot, RIP pancreatic cancer tissues, cell lines (PANC-1 and BxPC-3,HPDE6-C7) down-regulated GAS5 and PTEN protein were decreased in human PC tissues and cells, but miR-32-5p was increased. GAS5 induction greatly inhibited the proliferation, migration and invasion of PC cells PANC-1 and BxPC-3 in vitro and simultaneously induced cell apoptosis.GAS5 suppressed the proliferation, migration and invasion of PC cells through regulating miR-32-5p/PTEN axis. 29225772 2017 Long non-coding RNA GAS5 suppresses pancreatic cancer metastasis through modulating miR-32-5p/PTEN axis. 5-fluorouracil CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colon cancer C18 NA qPCR etc. cell lines (HCT-116, HT-29) up-regulated We have observed that modulated expression of CCAT2 regulates the expression of miR-145 in colon cancer HCT-116 and HT-29 cells. Knockout of CCAT2 increases miR-145 and negatively regulates miR-21 in HCT-116 cells, impairs proliferation and differentiation. In contrast, stable up-regulation of CCAT2 decreases mature miR-145 and increases the expression of several CSC markers in colon cancer cells. We have also observed that CCAT2 is enriched in the nucleus and correlates with the expression of pre-miR-145 but not pre-miR-21 in HCT-116 cells. These results indicate CCAT2 selectively blocks miR-145 maturation by inhibiting pre-miR-145 export to cytoplasm. Further, we revealed that CCAT2 blocks cleavage of pre-miR-145 by Dicer in vitro. 28964256 2017 A novel mechanism of lncRNA and miRNA interaction: CCAT2 regulates miR-145 expression by suppressing its maturation process in colon cancer cells 5-Fluorouracil ENSG00000244649 LINC02086 105371809 ENSG00000244649 XR_001752925 GRCh38_17:48646929-48704422 colorectal cancer C19.9 NA microarray, qPCR etc. cell line (HCT116) down-regulated To validate the microarray results, we randomly selected 6 differentially expressed lncRNAs (TCONS_00026506, ENST00000468960, NR_038990, ENST00000575202, ENST00000539009 and ENST00000544591) between CRR-HCT116 and parental HCT116 cells to confirm their expression levels by qPCR. Changes in lncRNA expression are involved in 5-FU-based CRR in CRC cells. 25921151 2015 Microarray Analysis of Long Non-coding RNA Expression Profile Associated with 5-Fluorouracil-Based Chemoradiation Resistance in Colorectal Cancer Cells. 5-Fluorouracil ENST00000468960 AC004893.11, LOC101927550 NA NA NA GRCh38_7:99013165-99036492 colorectal cancer C19.9 NA microarray, qPCR etc. cell line (HCT116) down-regulated To validate the microarray results, we randomly selected 6 differentially expressed lncRNAs (TCONS_00026506, ENST00000468960, NR_038990, ENST00000575202, ENST00000539009 and ENST00000544591) between CRR-HCT116 and parental HCT116 cells to confirm their expression levels by qPCR. Changes in lncRNA expression are involved in 5-FU-based CRR in CRC cells. 25921151 2015 Microarray Analysis of Long Non-coding RNA Expression Profile Associated with 5-Fluorouracil-Based Chemoradiation Resistance in Colorectal Cancer Cells. 5-Fluorouracil ENST00000539009 RP11-277P12.10 NA NA NA GRCh38_12:10332861-10338292 colorectal cancer C19.9 NA microarray, qPCR etc. cell line (HCT116) down-regulated To validate the microarray results, we randomly selected 6 differentially expressed lncRNAs (TCONS_00026506, ENST00000468960, NR_038990, ENST00000575202, ENST00000539009 and ENST00000544591) between CRR-HCT116 and parental HCT116 cells to confirm their expression levels by qPCR. Changes in lncRNA expression are involved in 5-FU-based CRR in CRC cells. 25921151 2015 Microarray Analysis of Long Non-coding RNA Expression Profile Associated with 5-Fluorouracil-Based Chemoradiation Resistance in Colorectal Cancer Cells. 5-Fluorouracil ENST00000544591 LINC02446 NA ENSG00000256039 NA GRCh38_12:10553363-10558049 colorectal cancer C19.9 NA microarray, qPCR etc. cell line (HCT116) down-regulated To validate the microarray results, we randomly selected 6 differentially expressed lncRNAs (TCONS_00026506, ENST00000468960, NR_038990, ENST00000575202, ENST00000539009 and ENST00000544591) between CRR-HCT116 and parental HCT116 cells to confirm their expression levels by qPCR. Changes in lncRNA expression are involved in 5-FU-based CRR in CRC cells. 25921151 2015 Microarray Analysis of Long Non-coding RNA Expression Profile Associated with 5-Fluorouracil-Based Chemoradiation Resistance in Colorectal Cancer Cells. 5-Fluorouracil ENST00000547547 NA NA NA GRCh38_12:69946543-69947081 colorectal cancer C19.9 NA qPCR, Western blot, RIP cell lines (HCT116 and LoVo) down-regulated Overexpression of ENST00000547547 promoted 5-FU-induced cell apoptosis and reduced the chemoresistance of 5-FU in-vitro.ENST00000547547 was a target of miR-31, miR-31 was upregulated in 5-FU-resistant CRC cells, and knockdown of miR-31 increased the chemosensitivity of 5-FU-resistant CRC cells. ENST00000547547 reduced chemoresistance in 5-FU of 5-FU-resistant CRC cells through competitive binding to miR-31 and has the potential to serve as a therapeutic target in CRC patients. 29115526 2017 The long non-coding RNA ENST00000547547 reduces 5-fluorouracil resistance of colorectal cancer cells via competitive binding to microRNA-31. 5-fluorouracil MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 chronic myeloid leukemia NA M9863/3 qPCR, western blot, RNAi etc. chronic myeloid leukemia tissues, cell lines (KCL22 and K562) down-regulated We found that MEG3 and PTEN expression were downregulated, whereas, MDM2, DNMT1 and miR-21 were up-regulated in the accelerated and blast phases of CML. demethylation drugs might also have potential clinical application in treating CML blast crisis. Due to the effect on MEG3 and miR-21, 5-azacytidine may be a possible new therapeutic option for CML blast crisis 29772439 2018 Long noncoding RNA MEG3 inhibits proliferation of chronic myeloid leukemia cells by sponging microRNA21 5-azacytidine PCGEM1 PCGEM1, LINC00071, NCRNA00071, PCAT9 64002 ENSG00000227418 NR_002769 GRCh38_2:192749845-192776899 prostate cancer C61.9 NA qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay, MTT assay etc. cell lines (LNCaP and CWR22Rv1) up-regulated We show transcriptional regulation of PCGEM1 in response to androgen deprivation by p54/nrb. While ectopic expression of p54/nrb increases, suppression of p54/nrb by RNAi or knockout (KO) reduces PCGEM1. Moreover, rescue experiments indicate that re-expression of p54/nrb in KO cells restores the ability to induce PCGEM1, leading to upregulation of the androgen receptor splice variant AR3 which has been shown to play a role in castration resistance. 27682980 2016 Regulation of PCGEM1 by p54/nrb in prostate cancer. 3,3′-Diindolylmethane (DIM) GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 squamous cell carcinoma NA M8070/3 microarray, qPCR, RNAi, Western blot, Flow cytometry assay etc. skin cancer tissues, cell line (A431) down-regulated The level of GAS5 was increased in MM1-treated cells, and inhibition of lncRNA GAS5 inhibited MM1-induced apoptosis. Conversely, overexpression of lncRNA GAS5 inhibited cell proliferation and promoted cell apoptosis in skin cancer cells. The expression of lncRNA GAS5 in the skin cancer tissues was found to be lower than that in the adjacent normal tissues in a majority of patients. 28252643 2017 2-O-Methylmagnolol upregulates the long non-coding RNA, GAS5, and enhances apoptosis in skin cancer cells. 2-O-Methylmagnolol GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 melanoma NA M8720/3 microarray, qPCR, RNAi, Western blot, Flow cytometry assay etc. skin cancer tissues, cell line (A375) down-regulated The level of GAS5 was increased in MM1-treated cells, and inhibition of lncRNA GAS5 inhibited MM1-induced apoptosis. Conversely, overexpression of lncRNA GAS5 inhibited cell proliferation and promoted cell apoptosis in skin cancer cells. The expression of lncRNA GAS5 in the skin cancer tissues was found to be lower than that in the adjacent normal tissues in a majority of patients. 28252643 2017 2-O-Methylmagnolol upregulates the long non-coding RNA, GAS5, and enhances apoptosis in skin cancer cells. 2-O-Methylmagnolol HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 prostate cancer C61.9 NA qPCR, Western blot, ChIP, Dot blot etc. cell lines (HUVEC, MDA-MB-361, MCF10, MCF7, PC3 etc.) differential expression HOTAIR and MALAT1 were present on pS2, hTERT and HOTAIR promoters at the ERE/eNOS peaks. Interestingly, upon treatment with17B-estradiol HOTAIR recruitment to chromatin increased significantly while that of MALAT1 was reduced, suggesting an opposite regulation and function for these lncRNAs. Similar results were obtained in cells and in an ex vivo prostate organotypic slice cultures. 27922078 2016 MALAT1 and HOTAIR Long Non-Coding RNAs Play Opposite Role in Estrogen-Mediated Transcriptional Regulation in Prostate Cancer Cells. 17b-estradiol SNHG8 SNHG8, LINC00060, NCRNA00060 100093630 ENSG00000269893 NR_003584 GRCh38_4:118278709-118279823 gastric cancer C16 NA RNA-seq, qPCR etc. EBV-associated gastric cancer tissues up-regulated SNHG8 expression in EBVaGC was significantly higher than in EBVnGC and in EBVaGC adjacent tissue. 27835598 2016 SNHG8 is identified as a key regulator of epstein-barr virus(EBV)-associated gastric cancer by an integrative analysis of lncRNA and mRNA expression. 1（SNHG8） SNHG6 SNHG6, HBII-276HG, NCRNA00058, U87HG 641638 ENSG00000245910 NR_002599 GRCh38_8:66921684-66926398 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, RNAi etc. HCC tissues, cell lines (BEL-7402, SMMC-7721, MHCC-97H, SK-Hep-1, Huh7 and HCC-LM3) up-regulated We found that five SNHG6 transcripts were differentially expressed in HCC tissues while only the SNHG6-003 had an oncogenic function.Ectopic expression of SNHG6-003 in HCC cells promoted cell proliferation and induced drug resistance, whereas SNHG6-003 knockdown promoted apoptosis.Moreover, SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-26a/b and thereby modulating the expression of transforming growth factor-B-activated kinase 1 (TAK1).Importantly, expression analysis revealed that both SNHG6-003 and TAK1 were upregulated in human cancers, exhibiting a co-expression pattern. 27530352 2017 The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma. 1（SNHG6-003） SLC6A9-5:2 SLC6A9, GCENSG, GLYT1 NA NA NA NA papillary thyroid cancer NA M8260/3 microarray, qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc. PTC tissues, cell lines (TPC-1 and BCPAP) down-regulated We demonstrated that SLC6A9-5:2 was remarkably downregulated in 131I-resistant thyroid cancer cell lines and 131I-insensitive patients and was positively correlated with Poly (ADP-ribose) polymerase 1 (PARP-1) expression and its activation. After downregulating SLC6A9 or blocking PARP-1 artificially, the sensitive thyroid cancer cells mostly displayed a tolerant phenotype under 131I exposure. Furthermore, SLC6A9-5:2 overexpression was positively correlated with PARP-1 mRNA and protein levels, which restored the sensitivity of resistant thyroid cancer cells. 28086241 2017 LncRNA-SLC6A9-5:2: A potent sensitizer in 131I-resistant papillary thyroid carcinoma with PARP-1 induction. 1（SLC6A9-5:2） RP11-58D2.1 ZBTB20-AS4 100874131 ENSG00000242767 NR_046877 GRCh38_3:115100423-115103061 pancreatic cancer C25 NA microarray, qPCR etc. cell lines (SW1990, SWl990/GZ etc.) up-regulated Six lncRNAs (RP11-58D2.1, lincRNA-ZNF532, AP000221.1, CTC-338M12.5, CR619813, DDX6P) were selected to validate the microarray consistency by using qPCR. The results demonstrated that RP11-58D2.1, lincRNA-ZNF532 and AP000221.1 were upregulated and that CTC-338M12.5, DDX6P and CR619813 were downregulated in the SW1990/GZ cells compared with SW1990 cells. 25755691 2015 Genomic analysis of drug resistant pancreatic cancer cell line by combining long non-coding RNA and mRNA expression profling. 1(pancreatic cancer chemotherapy resistance) PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 gastric cancer C16 NA microarray, qPCR etc. gastric cancer tissues, cell lines (SGC7901) up-regulated PVT1 showed higher expression in human gastric cancer tissues than in adjacent non-cancerous tissues and in SGC7901 paclitaxel-resistant cells compared with SGC7901 cells. PVT1 expression was correlated with lymph node invasion of gastric cancer. 25258543 2014 Expression and clinical significance of the long non-coding RNA PVT1 in human gastric cancer. 1（paclitaxel-resistant） PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 gastric cancer C16 NA qPCR, Western blot etc. gastric cancer tissues, cell lines (BGC823, SGC7901 etc.) up-regulated PVT-1 was highly expressed in gastric cancer tissues of cisplatin-resistant patients and cisplatin-resistant cells.Overexpression of LncRNA PVT1 in gastric carcinoma promotes the development of MDR,suggesting an eficacious target for reversing MDR in gastric cancer therapy. 25956062 2015 Overexpression of long non-coding RNA PVT1 in gastric cancer cells promotes the development of multidrug resistance. 1（multidrug resistance） RP11-137H2.4 RP11-137H2.4, LOC101929574 NA NA NA GRCh38_10:80529597-80535942 childhood acute lymphoblastic leukemia NA M9835/3 qPCR, RNAi, Cell proliferation assay etc. cell lines (Reh, NALM-6) up-regulated Here we report five lncRNAs specifically upregulated in pre-B cALL that had significant impacts on cancer hallmark traits such as cell proliferation, migration, apoptosis, and treatment response. In particular, silencing of the RP11-137H2.4 lncRNA effectively restored normal glucocorticoid (GC) response in a GC-resistant pre-B cALL cell line and specifically modulated expression of members of both the NRAS/BRAF/NF-kB MAPK cascade and cell cycle pathways. 27980230 2017 A childhood acute lymphoblastic leukemia-specific lncRNA implicated in prednisolone resistance, cell proliferation, and migration. 1（GC resistance） RP11-68I18.10 RP11-68I18.10 NA NA NA GRCh38_1:151130075-151131610 childhood acute lymphoblastic leukemia NA M9835/3 qPCR etc. cell lines (Reh, NALM-6) up-regulated We validated that five such lncRNA transcripts overexpressed in pre-B cALL samples (RP11-137H2.4, RP11-68I18.10, AC156455.1, KB-208E9.1, and CTA-331P3.1) were also overexpressed in the Reh and NALM-6 pre-B cALL cell lines that had significant impacts on cancer hallmark traits such as cell proliferation, migration, apoptosis, and treatment response. 27980230 2017 A childhood acute lymphoblastic leukemia-specific lncRNA implicated in prednisolone resistance, cell proliferation, and migration. 1（GC resistance） SOCS2-AS1 NA 144481 ENSG00000246985 NR_038263 GRCh38_12:93542463-93571768 prostate cancer C61.9 NA RNA-seq, qPCR, RIP, ChIP etc. cell lines (LNCaP, LTAD, VCaP) up-regulated we identified an androgen-regulated lncRNA, suppressor of cytokine signaling 2-antisense transcript 1 (SOCS2-AS1), the expression of which was higher in castration-resistant prostate cancer model cells, i.e long-term androgen-deprived (LTAD) cells, than in parental androgen-dependent LNCaP cells. SOCS2-AS1 promoted castration-resistant and androgen-dependent cell growth. We found that SOCS2-AS1 knockdown up-regulated genes related to the apoptosis pathway, including tumor necrosis factor superfamily 10 (TNFSF10), and sensitized prostate cancer cells to docetaxel treatment. 27342777 2016 Androgen-induced Long Noncoding RNA (lncRNA) SOCS2-AS1 Promotes Cell Growth and Inhibits Apoptosis in Prostate Cancer Cells. 1（docetaxel） RP1-179N16.3 RP1-179N16.3 NA NA NA NA nasopharyngeal cancer C11 NA microarray, qPCR, RNAi etc. nasopharyngeal carcinoma tissues, cell lines (CNE-2 etc.) up-regulated qPCR results were consistent with the microarray analysis results of six lncRNAs (AF086415, AK095147, RP1-179N16.3, MUDENG, AK056098, and AK294004) in terms of regulation direction and significance. 24379026 2014 Curcumin enhances the radiosensitivity in nasopharyngeal carcinoma cells involving the reversal of differentially expressed long non-coding RNAs. 1(curcumin) RP3-508I15.14 RP3-508I15.14 NA NA NA GRCh38_22:38739003-38749041 non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. 1（cisplatin-based chemotherapy） PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 malignant pleural mesothelioma NA M9050/3 microarray, qPCR, RNAi etc. MPM tissues, MPM cell lines up-regulated Our results suggest that C-MYC and PVT1 CNG promotes a malignant phenotype of MPM, with C-MYC CNG stimulating cell proliferation and PVT1 both stimulating proliferation and inhibiting apoptosis. 24926545 2014 Frequent coamplification and cooperation between C-MYC and PVT1 oncogenes promote malignant pleural mesothelioma. 1（cisplatin） RP11-134G8.8 RP11-134G8.10 NA NA NA GRCh38_1:201464383-201465146 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, Flow cytometry assay etc. cell line (HepG2) up-regulated After 12, 24 and 48 h of incubation, cisplatin significantly decreased the RP1-193H18.2 level by 2.75, 2.11 and 2.06-fold, respectively. RP11-134G8.8 expression increased by 1.77-2.13-fold, and the RP11-363E7.4 level was also upregulated by 1.89-2.94-fold. These trends in lncRNA expression are consistent with the microarray results. 28105167 2016 Cisplatin induces HepG2 cell cycle arrest through targeting specific long noncoding RNAs and the p53 signaling pathway. 1（Cisplatin） RP11-363E7.4 RP11-363E7.4 NA NA NA GRCh38_9:19453209-19455173 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, Flow cytometry assay etc. cell line (HepG2) up-regulated After 12, 24 and 48 h of incubation, cisplatin significantly decreased the RP1-193H18.2 level by 2.75, 2.11 and 2.06-fold, respectively. RP11-134G8.8 expression increased by 1.77-2.13-fold, and the RP11-363E7.4 level was also upregulated by 1.89-2.94-fold. These trends in lncRNA expression are consistent with the microarray results. 28105167 2016 Cisplatin induces HepG2 cell cycle arrest through targeting specific long noncoding RNAs and the p53 signaling pathway. 1（Cisplatin） RP1-193H18.2 RP1-193H18.2 NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR, Flow cytometry assay etc. cell line (HepG2) down-regulated After 12, 24 and 48 h of incubation, cisplatin significantly decreased the RP1-193H18.2 level by 2.75, 2.11 and 2.06-fold, respectively. RP11-134G8.8 expression increased by 1.77-2.13-fold, and the RP11-363E7.4 level was also upregulated by 1.89-2.94-fold. These trends in lncRNA expression are consistent with the microarray results. 28105167 2016 Cisplatin induces HepG2 cell cycle arrest through targeting specific long noncoding RNAs and the p53 signaling pathway. 1（Cisplatin） PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 cervical cancer C53 NA qPCR, RNAi, Western blot, Cell proliferation assay etc. cell lines (SiHa, HeLa, DoTc2 4510) up-regulated Our results demonstrate that PVT1 expression is significantly increased in ICC tissue versus normal cervix and that higher expression of PVT1 correlates with poorer overall survival. In cervical cancer cell lines, PVT1 knockdown resulted in significantly decreased cell proliferation, migration and invasion, while apoptosis and cisplatin cytotoxicity were significantly increased in these cells. Finally, we show that PVT1 expression is augmented in response to hypoxia and immune response stimulation and that this lncRNA associates with the multifunctional and stress-responsive protein, Nucleolin. 27232880 2016 The lncRNA PVT1 Contributes to the Cervical Cancer Phenotype and Associates with Poor Patient Prognosis. 1（cisplatin resistance） SLC25A25-AS1 SLC25A25-AS1 100289019 ENSG00000234771 NR_033374 GRCh38_9:128108581-128118693 colorectal cancer C19.9 NA qPCR, RNAi, Western blot etc. CRC tissues, cell lines (HCT-116 and HT-29) down-regulated We demonstrated that the expression of SLC25A25-AS1, which has not been reported previously, was significantly decreased in both the tumor tissues (27 out of 30) and serum of CRC patients. SLC25A25-AS1 overexpression significantly inhibited proliferation and colony formation in colorectal cancer cell lines, and downregulation of SLC25A25-AS1 obviously enhanced chemoresistance and promoted EMT process in vitro associated with Erk and p38 signaling pathway activation. 27553025 2016 Decreased expression of LncRNA SLC25A25-AS1 promotes proliferation, chemoresistance, and EMT in colorectal cancer cells. 1（chemoresistance） snaR SNAR-A1, SNAR-A53113498 NA NA NA GRCh19:47918429-47918550 colon cancer C18 NA qPCR etc. cell lines (SNU-C4R, SNU-C5R etc.) down-regulated We selected three lncRNAs, snaR, BACE1AS, and PRAS, and we detected their expression by RT-qPCR using specific primer sets. SnaR and BACE1AS were significantly down-regulated in both resistant cell lines (SNU-C4R and SNU-C5R), whereas PRAS was down-regulated in SNU-C4R cells but not in SNU-C5R cells. Down-regulation of snaR decreased cell death after 5-FU treatment, which indicates that snaR loss decreases in vitro sensitivity to 5-FU. 25078450 2014 A long non-coding RNA snaR contributes to 5-fluorouracil resistance in human colon cancer cells. 1（5-FU-resistant） PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 ovarian cancer C56.9 NA qPCR, Western blot etc. ovarian cancer tissues, cell lines (SKOV-3/DDP, A2780/DDP, A2780 and A2780/DDP) up-regulated Overexpression of PVT1 has been demonstrated in ovarian cancer. The mRNA level of PVT1 in ovarian cancer tissues of cisplatin-resistant patients and cisplatin-sensitive patients, cisplatin-resistant cells SKOV-3/DDP and A2780/DDP, cisplatin-sensitive cells SKOV-3 and A2780 were determined by qRT-PCR. 26884974 2015 Overexpression of long non-coding RNA PVT1 in ovarian cancer cells promotes cisplatin resistance by regulating apoptotic pathways 1（ Cisplatin） RRP1B RRP1B, KIAA0179, NNP1L, Nnp1, PPP1R136, RRP1 NA ENSG00000160208 NA GRCh38_21:43659548-43696079 laryngeal squamous cell cancer C32.3 NA qPCR etc. LSCC tissues down-regulated We discovered that five lncRNAs were differentially expressed between primary LSCC samples and adjacent normal tissues. Among them, three lncRNAs were up-expressed in tumor specimens, including CDKN2B-AS1, HOTAIR and MALAT1. More, two lncRNAs had significant down-expression, which were lncRNA RRP1B and SRA1. Cisplatin and paclitaxel have target function on significant lncRNAs in LSCC, which presents novel molecular targets to cure LSCC patients and also leads an orientation for developing new drugs. 25257554 2014 Cisplatin and paclitaxel target significant long noncoding RNAs in laryngeal squamous cell carcinoma. 1（ cisplatin and paclitaxel） lncRNA-PRAL PRAL, lncRNA-PRAL 109245082 ENSG00000279296 NA GRCh38_17:6772831-6776116 multiple myeloma C42.1 M9732/3 qPCR, Western blot, Flow cytometry, etc. cell lines (NCI-H929, ARH77, PRMI8226, OPM2, JJN3) down-regulated Survival curves showed that MM patients with low PRAL expression had a significantly shorter disease-free survival (DFS) and overall survival (OS) than the patients with high PRAL expression. We further identified and confirmed that miR-210 was the target of PRAL, and miR-210 overexpression overturned the potentiation effect of PRAL on BTZ efficacy. bone morphogenetic protein 2 (BMP2) was confirmed to be the target of miR-210. 29944867 2018 LncRNA PRAL is closely related to clinical prognosis of multiple myeloma and the bortezomib sensitivity. Bortezomib ADARB2-AS1 NA 642394 ENSG00000205696 NR_033387 GRCh38_10:1526637-1556984 Intraductal Papillary Mucinous Neoplasms of the Pancreas C25 M8453/0 qPCR etc. blood differential expression We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification. PVT1 has been shown to be upregulated in PDAC tissues, to be correlated with clinical stage and poor survival, to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study. 28874676 2017 Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas. 1 AF251187 NA NA NA NA GRCh38_2:168846243-168846834 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 AK123408 NA NA NA NA GRCh38_9:5832649-5835435 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) down-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 AK127565 LINC00683 NA ENSG00000266256 NA GRCh38_18:76615212-76625940 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 AL832444 NA NA NA NA GRCh38_8:123523808-123525468 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) down-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 AL833160 NA NA NA NA GRCh38_8:22679015-22684009 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 Intraductal Papillary Mucinous Neoplasms of the Pancreas C25 M8453/0 qPCR,etc. blood differential expression We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study. 28874676 2017 Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas. 1 BALR-2 NA NA NA NA NA B cell acute lymphoblastic leukemia NA M9826/3 microarray, qPCR etc. blood (mononuclear cells) up-regulated Importantly, high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. BALR-2 plays a functional role in the pathogenesis and/or clinical responsiveness of B-ALL and that altering the levels of particular lncRNAs may provide a future diretcion for therapeutic development. 25681502 2015 LncRNA Expression Discriminates Karyotype and Predicts Survival in B-lymphoblastic Leukemia. 1 BALR-2 NA NA NA NA NA B-lymphoblastic leukemia NA M9811/3 microarray, qPCR, Western blot etc. blood, cell line (HEK 293T) differential expression high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. In line with a function for this lncRNA in regulating cell survival, BALR-2 knockdown led to reduced proliferation, increased apoptosis, and increased sensitivity to prednisolone treatment. Conversely, overexpression of BALR-2 led to increased cell growth and resistance to prednisone treatment. Interestingly, BALR-2 expression was repressed by prednisolone treatment and its knockdown led to upregulation of the glucocorticoid response pathway in both human and mouse B-cells 25681502 2015 LncRNA Expression Discriminates Karyotype and Predicts Survival in B-Lymphoblastic Leukemia 1 BC016787 DEPDC1-AS1 NA ENSG00000234264 NA GRCh38_1:68496676-68538627 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 BC036599 GUCY1A2, GC-SA2, GUC1A2 NA NA NA GRCh38_11:106674027-106676271 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) down-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 BC038366 LINC02158 729083 ENSG00000225611 NR_122070 GRCh38_3:42770612-42773635 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 BC038580 LINC01293 NA ENSG00000230836 NA GRCh38_2:74940258-74942670 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 BC039678 LOC101928047 NA NA NA GRCh38_6:6724886-6725300 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 BC040572 NA NA NA NA GRCh38_8:90646441-90646633 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) up-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 BC040587 LINC00901, LSAMP-AS4, TCONS_00005428 100506724 ENSG00000242385 NR_121607 GRCh38_3:116921431-116932238 osteosarcoma NA M9180/3 microarray, qPCR, FISH etc. osteosarcoma tissues, cell lines (U2OS, SAOS-2, HOS etc.) down-regulated The osteo3q13.31 genes LOC285194, BC040587, and LSAMP commonly show loss of expression in primary osteosarcoma samples and cell lines. Depleting either LSAMP or LOC285194 promoted proliferation of normal osteoblasts by regulation of apoptotic and cell-cycle transcripts and also VEGF receptor 1. Moreover, genetic deletions of LOC285194 or BC040587 were also associated with poor survival of osteosarcoma patients. 20048075 2010 Recurrent focal copy-number changes and loss of heterozygosity implicate two noncoding RNAs and one tumor suppressor gene at chromosome 3q13.31 in osteosarcoma. 1 BC041455 LINC01671 101928233 ENSG00000225431 NR_131192 GRCh38_21:42599280-42615058 breast cancer C50 NA microarray, qPCR, RNAi, Western blot etc. cell lines (MCF-7 and T-47D) down-regulated From these 127 DE lncRNAs, we selected the top 25 most significant genes for further validation and analysis (electronic supplementary material, table S2). For 23 out of 25 (92%) of the lncRNAs tested, quantitative real-time PCR (qRTPCR) on cDNA templates confirmed the microarray results. Overexpression of BC041455 prevented ERK1/2 phosphorylation. The effects of BC041455 on hormone-dependent MAPK signalling were observed in both MCF-7 and T-47D cells. 28003470 2016 Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells. 1 BOKAS BOK-AS1, BOK-AS, BOKAS, NAToB, NCRNA00151 NA NA NA NA esophageal squamous cell cancer NA NA qPCR, Western blot, RIP etc. ESCC tissues up-regulated LncRNA BOKAS was up-regulated following radiation and promoted WISP1 expression and resultant radioresistance.WISP1 facilitated its own expression in response to radiation, creating a positive feedback loop and increased radioresistance. Our study revealed WISP1 as a potential target to overcome radioresistance in ESCC. 25749038 2015 Targeting WISP1 to sensitize esophageal squamous cell carcinoma to irradiation. 1 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 colorectal cancer C19.9 NA qPCR etc. CRC tissues up-regulated The expression of CCAT1, CCAT1-L, CCAT2, PVT1, and CASC19 were elevated in cancer tissues. Among these, high expression of CCAT1 and CCAT2 was significantly associated with poor RFS (P=0.049 and 0.022, respectively) and OS (P=0.028 and 0.015, respectively). These results were validated in an independent patient cohort, in which combined expression of CCAT1 and CCAT2 expression was significantly associated with a poor RFS (HR:2.60, 95% confidence interval [CI]: 1.04-6.06, P=0.042) and a poor OS (HR:8.38, 95%CI: 2.68-37.0,<0.001).High expression of CCAT1 and CCAT2 significantly associates with poor RFS and OS. The expression of these two lncRNAs independently, or in combination, serves as important prognostic biomarkers in CRC. 28838211 2017 CCAT1 and CCAT2 long noncoding RNAs, located within the 8q.24.21 ‘gene desert’, serve as important prognostic biomarkers in colorectal cancer 1 CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 colorectal cancer C19.9 NA qPCR etc. CRC tissue up-regulated The expression of CCAT1, CCAT1-L, CCAT2, PVT1, and CASC19 were elevated in cancer tissues. Among these, high expression of CCAT1 and CCAT2 was significantly associated with poor RFS (P=0.049 and 0.022, respectively) and OS. 28838211 2017 CCAT1 and CCAT2 long noncoding RNAs, located within the 8q.24.21 ‘gene desert’, serve as important prognostic biomarkers in colorectal cancer 1 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 myeloid leukemia NA M9860/3 qPCR, luciferase reporter assay etc. cell line (PBMCs) up-regulated Meanwhile, GAS5 is downregulated in breast cancer cells.Survival analysis indicated that GAS5 rs55829688 (T > C) was significantly associated with prognosis of AML (p=0.018).Patients with rs55829688 CC genotype showed higher GAS5 expression in peripheral blood mononuclear cells (PBMCs) (p=0.025) and harbored a longer platelets recovery (p=0.040) than carriers of rs55829688T allele. In conclusion, rs55829688 polymorphism could increase GAS5 expression by interacting with TP63, which might aggravate the myelosuppression and in turn lead to poor prognosis in AML. GAS5 is observed to be a key mediator of glucocorticoids (GCs) resistance rather than a growth arrest-specific transcript in PBMCs. 27951730 2017 Long non-coding RNA GAS5 polymorphism predicts a poor prognosis of acute myeloid leukemia in Chinese patients via affecting hematopoietic reconstitution. 1 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA qPCR etc. cell lines (MCF7, SKBR3, MDA-MB231) down-regulated GAS5 down-regulation can suppress many aspects of DNC anti-cancer effects in breast cancer cells, it seems that co-treatment with DNC and GAS5 over-expression may provide a clinically useful tool for drug-resistance breast cancer cells. 29655698 2018 Down-regulation of lncRNA, GAS5 decreases chemotherapeutic effect of dendrosomal curcumin (DNC) in breast cancer cells. 1 GLIS3-AS1 NA 84850 ENSG00000237009 NR_026663 GRCh38_9:3898642-3901248 Intraductal Papillary Mucinous Neoplasms of the Pancreas C25 M8453/0 qPCR etc. blood differential expression We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study. 28874676 2017 Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot Cell lines (HepG2, SMMC-7721, Hep3B, Huh7, Bel-7402 cells) up-regulated Our research reveals a novel relationship between HOTAIR and glucose metabolism in HCC cells, and it may be a therapeutic target for diagnosing and treating HCC. For example, lncRNAs correlate with tumor cell apoptosis, metastasis, drug resistance and autophagy (12). HOTAIR expression levels were significantly positively correlated with hepatocellular carcinoma (HCC) recurrence and metastasis and with the overall survival time of patients with HCC. 28731193 2017 Promotion of glycolysis by HOTAIR through GLUT1 upregulation via mTOR signaling. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 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 1 HOTTIP HOTTIP, HOXA-AS6, HOXA13-AS1, NCRNA00213 100316868 ENSG00000243766 NR_037843 GRCh38_7:27198575-27207259 gastric cancer C16 NA qPCR, RNAi, Western blot etc. cell line (CS12) differential expression Concurrent regulation of HoxA13-HOTTIP was mediated by the mixed lineage leukemia-WD repeat domain 5 complex, which caused the trimethylation of H3K4 and then stimulated cell proliferation. HoxA13 transactivated the IGFBP-3 promoter through the HOX-binding site. Activation of IGFBP-3 stimulated the oncogenic potential and invasion activity. Increased expression of HoxA13 (63.2%) and IGFBP-3 (28.6%) was detected in human gastric cancer tissues and was found in the gastric cancer data of The Cancer Genome Atlas 27144338 2016 Oncogenic function of the homeobox A13-long noncoding RNA HOTTIP-insulin growth factor-binding protein 3 axis in human gastric cancer 1 HOXD-AS1 HAGLR, HOXD-AS1, Mdgt 401022 ENSG00000224189 NR_033979 GRCh38_2:176164051-176188958 prostate cancer C61.9 NA Microarray Analysis, western blot, RNAi, GhIP etc. cell lines (LNCaP and PC-3) up-regulated we discovered that an lncRNA HOXD-AS1 is highly expressed in CRPC cells and correlated closely with Gleason score, T stage, lymph nodes metastasis, and progression-free survival. Knockdown of HOXD-AS1 inhibited the proliferation and chemo-resistance of CRPC cells in vitro and in vivo. Furthermore, we identified several cell cycle, chemo-resistance, and castration-resistance- related genes, including PLK1, AURKA, CDC25C, FOXM1, and UBE2C, that were activated transcriptionally by HOXD-AS1. Further investigation revealed that HOXD-AS1 recruited WDR5 to directly regulate the expression of target genes by mediating histone H3 lysine 4 tri-methylation (H3K4me3). In conclusion, our finndings indicate that HOXD-AS1 promotes proliferation, castration resistance, and chemo-resistance in prostate cancer by recruiting WDR5. This sheds a new insight into the regulation of CRPC by lncRNA and provides a poten-tial approach for the treatment of CRPC. 28487115 2017 lncRNA HOXD-AS1 Regulates Proliferation and Chemo-Resistance of Castration-Resistant Prostate Cancer via Recruiting WDR5 1 KB-208E9.1 KB-208E9.1 NA NA NA GRCh38_22:23580880-23583859 childhood acute lymphoblastic leukemia NA M9835/3 qPCR etc. cell lines (Reh, NALM-6) up-regulated We validated that five such lncRNA transcripts overexpressed in pre-B cALL samples (RP11-137H2.4, RP11-68I18.10, AC156455.1, KB-208E9.1, and CTA-331P3.1) were also overexpressed in the Reh and NALM-6 pre-B cALL cell lines that had significant impacts on cancer hallmark traits such as cell proliferation, migration, apoptosis, and treatment response. 27980230 2017 A childhood acute lymphoblastic leukemia-specific lncRNA implicated in prednisolone resistance, cell proliferation, and migration. 1 LINC00472 LINC00472, C6orf155 79940 ENSG00000233237 NR_121612 GRCh38_6:71344344-71420769 Intraductal Papillary Mucinous Neoplasms of the Pancreas C25 M8453/0 qPCR etc. blood differential expression We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study. 28874676 2017 Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas. 1 linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 colon cancer C18 NA qPCR, Western blot, luciferase reporter assay etc. cell lines (HB56, HB96,TSCC, Tca8113, SCC-9 and CAL27, HEK-293T), Oral cancer tissues up-regulated LincRNA-ROR was frequently up-regulated and inversely correlated with miR-145 down-regulation in the colon cancer specimens. The levels of CD44, CD133, Oct4, Sox2, Nanog, lincRNA-ROR in CD44(+) CD133(+) cells were significantly increased,while miR-145 was decreased compared with CD44(-)CD133(-)cells(P<0.05). The levels of CD44,CD133,lnc-ROR in CD44(+) CD133(+) cells were significantly reduced upon cell adherence, while miR-145 was significantly increased. Bioinformatics analysis revealed that lincRNA-ROR shared miRNA response elements with core transcription factors Oct4,Sox2 and Nanog. MiR-145 significantly inhibited the expression of lincRNA-ROR, Oct4, Sox2 and Nanog. Silencing lincRNA-ROR significantly inhibited colon cancer stem cells proliferation and increased the sensitivity to chemotherapy. Linc-ROR functions as a key ceRNA to prevent core TFs,e.g.Oct4, Sox2, Nanog, from miR-145-mediated suppression in colon cancer stem cells and regulates cell proliferation and chemosensitivity. 29690669 2018 LincRNA-ROR functions as a ceRNA to regulate Oct4, Sox2, and Nanog expression by sponging miR-145 and its effect on biologic characteristics of colonic cancer stem cells 1 linc-ROR LINC-ROR, ROR, lincRNA-RoR 100885779 ENSG00000258609 NR_048536 GRCh38_18:57054558-57072119 breast cancer C50 NA qPCR breast cancer cell lines, breast cancer tissues and plasma up-regulated Among lncRNAs, large intergenic non-coding RNA regulator of reprogramming (lincRNA-ROR or linc-ROR) is a member of subvariety of lncRNAs, was first discovered in induced pluripotent stem cells (iPSCs), and plays a central role in promoting survival in iPSCs and embryonic stem cells (ESCs) through preventing the activation of cellular stress pathways.And linc-ROR also acts as a ceRNA to increase stemness gene Nanog expression by sponging miR-145 in cancer cells. 28869448 2017 Large intergenic non-coding RNA-ROR as a potential biomarker for the diagnosis and dynamic monitoring of breast cancer 1 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assays etc. cell lines (U251 and U87) up-regulated MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101. The present study elucidates a novel MALAT1-miR-101-Rap1B regulatory axis in glioma, contributing to a better understanding of the glioma pathogenesis and providing a promising therapeutic target for glioma patients. MALAT1 was found to be upregulated in glioma tissues and correlated with the progression of glioma.Although enormous efforts have been made to improve therapeutic strategies, the mortality of malignant glioma remains high and the median survival is less than 14 months. At present, the main treatment methods of glioma include surgical techniques, radiotherapy and chemotherapy, however, these traditional treatments obtain a poor prognosis due to the highly invasive nature and resistance to radiation and chemotherapy of glioma. 28551849 2017 Long non-coding RNA MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101. 1 MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, Luciferase report assay etc. PDAC tissues, cell lines (Panc-1, Aspc-1, Mia Paca-2 and Bxpc-3) up-regulated MALAT1 is expressed at higher levels in pancreatic ductal adenocarcinoma (PDAC) tissues than in nontumour tissues and in metastatic PDAC than in localized tumours. Plasma levels of MALAT1-derived fragments are significantly elevated in patients with prostate cancer compared with those without prostate cance. MALAT1 regulates KRAS expression by influencing the spatial distribution of miR-217. MALAT1 inhibits the translocation of miR-217 from the nucleus to the cytoplasm. Patients with PDAC and high MALAT1 expression levels have shorter overall survival than patients with PDAC and low MALAT1 expression levels. Resistance to KRAS inhibition has been observed experimentally in studies regarding pancreatic cancer treatment34; thus, targeting MALAT1 may be another way to achieve KRAS/MAPK pathway inactivation. 28701723 2017 The lncRNA MALAT1 acts as a competing endogenous RNA to regulate KRAS expression by sponging miR-217 in pancreatic ductal adenocarcinoma. 1 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 Intraductal Papillary Mucinous Neoplasms of the Pancreas C25 M8453/0 qPCR etc. blood differential expression We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study. 28874676 2017 Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas. 1 MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 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. 1 NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 leukemia NA M9800/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. blood, cell lines (K562, THP-1, HL-60, Jurkat) down-regulated NEAT1 messenger RNA (mRNA) expression levels were significantly downregulated in leukemia patient samples compared with those from healthy donors. Furthermore, NEAT1 mRNA expression was repressed in a number of leukemia cell lines, including K562, THP-1, HL-60 and Jurkat cells, compared with peripheral white blood control cells, consistent with the expression observed in patients with leukemia. In addition, the transfection of a NEAT1 overexpression plasmid into K562 and THP-1 leukemia cell lines alleviated MDR induced by cytotoxic agents, such as Alisertib and Bortezomib, through inhibition of ATP-binding cassette G2. 27446393 2016 Overexpression of lncRNA NEAT1 mitigates multidrug resistance by inhibiting ABCG2 in leukemia. 1 PANDAR PANDAR, PANDA 101154753 ENSG00000281450 NR_109836 GRCh38_6:36673621-36675126 Intraductal Papillary Mucinous Neoplasms of the Pancreas C25 M8453/0 qPCR etc. blood differential expression We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study. 28874676 2017 Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas. 1 PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 Intraductal Papillary Mucinous Neoplasms of the Pancreas C25 M8453/0 qPCR etc. blood differential expression We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study. 28874676 2017 Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas. 1 SNHG15 SNHG15, C7orf40, Linc-Myo1g, MYO1GUT 285958 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-kB 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-kB signaling pathway. 1 TUG1 TUG1, LINC00080, NCRNA00080, TI-227H 55000 ENSG00000253352 NR_002323 GRCh38_22:30969245-30979395 bladder urothelial cancer NA M8120/3 qPCR, Western blot, Luciferase assay etc. Human BUC T24 cell lines, BUC tissues up-Regulated In conclusion, up-regulation of lncRNA TUG1 was related with the poor response of BUC patients to Dox chemotherapy, knockdown of TUG1 inhibited the Dox resistance of BUC cells via Wnt/B-catenin pathway. These findings might assist in the discovery of novel potential diagnostic and therapeutic target for BUC, thereby improve the effects of clinical treatment in patients. 29179467 2017 Knockdown of long non-coding RNA Taurine Up-Regulated 1 inhibited doxorubicin resistance of bladder urothelial carcinoma via Wnt/B-catenin pathway. 1 UCA1 UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 652995 ENSG00000214049 NR_015379 GRCh38_19:15828206-15836326 Intraductal Papillary Mucinous Neoplasms of the Pancreas C25 M8453/0 qPCR etc. blood differential expression We hypothesized that circulating long non-coding RNAs (lncRNAs) may act as diagnostic markers of incidentally-detected cystic PDAC precursors known as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological classification.PVT1 has been shown to be upregulated in PDAC tissues,to be correlated with clinical stage and poor survival,to be overexpressed in the saliva of PDAC cases versus healthy controls, and to contribute to susceptibility to PDAC as part of a genome-wide association study. 28874676 2017 Linc-ing Circulating Long Non-coding RNAs to the Diagnosis and Malignant Prediction of Intraductal Papillary Mucinous Neoplasms of the Pancreas. 1 AB019562 NA NA NA NA NA hypopharyngeal squamous cell carcinoma C13 M8070/3 microarray, qPCR etc. primary HSCC tissues up-regulated AB209630 expression was significantly lower in carcinomas than in adjacent nontumor tissues. AB019562 expression was significantly higher in carcinomas than in adjacent nontumor tissues. 26131061 2015 Gene microarray analysis of lncRNA and mRNA expression profiles in patients with hypopharyngeal squamous cell carcinoma. 1 AB209630 NA NA NA NA GRCh38_9:69248696-69251364 hypopharyngeal squamous cell carcinoma C13 M8070/3 microarray, qPCR etc. primary HSCC tissues down-regulated AB209630 expression was significantly lower in carcinomas than in adjacent nontumor tissues. AB019562 expression was significantly higher in carcinomas than in adjacent nontumor tissues. 26131061 2015 Gene microarray analysis of lncRNA and mRNA expression profiles in patients with hypopharyngeal squamous cell carcinoma. 1 AC005550.4 MEOX2, GAX, MOX2, MEOX2-AS1 101927524 ENSG00000229108 NR_110094 GRCh38_7:15688378-15695491 urothelial cancer NA M8120/3 microarray, qPCR etc. urothelial cancer tissues down-regulated We randomly chose five differentially expressed lncRNAs and determined their expression levels by RT-PCR in the six pairs of UC and corresponding normal urothelial tissues in RTx recipients. The fold changes were also similar to those of microarray results. 27448299 2016 Profiling of mRNA and long non-coding RNA of urothelial cancer in recipients after renal transplantation. 1 AC023115.3 NA 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-GSK3B-Mcl1 signalling. 28499919 2017 Long non-coding RNA AC023115.3 suppresses chemoresistance of glioblastoma by reducing autophagy 1 AC090952.4.1 RHBDF1P1 NA ENSG00000234123 NA GRCh38_3:14572852-14574792 non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. 1 AC156455.1 AC156455.1, LOC100506691 NA ENSG00000256546 NA GRCh38_12:122063306-122068616 childhood acute lymphoblastic leukemia NA M9835/3 qPCR etc. cell lines (Reh, NALM-6) up-regulated We validated that five such lncRNA transcripts overexpressed in pre-B cALL samples (RP11-137H2.4, RP11-68I18.10, AC156455.1, KB-208E9.1, and CTA-331P3.1) were also overexpressed in the Reh and NALM-6 pre-B cALL cell lines that had significant impacts on cancer hallmark traits such as cell proliferation, migration, apoptosis, and treatment response. 27980230 2017 A childhood acute lymphoblastic leukemia-specific lncRNA implicated in prednisolone resistance, cell proliferation, and migration. 1 AF268386 DDR2, MIG20a, NTRKR3, TKT, TYRO10, uc001gch.1 NA NA NA GRCh38_1:162785489-162786465 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). 1 AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, Flow cytometry assay etc. HCC cell lines (SMCC7721 and HepG2) up-regulated We found that increased expression of AFAP1-AS1 was significantly correlated with pathological staging and lymph-vascular space invasion (LVSI) in HCC patients. Multivariate analyses indicated that AFAP1-AS1 represented an independent predictor for overall survival of HCC. Further experiments showed that knockdown of AFAP1-AS1 by si-AFAP1-AS1 decreased the proliferation and invasion in vitro and in vivo, induced cell apoptosis and blocked cell cycle in S phase via inhibition of the RhoA/Rac2 signaling 26892468 2016 Long noncoding RNA AFAP1-AS1 indicates a poor prognosis of hepatocellular carcinoma and promotes cell proliferation and invasion via upregulation of the RhoA/Rac2 signaling 1 AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 esophageal squamous cell cancer NA NA qPCR, MTT assay etc. ESCC tissues, cell lines (KYSE30, KYSE70, KYSE150, KYSE450, KYSE510, and TE10) up-regulated Three lncRNAs (AFAP1-AS1, UCA1, HOTAIR) were found to be deregulated in cisplatin-resistant cells compared with their parent cells. AFAP1-AS1 was significantly up-regulated in tumor tissues compared with adjacent normal tissues. Furthermore, overexpression of AFAP1-AS1 was closely associated with lymph node metastasis, distant metastasis, advanced clinical stage, and response to dCRT. 26756568 2016 High expression of long non-coding RNA AFAP1-AS1 predicts chemoradioresistance and poor prognosis in patients with esophageal squamous cell carcinoma treated with definitive chemoradiotherapy. 1 AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 laryngeal squamous cell cancer C32.3 NA qPCR,Luciferase reporter assay,Western blot,etc. laryngeal specimens and normal tissues up-regulated Taken together,these results suggest that, AFAP1-AS1 can serve as a prognostic biomarker in laryngeal carcinoma and that, miR-320a has the potential to improve standard therapeutic approaches to the disease, especially for cases in which cancer cell stemness and drug resistance. 29971915 2018 Long non-coding RNA AFAP1-AS1/miR-320a/RBPJ axis regulates laryngeal carcinoma cell stemness and chemoresistance. 1 AFAP1-AS1 AFAP1-AS1, AFAP1-AS, AFAP1AS, LOC84740 84740 ENSG00000272620 NR_026892 GRCh38_4:7754090-7778928 non small cell lung cancer C34 M8046/3 qPCR, etc. lung cancer tissues, normal tissues. up-regulated In conclusion, it was demonstrated that lncRNA AFAP1?AS1 is overexpressed in NSCLC and an unfavorable biomarker for patients with NSCLC. Upregulation of HOTAIR in lung tumor tissues is associated with metastasis, drug resistance and poor survival time in patients with lung cancer. 29963138 2018 Long noncoding RNA AFAP1-AS1 is upregulated in NSCLC and associated with lymph node metastasis and poor prognosis. 1 AK022798 C1orf74, URLC4, FLJ25078 148304 ENSG00000162757 NA GRCh38_1:209779208-209784559 gastric cancer C16 NA qPCR, Western blot etc. cell lines (SGC7901, BGC823, SGC7901/DDP, BGC823/DDP etc.) up-regulated The expression of lncRNA AK022798 was significantly higher in all pcDNA3-Notch 1 plasmid treatment groups than in the pcDNA3 plasmid treatment group. Overexpression of lncRNA AK022798 promotes SGC7901/DDP and BGC823/DDP cells apoptosis.the expression of MRP1 and P-glycoprotein decreased significantly in SGC7901/DDP and BGC823/DDP cells, and their apoptosis as well as the expressions of caspase 3 and caspase 8. 25763542 2015 Notch 1 promotes cisplatin-resistant gastric cancer formation by upregulating lncRNA AK022798 expression. 1 AK054908 SNORA17B, ACA43, SNORA43 677824 ENSG00000276161 NA GRCh38_9:136726105-136726234 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). 1 AK056988 NA NA NA NA GRCh38_11:114060305-114061539 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues down-regulated The results showed that BC017743, ENST00000395084, NR_026591, NR_015378 and NR_024284 were up-regulated and NR_027151, AK056988 and uc003yqb.1 were down-regulated in HCC samples compared with adjacent NT samples. 25025236 2014 The long noncoding RNA expression profile of hepatocellular carcinoma identified by microarray analysis. 1 AK096725 LBX2-AS1 151534 ENSG00000257702 NR_024606 GRCh38_2:74502595-74504678 renal cell carcinoma C64.9 NA microarray, qPCR etc. RCC tissues up-regulated We chose the lncRNAs AK096725 (upregulated) and ENST00000453068 (downregulated) to confirm their differential expression levels in 70 paired RCC tissues and adjacent non-tumor tissues. Levels of AK096725 were significantly greater in RCC tissues while those of ENST00000453068 was significantly lower compared to the non-tumor tissues. These results are consistent with the microarray data. 24905231 2014 Expression pattern of long non-coding RNAs in renal cell carcinoma revealed by microarray. 1 AK123263 LOC100506974 NA NA NA GRCh38_17:13776832-13777349 non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. 1 AK126698 NA NA NA NA NA non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. 1 AK129685 NA NA NA NA GRCh38_19:13837806-13840186 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). 1 AK130275 PAX8-AS1 654433 ENSG00000189223 NR_015377 GRCh38_2:113211522-113276581 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). 1 AK130977 NA NA NA NA GRCh38_20:36550794-36551444 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). 1 ANRASSF1 RASSF1-AS1, ANRASSF1 102060282 ENSG00000281358 NR_109831 GRCh38_3:50337511-50338300 prostate cancer C61.9 NA RNA-seq, qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. cell lines (HeLa, MDA-MB-231, LNCaP and MCF-8) up-regulated ANRASSF1 endogenous expression is higher in breast and prostate tumor cell lines compared with non-tumor, and an opposite pattern is observed for RASSF1A. ANRASSF1 ectopic overexpression reduces RASSF1A abundance and increases the proliferation of HeLa cells, whereas ANRASSF1 silencing causes the opposite effects. These changes in ANRASSF1 levels do not affect the RASSF1C isoform abundance. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region. 23990798 2013 The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation. 1 ANRASSF1 RASSF1-AS1, ANRASSF1 102060282 ENSG00000281358 NR_109831 GRCh38_3:50337511-50338300 cervical cancer C53 NA RNA-seq, qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. cell lines (HeLa, MDA-MB-231, LNCaP and MCF-9) differential expression Overexpression of ANRASSF1 increases the cell proliferation rate and decreases cell death. 23990798 2013 The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation. 1 ANRASSF1 RASSF1-AS1, ANRASSF1 102060282 ENSG00000281358 NR_109831 GRCh38_3:50337511-50338300 breast cancer C50 NA RNA-seq, qPCR, RNAi, Western blot, RIP, ChIP, Cell proliferation assay etc. cell lines (HeLa, MDA-MB-231, LNCaP and MCF-7) up-regulated ANRASSF1 endogenous expression is higher in breast and prostate tumor cell lines compared with non-tumor, and an opposite pattern is observed for RASSF1A. ANRASSF1 ectopic overexpression reduces RASSF1A abundance and increases the proliferation of HeLa cells, whereas ANRASSF1 silencing causes the opposite effects. These changes in ANRASSF1 levels do not affect the RASSF1C isoform abundance. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region. 23990798 2013 The intronic long noncoding RNA ANRASSF1 recruits PRC2 to the RASSF1A promoter, reducing the expression of RASSF1A and increasing cell proliferation. 1 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 laryngeal squamous cell cancer C32.3 NA qPCR etc. LSCC tissues up-regulated We discovered that five lncRNAs were differentially expressed between primary LSCC samples and adjacent normal tissues. Among them, three lncRNAs were up-expressed in tumor specimens, including CDKN2B-AS1, HOTAIR and MALAT1. More, two lncRNAs had significant down-expression, which were lncRNA RRP1B and SRA1. Cisplatin and paclitaxel have target function on significant lncRNAs in LSCC, which presents novel molecular targets to cure LSCC patients and also leads an orientation for developing new drugs. 25257554 2014 Cisplatin and paclitaxel target significant long noncoding RNAs in laryngeal squamous cell carcinoma. 1 ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 gastric cancer C16 NA qPCR, RNAi etc. primary gastric cancer tissues, cell line (BGC823) up-regulated ANRIL was highly expressed in gastric cancer tissues of cisplatin-resistant and 5-fluorouracil (5-FU)-resistant patients, and the same upregulation trends were observed in cisplatin-resistant cells (BGC823/DDP) and 5-FU-resistant cells (BGC823/5-FU). In addition, BGC823/DDP and BGC823/5-FU cells transfected with ANRIL siRNA and treated with cisplatin or 5-FU, respectively, exhibited significant lower survival rate, decreased invasion capability, and high percentage of apoptotic tumor cells. The influence of ANRIL knockdown on MDR was assessed by measuring IC50 of BGC823/DDP and BGC823/5-FU cells to cisplatin and 5-FU, the result showed that silencing ANRIL decreased the IC50 values in gastric cancer cells. Moreover, qRT-PCR and western blotting revealed that ANRIL knockdown decreased the expression of MDR1 and MRP1, both of which are MDR related genes; regression analysis showed that the expression of ANRIL positively correlated with the expression of MDR1 and MRP1 27121324 2016 Silencing of long non-coding RNA ANRIL inhibits the development of multidrug resistance in gastric cancer cells 1 AOC4P AOC4P, AOC4, UPAT 90586 ENSG00000260105 NA GRCh38_17:42865922-42874369 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, RNA pull-down assay etc. HCC tissues, cell lines (J7 and SK-Hep1) down-regulated we identified a differentially expressed novel tumor suppressive lncRNA termed amine oxidase, copper containing 4, pseudogene (AOC4P). The level of AOC4P expression was significantly downregulated in 68% of HCC samples and negatively correlated with advanced clinical stage, capsule invasion and vessel invasion. Low AOC4P expression correlated with poor prognostic outcomes, serving as an independent prognostic factor for HCC. In vitro functional assays indicated that AOC4P overexpression significantly reduced cell proliferation, migration and invasion by inhibiting the epithelial-mesenchymal transition (EMT). 26160837 2015 Long non-coding RNA AOC4P suppresses hepatocellular carcinoma metastasis by enhancing vimentin degradation and inhibiting epithelial-mesenchymal transition 1 AP000221.1 LOC105372753 NA ENSG00000229962 NA GRCh38_21:25515473-25518338 pancreatic cancer C25 NA microarray, qPCR etc. cell lines (SW1990, SWl990/GZ etc.) up-regulated Six lncRNAs (RP11-58D2.1, lincRNA-ZNF532, AP000221.1, CTC-338M12.5, CR619813, DDX6P) were selected to validate the microarray consistency by using qPCR. The results demonstrated that RP11-58D2.1, lincRNA-ZNF532 and AP000221.1 were upregulated and that CTC-338M12.5, DDX6P and CR619813 were downregulated in the SW1990/GZ cells compared with SW1990 cells. 25755691 2015 Genomic analysis of drug resistant pancreatic cancer cell line by combining long non-coding RNA and mRNA expression profling. 1 ASHGA5P014130 ULK4P2, D-X, FAM7A1 89838 ENSG00000260128 NA GRCh38_15:30572738-30600647 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 ASHGA5P014632 AL589743.1, PCAN-2 NA ENSG00000244306 NA GRCh38_14:19284653-19337730 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 ASHGA5P018902 LRRC75A-AS1, C17orf45, C17orf76-AS1, FAM211A-AS1, NCRNA00188, TSAP19 125144 ENSG00000175061 NA GRCh38_17:16438822-16478678 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues down-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 ASHGA5P022276 NA NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 ASHGA5P028603 NA NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 ASHGA5P036884 HAR1B, HAR1R, LINC00065, NCRNA00065 NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 ASHGA5P039672 ANP32C, PP32R1 NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues down-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 ASHGA5P043753 LOC100133091 NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 ASHGA5P051732 TIPARP-AS1 100287227 ENSG00000243926 NR_027954 GRCh38_3:156671862-156674378 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 AX746718 NA NA NA NA NA malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). 1 BACE1-AS BACE1-AS, BACE1-AS1, BACE1AS, NCRNA00177 100379571 ENSG00000278768 NR_037803 GRCh38_11:117290874-117293571 ovarian cancer C56.9 NA qPCR, Western blot, Northern blot, MTT assay etc. ovarian cancer stem cell up-regulated The mRNA expression levels of BACE1-AS were significantly increased in anisomycin-treated OCSCs compared to controls. In addition, mRNA and protein levels of BACE1 and AB1-42 were increased in anisomycin-treated OCSCs compared to controls. We confirmed that anisomycin suppressed the growth of xenograft tumors formed by OCSCs in vivo. Finally, when expression of lncRNA BACE1-AS was silenced using siRNA, BACE1 expression was downregulated and the antiproliferative and anti-invasive effects of anisomycin were reduced. 26783004 2016 Long non-coding RNA BACE1-AS is a novel target for anisomycin-mediated suppression of ovarian cancer stem cell proliferation and invasion. 1 BACE1-AS BACE1-AS, BACE1-AS1, BACE1AS, NCRNA00177 100379571 ENSG00000278768 NR_037803 GRCh38_11:117290874-117293571 colon cancer C18 NA qPCR etc. cell lines (SNU-C4R, SNU-C5R etc.) down-regulated We selected three lncRNAs, snaR, BACE1AS, and PRAS, and we detected their expression by RT-qPCR using specific primer sets. SnaR and BACE1AS were significantly down-regulated in both resistant cell lines (SNU-C4R and SNU-C5R), whereas PRAS was down-regulated in SNU-C4R cells but not in SNU-C5R cells. Down-regulation of snaR decreased cell death after 5-FU treatment, which indicates that snaR loss decreases in vitro sensitivity to 5-FU. 25078450 2014 A long non-coding RNA snaR contributes to 5-fluorouracil resistance in human colon cancer cells. 1 BC032020 NA 101927211 ENSG00000226803 NR_110742 GRCh38_6:57114894-57174236 pancreatic ductal adenocarcinoma C25.3 M8500/3 qPCR, Western blot,in vitro knockdown etc. cell lines (AsPC-1(CRL-1682), BxPC-3 (CRL-1687), PANC-1 (CRL-1469),CFPAC-1 (CRL-1918), MIA PaCa-2 (CRL-1420)), pancreatic cancer tissues down-regulated BC032020 levels in the PDAC tumor tissues were lower than those in the adjacent normal tissues, and ZNF451 expression inversely correlated with the BC032020 levels in the PDAC tumor tissues and cell lines. BC032020 overexpression led to a decrease in ZNF451 expression; it also suppressed the proliferation and migration of the AsPC-1 and PANC-1 cells, and induced G1 phase arrest and cell apoptosis. The results of in vivo experiments revealed that BC032020 suppressed tumor growth in a xenograft model by inhibiting ZNF451 expression. Taken together, the findings of this study indicate that BC032020 suppresses the survival of PDAC cells by inhibiting ZNF451 expression. 29532883 2018 LncRNA BC032020 suppresses the survival of human pancreatic ductal adenocarcinoma cells by targeting ZNF451. 1 BC047917 TMEM179, C14orf90, TMEM179A NA NA NA GRCh38_14:104590865-104592156 renal cell carcinoma C64.9 NA microarray, qPCR etc. RCC tissues up-regulated From five paired samples we identified hundreds of significantly differentiated lncRNAs. Specifically, the most upregulated lncRNAs were: uc001vjj.1, ENST00000414223, BC047917, uc003erl.1, and uc009wkz.1, of which uc001vjj.1 was the highest. The most highly downregulated were: ENST00000507950, uc001aka.2, NR_026860, NR_024256, and BC070168, of which ENST00000507950 showed the largest downregulation. 24905231 2014 Expression pattern of long non-coding RNAs in renal cell carcinoma revealed by microarray. 1 BC070168 TSPAN8, CO-029, TM4SF3 NA ENSG00000127324 NA GRCh38_12:71125085-71441898 renal cell carcinoma C64.9 NA microarray, qPCR etc. RCC tissues down-regulated From five paired samples we identified hundreds of significantly differentiated lncRNAs. Specifically, the most upregulated lncRNAs were: uc001vjj.1, ENST00000414223, BC047917, uc003erl.1, and uc009wkz.1, of which uc001vjj.1 was the highest. The most highly downregulated were: ENST00000507950, uc001aka.2, NR_026860, NR_024256, and BC070168, of which ENST00000507950 showed the largest downregulation. 24905231 2014 Expression pattern of long non-coding RNAs in renal cell carcinoma revealed by microarray. 1 BC087858 NA NA NA NA NA non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) up-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. 1 BC087858 NA NA NA NA NA non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Cell proliferation assay, Cell apoptosis assay etc. NSCLC tissues, cell lines (PC9, H1975, H460 and H23) up-regulated Over-expression was observed in NSCLC cells and patients with acquired resistance to EGFR-TKIs and significantly associated with a shorter progression-free survival (PFS) in tumors with respond to EGFR-TKIs. The significant relationship was not observed in patients with T790M mutation but in patients with non-T790M. Down-regulation of BC087858 could significantly promote PC9/R and PC9/G2 cells invasion. BC087858 knockdown restored gefitinib sensitivity in acquired resistant cells with non-T790M and inhibited the activation of the PI3K/AKT and MEK/ERK pathways and epithelial-mesenchymal transition (EMT) via up-regulating ZEB1 and Snail. 27409677 2016 Long non-coding RNA BC087858 induces non-T790M mutation acquired resistance to EGFR-TKIs by activating PI3K/AKT and MEK/ERK pathways and EMT in non-small-cell lung cancer. 1 BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) up-regulated Overexpression of H19 and BC200 were observed in gefitinib-resistant lung cancer cell lines (PC9/R, A549, H1299 and H1975). However, in the gefitinib-sensitive cell line (PC9), MALAT1 and HOTAIR were downregulated. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. 1 BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 glioma NA M9380/3 qPCR etc. cell lines (U251, U87) down-regulated MEG3 and ST7OT1 are up-regulated in both cell lines under apoptosis induced using both agents. The induction of GAS5 is only clearly detected during DOX-induced apoptosis, whereas the up-regulation of neat1 and MIR155HG is only found during RES-induced apoptosis in both cell lines. However, TUG1, BC200 and MIR155HG are down regulated when necrosis is induced using a high dose of DOX in both cell lines. 25645334 2015 Altered expression of long non-coding RNAs during genotoxic stress-induced cell death in human glioma cells 1 BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 ovarian cancer C56.9 NA qPCR, RNAi etc. cell lines (SKOV3 and A2780) down-regulated The results demonstrated that BC200 expression was reduced in ovarian cancer compared with normal ovarian tissue samples. In the SKOV3 and A2780 cells, BC200 exerted no effect on invasive or migratory ability, however, the inhibition of BC200 was demonstrated to promote cell proliferation. Additionally, it was observed that carboplatin induced BC200 expression in the cell lines, and that the inhibition of BC200 decreased the sensitivity of the cells to the drug. BC200 is therefore likely to have a tumor suppressive function in ovarian cancer by affecting cell proliferation. Furthermore, BC200 appears to serve a role in the mediation of carboplatin-induced ovarian cancer cell death 26893717 2016 Downregulation of BC200 in ovarian cancer contributes to cancer cell proliferation and chemoresistance to carboplatin 1 BC200 BCYRN1, BC200, BC200a, LINC00004, NCRNA00004 618 ENSG00000236824 NR_001568 GRCh38_2:47335315-47335514 breast cancer C50 NA qPCR, ChIP etc. cell lines (MCF-7, T47D, MDA-MB-231) up-regulated In this study, we show that BC200 is upregulated in breast cancer; among breast tumor specimens there is a higher level of BC200 in estrogen receptor (ER) positive than in ER-negative tumors. Further experiments show that activation of estrogen signaling induces expression of BC200. 27277684 2016 Regulation of alternative splicing of Bcl-x by BC200 contributes to breast cancer pathogenesis. 1 BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA microarray, qPCR, RNAi etc. cell lines (ZR-75-1, MCF7, BCAR4 etc.) differential expression As BCAR4 expression in cell lines did not change the sensitivity to different chemotherapeutic agents, the increased sensitivity to lapatinib is not due to a general mechanism of drug resistance. Also in our BCAR4-expressing cell models, the combination of lapatinib and antioestrogens was more potent in inhibiting cell growth than lapatinib alone; indicating that blocking the ERBB2 pathway with lapatinib re-sensitises BCAR4-expressing cells to antioestrogens. BCAR4 expression strongly sensitised ZR-75-1 and MCF7 breast cancer cells to the combination of lapatinib and antioestrogens. 22892392 2012 BCAR4 induces antioestrogen resistance but sensitises breast cancer to lapatinib. 1 BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA qPCR etc. cell line (ZR-75-1) up-regulated Forced expression of BCAR4 in human ZR-75-1 and MCF7 breast cancer cells resulted in cell proliferation in the absence of estrogen and in the presence of various antiestrogens. Inhibition of estrogen receptor 1 (ESR1) expression with small interfering RNA (siRNA), implied that the BCAR4-induced mechanism of resistance is independent of ESR1. BCAR4 is a strong transforming gene causing estrogen-independent growth and antiestrogen resistance, and induces tumor formation in vivo. Due to its restricted expression, BCAR4 may be a good target for treating antiestrogen-resistant breast cancer. 21506106 2011 Characterization of BCAR4, a novel oncogene causing endocrine resistance in human breast cancer cells. 1 BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA qPCR, Western blot etc. cell lines (ZR-75-1, BCAR3, EGFR etc.) up-regulated Multivariate analyses established high BCAR4 mRNA levels as an independent predictive factor for poor PFS after start of tamoxifen therapy for recurrent disease. BCAR4 may have clinical relevance for tumour aggressiveness and tamoxifen resistance. Our cell model suggests that BCAR4-positive breast tumours are driven by ERBB2/ERBB3 signalling. Patients with such tumours may benefit from ERBB-targeted therapy. 20859285 2010 Relevance of BCAR4 in tamoxifen resistance and tumour aggressiveness of human breast cancer. 1 BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA qPCR etc. cell line (ZR-75-1) up-regulated We showed that ectopic expression of this gene, designated as breast cancer antiestrogen resistance 4 (BCAR4), caused OH-TAM resistance and anchorage-independent cell growth in ZR-75-1 cells and that the intact open reading frame was required for its function. We conclude that retroviral transfer of cDNA libraries into human breast cancer cells is an efficient method for identifying genes involved in tamoxifen resistance. 16778085 2006 Functional screen for genes responsible for tamoxifen resistance in human breast cancer cells. 1 BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell lines (BEAS-2B, A549), NSCLC tissues up-regulated lncRNA BCAR4 in NSCLC tissues and cells was significantly higher than normal level. The overexpression of BCAR4 promoted NSCLC cell viability, migration, and invasion. The suppression of BCAR4 and GLI2 showed the opposite effects. The overexpression of BCAR4 led to the increase in the expression of GLI2 downstream proteins, while the suppression of BCAR4 and GLI2 reduced their expression. In tumor xenograft assay, tumors in mice of BCAR4 group showed the biggest volume, while those in mice of si-GLI2 group showed the smallest volume. Ki67 showed much higher level in BCAR4 overexpression group but much lower level in si-GLI2 group. 29615150 2018 LncRNA BCAR4 increases viability, invasion and migration non-small cell lung cancer cells by targeting glioma-associated oncogene 2(GLI2) 1 BCAR4 NA 400500 ENSG00000262117 NR_024049 GRCh38_16:11819829-11828845 breast cancer C50 NA qPCR, Western blot, Cell proliferation assay etc. primary breast cancer tissues, cell lines (ZR-75-1,IPH-926 etc.) up-regulated Relative high BCAR4 mRNA expression was identified in IPH-926, a cell line derived from an endocrine-resistant lobular breast cancer. Moderate BCAR4 expression was evident in MDA-MB-134 and MDA-MB-453 breast cancer cells. BCAR4 protein was detected in breast cancer cells with ectopic (ZR-75-1-BCAR4) and endogenous (IPH-926, MDA-MB-453) BCAR4 mRNA expression. Knockdown of BCAR4 inhibited cell proliferation. 26317614 2015 Breast Cancer Anti-Estrogen Resistance 4 (BCAR4) Drives Proliferation of IPH-926 lobular Carcinoma Cells. 1 BE244504 NA NA NA NA GRCh38_20:856476-856922 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) down-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. 1 BG188549 NA NA NA NA GRCh38_4:120005942-120006438 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) down-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. 1 BLACAT1 BLACAT1, LINC00912, UBC1, onco-lncRNA-30 101669762 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. 1 CAR10 ADAM12, ADAM12-OT1, CAR10, MCMP, MCMPMltna, MLTN, MLTNA 8038 ENSG00000148848 NA GRCh38_10:126012381-126388455 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell line (MHCC97H-OXA) up-regulated qPCR results demonstrated that lncRNA ENST00000438347, NR_073453, ENST00000460497, NR_033928, NEST00000480069, ENST00000421965, AK055628 and TCONS_00014652 were up-regulated in MHCC97H-OXA cells in consistent with microarray results. 27729273 2017 Identification of long noncoding RNA expression profile in oxaliplatin-resistant hepatocellular carcinoma cells. 1 CAR10 ADAM12, ADAM12-OT1, CAR10, MCMP, MCMPMltna, MLTN, MLTNA 8038 ENSG00000148848 NA GRCh38_10:126012381-126388455 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated To identify lncRNAs that are critical to lung carcinogenesis, we selected three lncRNAs, CAR intergenic 10 (hereafter, CAR10), AK311218, and RP11-480I12.3, from the most up-regulated lncRNAs in the HPR NSCLCs (Table S3) and tested their expression by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The expression of these lncRNAs was consistent with the microarray analysis. 27322209 2016 Long non-coding RNA stabilizes the Y-box-binding protein 1 and regulates the epidermal growth factor receptor to promote lung carcinogenesis. 1 CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 glioma NA M9380/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, MTT assay etc. glioma tissues, cell lines (U251, U373, SNB19, U118, and LN229) down-regulated CASC2 expression was down-regulated in glioma tissues and cell lines. Exogenous CACS2 alone was sufficient to inhibit glioma cells' proliferation and amplified TMZ-induced repression of cell proliferation, while CACS2 knockdown could reverse this process. CASC2 up-regulates PTEN through direct inhibiting miR-181a and plays an important role in glioma sensitivity to TMZ and may serve as a potential target for cancer diagnosis and treatment. 28121023 2017 LncRNA CASC2 Interacts With miR-181a to Modulate Glioma Growth and Resistance to TMZ Through PTEN Pathway. 1 CASC9 CASC9, ESCCAL-1, ESSCAL1, LINC00981 101805492 ENSG00000249395 NR_103848 GRCh38_8:75223404-75324741 non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Cell proliferation assay etc. cell lines (PC9, PC9G) up-regulated CASC9 expression was upregulated in PC9G and knockdown of its expression could increase the sensitivity of PC9G cells to gefitinib. 28040594 2017 Transcriptome analysis of EGFR tyrosine kinase inhibitors resistance associated long noncoding RNA in non-small cell lung cancer. 1 CASC9 CASC9, ESCCAL-1, ESSCAL1, LINC00981 101805492 ENSG00000249395 NR_103848 GRCh38_8:75223404-75324741 gastric cancer C16 NA qPCR, Cell transfection, Western blot, Cell proliferation assay etc. gastric cancer tissues, cell lines (BGC823 and SGC7901) up-regulated CASC9 was overexpressed in gastric cancer (GC) compared to normal gastric tissue. Moreover, the expression of CASC9 was even higher in BGC823/DR and SGC7901/DR cells that are resistant to paclitaxel or adriamycin. CASC9 knockdown inhibited proliferation and promoted cell apoptosis In BGC823/DR and SGC7901/DR cells. The invasion potential was also significantly inhibited measured by Transwell assay. In addition, CASC9 knockdown in BGC823/DR and SGC7901/DR cells restored chemosensitivity to paclitaxel and adriamycin. 28146436 2017 Silence of cancer susceptibility candidate 9 inhibits gastric cancer and reverses chemoresistance. 1 CCAL NA NA NA NA NA colorectal cancer C19.9 NA microarray, qPCR etc. CRC tissues up-regulated We identified colorectal cancer-associated lncRNA (CCAL) as a key regulator of CRC progression. Patients whose tumours had high CCAL expression had a shorter overall survival and a worse response to adjuvant chemotherapy than patients whose tumours had low CCAL expression.Our results suggest that CCAL is a crucial oncogenic regulator involved in CRC tumorigenesis and progression. 25994219 2015 Long non-coding RNA CCAL regulates colorectal cancer progression by activating Wnt/B-Catenin signalling pathway via suppression of activator protein 2a. 1 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 NA NA NA NA pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues down-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot, RIP, Dual-luciferase reporter assay, Flow cytometry assay etc. LAD tissues, cell lines (SPC-A1, H1299, SPC-A1/DTX and H1299/DTX) up-regulated Here, we showed that CCAT1 was upregulated in docetaxel-resistant LAD cells. Furthermore, downregulation of CCAT1 decreased chemoresistance, inhibited proliferation, enhanced apoptosis and reversed the epithelial-to-mesenchymal transition phenotype of docetaxel-resistant LAD cells. We also found that the oncogenic function of CCAT1 in docetaxel-resistant LAD cells depended on the sponging of let-7c. In turn, the sponging of let-7c by CCAT1 released Bcl-xl (a let-7c target), thereby promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes in docetaxel-resistant LAD cells. 27566568 2016 Long noncoding RNA CCAT1 acts as an oncogene and promotes chemoresistance in docetaxel-resistant lung adenocarcinoma cells. 1 CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 bladder cancer C67 NA qPCR, RNAi, Cell proliferation assay, Cell migration assay etc. bladder cancer tissues, cell lines (SV-HUC-1, T24, 5637) up-regulated Here, we found that CCAT2 was upregulated in bladder cancer tissues and cell lines. Through the statistical analyses, we also found that the high expression level of CCAT2 was positively correlated with histological grade and TNM stage of bladder cancer. Further experimental results revealed that knockdown of CCAT2 could decrease cell proliferation and migration as well as induce apoptosis in bladder cancer cells. 27015551 2016 shRNA targeting long non-coding RNA CCAT2 controlled by tetracycline-inducible system inhibits progression of bladder cancer cells. 1 CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 breast cancer C50 NA microarray, qPCR, RNAi etc. breast cancer tissues, cell lines (SUM149, SUM190, MDA-MB-231, MDA-MB-436 etc.) up-regulated Although, after dividing the tumors at the median in groups containing a low or high percentage of invasive tumor cells, CCAT2 RNA levels were significantly higher in the group of tumors with high invasive tumor cells. 24077681 2013 CCAT2, a novel long non-coding RNA in breast cancer: expression study and clinical correlations. 1 CES1P1-001 CES1P1, CES1A2, CES1A3, CES4, CESR, PCE-3 NA NA NA NA non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. 1 CILA1 NA NA NA NA NA tongue squamous cell carcinoma C02 M8070/3 qPCR, Western blot etc. cell lines (CAL27, SCC9), TSCC tissues up-regulated lncRNA 1 (CILA1) was discovered by using microarrays and was functionally identified as a regulator of chemo-sensitivity in TSCC cells. Upregulation of CILA1 promotes EMT, invasiveness, and chemo-resistance in TSCC cells, whereas the inhibition of CILA1 expression induces mesenchymal-epithelial transition (MET) and chemo-sensitivity, and inhibits the invasiveness of cisplatin-resistant cells both in vitro and in vivo. We also found that CILA1 exerts its functions via the activation of the Wnt/B-catenin signaling pathway. High CILA1 expression levels and low levels of phosphorylated B-catenin were closely associated with cisplatin resistance and advanced disease stage, and were predictors of poor prognosis in TSCC patients. These findings provided a new biomarker for the chemo-sensitivity of TSCC tumors and a therapeutic target for TSCC treatment. 29699939 2018 Chemotherapy-Induced Long Non-coding RNA 1 Promotes Metastasis and Chemo-Resistance of TSCC via the Wnt/B-Catenin Signaling Pathway. 1 CR619813 NA NA NA NA NA pancreatic cancer C25 NA microarray, qPCR etc. cell lines (SW1990, SWl990/GZ etc.) down-regulated Six lncRNAs (RP11-58D2.1, lincRNA-ZNF532, AP000221.1, CTC-338M12.5, CR619813, DDX6P) were selected to validate the microarray consistency by using qPCR. The results demonstrated that RP11-58D2.1, lincRNA-ZNF532 and AP000221.1 were upregulated and that CTC-338M12.5, DDX6P and CR619813 were downregulated in the SW1990/GZ cells compared with SW1990 cells. 25755691 2015 Genomic analysis of drug resistant pancreatic cancer cell line by combining long non-coding RNA and mRNA expression profling. 1 CRALA NA NA NA NA NA breast cancer C50 NA qPCR etc. breast tissues up-regulated CRALA is upregulated in chemoresistant breast cancer cell lines compared to their parental lines. Silencing of CRALA in chemoresistant breast cancer cells resensitizes the cells to chemotherapy in vitro. Furthermore, univariate and multivariate analysis showed that higher CRALA expression was significantly associated with poor prognosis in 144 breast cancer patients. 28834648 2017 Long non-coding RNA CRALA is associated with poor response to chemotherapy in primary breast cancer 1 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 bladder cancer C67 NA qPCR, in vitro knockdown etc. cell lines (5637,T24), BC tissues up-regulated CRNDE was significantly increased in bladder cancer, and overexpressed expression of CRNDE was positively related with advanced TNM stage of bladder cancer patients. In addition, in vitro experiments showed that CRNDE strengthened cell migration/proliferation and inhibited cell apoptosis in bladder cancer.CRNDE can suppress E2F3 expression to increase miR-145 expression. 29710461 2018 Overexpression of CRNDE promotes the progression of bladder cancer. 1 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 lung adenocarcinoma C34 M8140/3 qPCR, Western blot, RIP lung adenocarcinoma tissues, cell lines (A549, H1299) up-regulated In our present study, we identified that CRNDE was significantly upregulated in LAD tissue and radio-resistant LAD cell lines. And high level of CRNDE expression was significantly correlated with poor differentiation, TNM stage and lymph node metastasis, radiotherapy response and high level of CRNDE expression had a significantly shorter overall survival. 28550688 2017 Long Noncoding RNA CRNDE/PRC2 Participated in the Radiotherapy Resistance of Human Lung Adenocarcinoma Through Targeting p21 Expression 1 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA ENSG00000245694 NA GRCh38_16:54845189-54929189 colorectal cancer C19.9 NA qPCR, RNAi, Western blot, Luciferase reporter assay, FISH, MTT assay etc. CRC tissues, cell lines (HCT116 and SW480) up-regulated The expression levels of the CRNDE were upregulated in CRC clinical tissue samples. Significantly, we found that the repression of cell proliferation, the reduction of chemoresistance, and the inhibition of Wnt/B-catenin signaling induced by CRNDE knockdown would require the increased expression of miR-181a-5p. 28086904 2017 The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/B-catenin signaling. 1 CRNDE CRNDE, CRNDEP, LINC00180, NCRNA00180, PNAS-108, lincIRX5 NA 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. 1 CTA-331P3.1 CTA-331P3.1 NA NA NA GRCh38_6:110477907-110479436 childhood acute lymphoblastic leukemia NA M9835/3 qPCR etc. cell lines (Reh, NALM-6) up-regulated We validated that five such lncRNA transcripts overexpressed in pre-B cALL samples (RP11-137H2.4, RP11-68I18.10, AC156455.1, KB-208E9.1, and CTA-331P3.1) were also overexpressed in the Reh and NALM-6 pre-B cALL cell lines that had significant impacts on cancer hallmark traits such as cell proliferation, migration, apoptosis, and treatment response. 27980230 2017 A childhood acute lymphoblastic leukemia-specific lncRNA implicated in prednisolone resistance, cell proliferation, and migration. 1 CTC-338M12.5 CTC-338M12.5 NA NA NA GRCh38_5:181191924-181194429 pancreatic cancer C25 NA microarray, qPCR etc. cell lines (SW1990, SWl990/GZ etc.) down-regulated Six lncRNAs (RP11-58D2.1, lincRNA-ZNF532, AP000221.1, CTC-338M12.5, CR619813, DDX6P) were selected to validate the microarray consistency by using qPCR. The results demonstrated that RP11-58D2.1, lincRNA-ZNF532 and AP000221.1 were upregulated and that CTC-338M12.5, DDX6P and CR619813 were downregulated in the SW1990/GZ cells compared with SW1990 cells. 25755691 2015 Genomic analysis of drug resistant pancreatic cancer cell line by combining long non-coding RNA and mRNA expression profling. 1 DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 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-kB 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-kB signaling pathway in glioma cells. Inhibiting AXL/PI3K/Akt/NF-kB signaling pathway reversed the effects of DANCR on cisplatin resistance.DANCR promotes cisplatin resistance via activating AXL/PI3K/Akt/NF-kB 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-kB signaling pathway. 1 DANCR DANCR, AGU2, ANCR, KIAA0114, SNHG13, lncRNA-ANCR 57291 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. 1 DDX6P DDX6P1, DDX6-Lp, DDX6P, bA150A6.3 NA ENSG00000230056 NA GRCh38_6:29329626-29331061 pancreatic cancer C25 NA microarray, qPCR etc. cell lines (SW1990, SWl990/GZ etc.) down-regulated Six lncRNAs (RP11-58D2.1, lincRNA-ZNF532, AP000221.1, CTC-338M12.5, CR619813, DDX6P) were selected to validate the microarray consistency by using qPCR. The results demonstrated that RP11-58D2.1, lincRNA-ZNF532 and AP000221.1 were upregulated and that CTC-338M12.5, DDX6P and CR619813 were downregulated in the SW1990/GZ cells compared with SW1990 cells. 25755691 2015 Genomic analysis of drug resistant pancreatic cancer cell line by combining long non-coding RNA and mRNA expression profling. 1 DSCAM-AS1 DSCAM-AS1, M41 100506492 ENSG00000235123 NR_038896 GRCh38_21:40383083-40385358 breast cancer C50 NA RNA-seq, qPCR, RNAi, RIP, ChIP, Cell proliferation assay etc. cell lines (T47D, ZR75-1, HEK293, MCF7) up-regulated Among the luminal breast cancers, DSCAM-AS1 is expressed significantly higher in luminal B, a clinical subtype containing most of the clinically aggressive ER-positive breast cancers. We demonstrate that DSCAM-AS1 mediates tumour progression and tamoxifen resistance and identify hnRNPL as an interacting protein involved in the mechanism of DSCAM-AS1 action. 27666543 2016 The lncRNA landscape of breast cancer reveals a role for DSCAM-AS1 in breast cancer progression. 1 ENST00000381279 AL390205.1 NA ENSG00000205695 NA GRCh38_6:139659928-139661513 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) down-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. 1 ENST00000413580 PHOSPHO1 NA ENSG00000173868 NA GRCh38_17:49223362-49230766 ovarian cancer C56.9 NA microarray, qPCR etc. cell lines (A2780, CP70, SKOV3, and SKOV3/DDP) down-regulated The lncRNA microarray analysis and qPCR identified seven lncRNAs that were significantly downregulated. 28128423 2017 Long non-coding RNA ENST00000457645 reverses cisplatin resistance in CP70 ovarian cancer cells. 1 ENST00000418077 RPL23P11, RPL23_6_1032 NA NA NA GRCh38_10:33864313-33864723 non small cell lung cancer C34 M8046/3 microarray, qPCR, Cell proliferation assay etc. cell lines (PC9, H1975, H1299 and A549) down-regulated Four upregulated and four downregulated lncRNAs from differentially expressed lncRNAs were randomly selected. Using RT-qPCR the results of microarray in PC9/R vs. PC9 were validated. The expression levels of ENST00000507437, ENST00000508827, NR_026685 and BC087858 were upregulated and ENST00000381279, ENST00000418077, BG188549 and BE244504 were downregulated. Thus, the microarray data were confirmed by RT-qPCR. 25482516 2015 Microarray expression profile of long non-coding RNAs in EGFR-TKIs resistance of human non-small cell lung cancer. 1 ENST00000434951 AC079742.4 NA NA NA GRCh38_7:6578565-6588974 lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. cell lines (HCC827 and HCC827-8-1) down-regulated To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance. 27108960 2016 Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray. 1 ENST00000447565 Lnc-LIF-AS NA NA NA GRCh38_22:30239194-30240538 cervical cancer C53 NA qPCR, Western blot, Microarray hybridization etc. cervical tissues, cell lines (SiHa and ME-180) down-regulated ENST00000422259, ENST00000447565 (Lnc-LIF-AS) and ENST00000469965, together with their related antisense mRNA DPYD (dihydropyrimidine dehydrogenase, a pyrimidine catabolic pathway gene), LIF (leukemia inhibitor factor) and FLNC (filamin C) were all notably differentially expressed in both ΔNp63a overexpression cells and knockdown cells.An inverse interaction of LIF and ΔNp63a expression was as well validated in clinical samples of cervical cancer, and high level of LIF in cervical cancers was related with poor patient survival. 28391028 2017 LncRNA expression profile of ΔNp63a in cervical squamous cancers and its suppressive effects on LIF expression. 1 ENST00000449694 AP003774.5 NA NA NA GRCh38_11:64420535-64432670 ovarian cancer C56.9 NA microarray, qPCR etc. cell lines (A2780, CP70, SKOV3, and SKOV3/DDP) down-regulated The lncRNA microarray analysis and qPCR identified seven lncRNAs that were significantly downregulated. 28128423 2017 Long non-coding RNA ENST00000457645 reverses cisplatin resistance in CP70 ovarian cancer cells. 1 ENST01108 NA NA NA NA NA glioma NA M9380/3 qPCR, Western blot, Luciferase reporter assay etc. cell lines (U251 and U87), glioma tissues up-regulated lncRNA ENST01108 (ENST01108) has oncogenic role in glioma. Clinical data suggest that ENST01108 is closely associated with the malignant status in glioma. In vitro experiment demonstrated that overexpression of ENST01108 promoted glioma cell proliferation, migration, invasion, EMT process and survival, while knockdown of ENST01108 has an opposite effect,indicating that ENST01108 serves as an oncogenic property in glioma carcinogenesis.Further, we identified miR-489 as a direct target of ENST01108 and ENST01108 negatively regulate miR-489 by act as a sponge. SIK1 is verified as the direct target of miR-489 and it is negatively regulated by miR-489. ENST01108 also positively regulate SIKI and it promotes SIKI expression by suppressing miR-489. Taken together, the reciprocal repression of ENST011081 and miR-489 may be served as potential targets for cancer therapeutics in glioma. 29421578 2018 Long non-coding RNA ENST01108 promotes carcinogenesis of glioma by acting as a molecular sponge to modulate miR-489. 1 FR165245 NA NA NA NA NA lung adenocarcinoma C34 M8140/3 microarray, qPCR etc. cell lines (HCC827 and HCC827-8-1) up-regulated To validate the results of the microarray, we chose a total of 7 differentially expressed lncRNA transcripts for RT-qPCR. The RT-qPCR results were consistent with that of the microarray, in that all 7 lncRNA transcripts were differentially expressed with the same trend (upregulated or downregulated) and reached statistical significance. 27108960 2016 Genome-wide profiling of long non-coding RNA expression patterns in the EGFR-TKI resistance of lung adenocarcinoma by microarray. 1 FTH1P3 FTH1P3,FTHL3,FTHL3P NA ENSG00000213453 NA GRCh38_2:27392784-27393367 breast cancer C50 NA qPCR,Flow cytometry assay,Western blot,Luciferase reporter assay,etc. Human breast cancer cell lines (MCF-7,MDA-MB-231,MDA-MB-468,MDA-MB-453) and normal human breast epithelial cell (MCF-10A) were purchased from ATCC (Manassas,VA,USA). breast cancer tumorous tissue. up-regulated Bioinformatics tools and luciferase reporter assay validated that,FTH1P3 promoted ABCB1 protein expression through targeting miR-206,acting as,a miRNA sponge. In summary,our results reveal the potential regulatory mechanism ,of FTH1P3 on breast cancer paclitaxel resistance through miR-206/ABCB1,providing a novel insight for the breast cancer chemoresistance. However,the occurrence of chemoresistance causes the poor prognosis,high recurrence rate and low 5-year survival rate.In the present study,we investigate the role of lncRNA FTH1P3 in breast cancer paclitaxel resistance and explore the underlying mechanism for the drug resistance generation. 29971911 2018 Long non-coding RNA FTH1P3 activates paclitaxel resistance in breast cancer through miR-206/ABCB1. 1 FTX FTX, LINC00182, MIR374AHG, NCRNA00182 100302692 ENSG00000230590 NR_028379 GRCh38_X:73946555-74293574 acute myeloid leukemia NA M9861/3 Microarray, qPCR, Western blot, Flow cytometry assay, RIP, etc. AML cell lines(U937, THP-1). up-regulated The observation suggested that high-mannose N-glycans and mannosyltransferase ALG3 affected drug-resistance in AML cells. FTX/miR-342/ALG3 axis could potentially be used for the targets to overcome therapeutic resistance in AML. Functionally, we found that FTX directly interacted with miR-342 to regulate ALG3 expression and function, including ADR-resistant cell growth and apoptosis. Kaplan–Meier overall survival curves (OS) was observed based on ALG3 level. Data were the means±SD of triplicate determinants (*p < 0.05). 29880818 2018 Aberrant mannosylation profile and FTX/miR-342/ALG3-axis contribute to development of drug resistance in acute myeloid leukemia. 1 GACAT3 GACAT3, LINC01458, lncRNA-AC130712 104797537 ENSG00000236289 NR_126559 GRCh38_2:16050427-16085801 non small cell lung cancer C34 M8046/3 qPCR, Western blot, Luciferase reporting assay etc. cell lines (A549, H157,HCC827, H838), NSCLC tissue up-regulated Overexpression of ectopic GACAT3 in A549 cells promoted cell proliferation and migration, and enhanced the sensitivity of lung cancer cells to radiotherapy. 29565489 2018 High expression of lncRNA GACAT3 inhibits invasion and metastasis of non-small cell lung cancer to enhance the effect of radiotherapy. 1 GAPLINC GAPLINC, LINC01540 100505592 ENSG00000266835 NR_110429 GRCh38_18:3466250-3478978 colorectal cancer C19.9 NA qPCR, Western blot, Luciferase reporter assay, in vitro knockdown etc. cell line (HCT116), CRC tissue up-regulated GAPLINC expression was obviously increased in CRC tissues.In HCT116, silencing of GAPLINC weakened cell migration and invasion, while overexpression of GAPLINC significantly promoted cell migration and invasion. Through dual-luciferase, RNA pull-down, and Transwell assays, we verified that miR-34a was the downstream molecule of GAPLINC and that miR-34a negatively regulated the migration and invasion of HCT116 cell.Furthermore, we found that GAPLINC positively regulated the miR-34a target gene c-MET in CRC tissues. 29427222 2017 Long Noncoding RNA GAPLINC Promotes Cells Migration and Invasion in Colorectal Cancer Cell by Regulating miR-34a/c-MET Signal Pathway. 1 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 malignant pleural mesothelioma NA M9050/3 qPCR, RNAi etc. MPM tissues, cell lines (SPC111, SPC212, ZL34, ZL55) down-regulated GAS5 expression was lower in MPM cell lines compared to normal mesothelial cells. GAS5 was upregulated upon growth arrest induced by inhibition of Hedgehog and PI3K/mTOR signalling in in vitro MPM models. The increase in GAS5 lncRNA was accompanied by increased promoter activity. Silencing of GAS5 increased the expression of glucocorticoid responsive genes glucocorticoid inducible leucine-zipper and serum/glucocorticoid-regulated kinase-1 and shortened the length of the cell cycle. Drug induced growth arrest was associated with GAS5 accumulation in the nuclei. GAS5 was abundant in tumoral quiescent cells and it was correlated to podoplanin expression. 24885398 2014 GAS5 long non-coding RNA in malignant pleural mesothelioma. 1 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 prostate cancer C61.9 NA qPCR, RNAi, Cell proliferation assay etc. cell lines (22Rv1, LNCaP, PC-3, DU 145, PNT2C2) down-regulated First generation mTORC1, combined mTORC1/mTORC2 and dual PI3K/mTOR inhibitors all increased cellular GAS5 levels and inhibited culture growth in androgen-dependent (LNCaP) and androgen-sensitive (22Rv1) cell lines, but not in androgen-independent (PC-3 and DU 145) cell lines. The latter exhibited low endogenous GAS5 expression, and GAS5 silencing in LNCaP and 22Rv1 cells decreased the sensitivity to mTOR inhibitors, whereas transfection of GAS5 lncRNA sensitized PC-3 and DU 145 cells to these agents. 25650269 2015 Reciprocal regulation of GAS5 lncRNA levels and mTOR inhibitor action in prostate cancer cells. 1 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 prostate cancer C61.9 NA qPCR, RNAi etc. cell lines (22Rv1, PC-3 etc.) up-regulated GAS5 promotes the apoptosis of prostate 34 cells, and exonic sequence, i.e. GAS5 lncRNA, is sufficient to mediate this activity. Abnormally low levels of 35 GAS5 expressionmay therefore reduce the effectiveness of chemotherapeutic agents. 23676682 2013 Long non-coding RNA GAS5 regulates apoptosis in prostate cancer cell lines. 1 GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 breast cancer C50 NA Microarray, qPCR, Western blot, RIP, luciferase reporter assay, Flow cytometry assay, etc. human breast cancer cell line (MCF-7, MCF-7R). breast cancer tissues. down-regulation Collectively, our study demonstrates that GAS5 enhances the efficacy of tamoxifen in the treatment of breast cancer and could be a novel prognostic biomarker. Tamoxifen is a frequently used drug for hormonal therapy in patients with breast cancer, however, development of resistance to tamoxifen remains a serious clinical problem.Kaplan-Meier survival analysis was used to analyze the relationship between the expression of GAS5 and survival rate. P < 0.05 indicates a significant difference. Moreover, GAS5 increased sensitivity of breast cancer cells to tamoxifen by serving as a molecular sponge for miR-222, contributing to suppression of phosphatase and tensin homologs (PTEN) (one endogenous target of miR-222). 29969658 2018 Downregulation of lncRNA GAS5 confers tamoxifen resistance by activating miR-222 in breast cancer. 1 GHET1 GHET1, lncRNA-GHET1 102723099 ENSG00000281189 NR_130107 GRCh38_7:148987527-148989432 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tissues up-regulated The expression of lncRNA GHET1 in lung cancer specimen was significantly higher than that in the cancer-adjacent tissues, which was related to the tumor size, differentiation degree of tumor cells, and lymph node metastasis of clinical specimens. Moreover, lncRNA GHET1 predicted a poor prognosis for the patients with lung cancer.LncRNA GHET1 might be a biomarker and molecular target of NSCLC, providing a potential therapeutic target of NSCLC. 29762836 2018 LncRNA GHET1 predicts a poor prognosis of the patients with non-small cell lung cancer. 1 GHET1 GHET1, lncRNA-GHET1 102723099 ENSG00000281189 NR_130107 GRCh38_7:148987527-148989432 gastric cancer C16 NA qPCR, Western blot etc. gastric carcinoma tissues, cell lines (BGC823 and SGC7901) up-regulated Highly expressing GHET1 promoted the development of MDR which was related to the Bax, Bcl-2, MDR1 and MRP1 genes expression in gastric cancer cells. In the BGC823 and SGC7901 cell, overexpression of GHET1 downregulated Bax expression and upregulated Bcl-2, MDRA and MRP1 expression, which resulted in increasing cisplatin resistance and inhibiting cell apoptosis. In the BGC823/DPP and SGC7901/DDP cell, knockdown of GHET1 leaded to increase cisplatin sensitivity and promote cell apoptosis. In the present study, we examined the GHET1 expression level in gastric carcinoma tissues of cisplatin sensitive patients and drug-resistant patients, as well as the MDR gastric cancer cell lines and their chemo-sensitive parental line. We also identified the function of GHET1 in cisplatin resistant strains (BGC823/DPP and SGC7901/ DDP cells) and their parental line (BGC823 and SGC7901 cells) using gain-of-function and loss-of-function approaches in vitro. 28578256 2017 Overexpression of long non-coding RNA GHET1 promotes the development of multidrug resistance in gastric cancer cells. 1 GRP78 NA 3309 ENSG00000044574 NA GRCh38_9:125234853-125241330 prostate cancer C61.9 NA qPCR etc. cell line (PC3PCA+ ) up-regulated Three proteins were found down-regulated and 7 proteins up-regulated in PC3PCA+ cells compared to PC3NC cells,including GRP78.Higher GRP78 was also found in PCa clinical specimens.This study confirmed that in PCa, PCA3 plays a pro-cancer role through promoting cell proliferation, migration and invasion while inhibiting cell apoptosis. This process might involve the up-regulation of GRP78.GRP78 was also reported to be preferentially expressed in the camptothecin (CPT)- resistant PC3 prostate cancer cell line in comparison to the CPT-sensitive LNCaP prostate cancer cell line, which indicated its involvement in chemotherapy resistant in PCa. 28739722 2017 GRP78 Participates in PCA3-regulated Prostate Cancer Progression. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 small cell lung cancer C56.9 M8441/3 qPCR, Northern blot etc. cell line (NCI-HI688) up-regulated We discovered that the mRNA of the H19 gene is overexpressed in MCF-7/AdrVp cells relative to parental MCF-7 cells or drug-sensitive MCF-7/AdrVp revertant cells. H19 is an imprinted gene with an important role in fetal differentiation, as well as a postulated function as a tumor suppressor gene. Another p95-overexpressing multidrug-resistant cell line, human lung carcinoma NCI-H1688, also displays high levels of H19 mRNA. 8674037 1996 H19 gene overexpression in atypical multidrug-resistant cells associated with expression of a 95-kilodalton membrane glycoprotein. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 pancreatic cancer C25 NA Microarray, qPCR etc. cell lines (PK-1, AsPC-1, PK-45P, PK-45H, PK-9, PK-8, PANC-1, MIAPaCa-2, HPDE4, HPDE6), pancreas tissue up-regulated H19 expression positively correlated with higher histological grades. Overexpression of H19 in PANC-1 pancreatic cancer cells induced higher motilities. 29581580 2018 Reduced expression of the H19 long non-coding RNA inhibits pancreatic cancer metastasis. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 lung adenocarcinoma C34 M8140/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. LUAD tissues, cell lines (A549, A549/DDP) up-regulated In our study, the expression of H19 in cisplatin-resistant A549/DDP cells was unregulated. Knockdown of H19 restored the response of A549/DDP cells to cisplatin. H19-mediated chemosensitivity enhancement was associated with metastasis, induction of G0/G1 cell-cycle arrest, cell proliferation, and increased apoptosis. Furthermore, lncRNA H19 expression was significantly related to TNM stage and metastasis. Overexpression of H19 was negatively correlated with cisplatin-based chemotherapy response in patients. 27911863 2017 Correlation of long non-coding RNA H19 expression with cisplatin-resistance and clinical outcome in lung adenocarcinoma. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 lung cancer C34 NA qPCR etc. cell line (KYSE31-R) up-regulated We observed that three lncRNAs, MALAT1 , H19 , and CUDR , could be clinically useful as biomarkers for LC-MPE diagnosis. Moreover, the combination of MALAT2 and CEA provided higher sensitivity and accuracy in predicting LC-MPE than CEA alone. 29731641 2018 Combination of long noncoding RNA MALAT2 and carcinoembryonic antigen for the diagnosis of malignant pleural effusion caused by lung cancer. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 ovarian cancer C56.9 NA qPCR, RNAi etc. cell lines (PC3, C2C12 etc.) up-regulated This nuclear and short-lived RNA is not imprinted in mouse but is expressed predominantly from the maternal allele in both mice and humans within the H19 gene region. Moreover, the transcript is stabilized in breast cancer cells and overexpressed in human breast tumors. Finally, knockdown experiments showed that, in humans, 91H, rather than affecting H19 expression, regulates IGF2 expression in trans. 19656414 2009 Development of targeted therapy for ovarian cancer mediated by a plasmid expressing diphtheria toxin under the control of H19 regulatory sequences. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 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. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioma NA M9380/3 qPCR, Western blot, Flow cytometry assay etc. cell lines (U87MG and U251) down-regulated In this study, we discovered that the expression of H19 increased in GBM cell lines. H19 knocked down GBM cells also displayed decreased cellular proliferation and a higher apoptosis rate when induced by temozolomide. Interestingly, the GBM cell lines U87MG and U251 were found to express cancer stem cell markers CD133, NANOG, Oct4 and Sox2. Expression of these markers was downregulated in H19-deficient cells 26983719 2016 Suppressing H19 Modulates Tumorigenicity and Stemness in U251 and U87MG Glioma Cells 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 non small cell lung cancer C34 M8046/3 qPCR etc. NSCLC tumor tissue, cell line (A549) up-regulated H19 and miR-21 expression was measured in tumor tissues and corresponding non-tumor lung tissues from 200 patients by quantitative reverse transcription polymerase chain reaction. Expression of both H19 and miR-21 was significantly higher in lung tissues from patients with NSCLC than in normal lung tissues. Increased expression of H19 and miR-21 was positively correlated with advanced tumor-node-metastasis stage and tumor size. miR-21 expression was highest in stage I and II NSCLC, whereas H19 expression was highest in stage III and IV NSCLC. The results show that H19 may mainly contributes to the progression of NSCLC, and its expression levels can reflect the invasive and metastatic status to some extent. New H19 and miR-targeting anticancer drugs will soon enter the clinical stage of development and ultimately become available for the treatment of patients with lung cancer. 28799568 2017 Association of long non-coding RNA H19 and microRNA-21 expression with the biological features and prognosis of non-small cell lung cancer. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, Western blot, RIP, ChIP etc. cell lines (MCF-7, ZR-75-1) up-regulated In the present study, the high expression of lncRNA H19 was identified as a powerful factor associated with paclitaxel (PTX) resistance in ERa-positive breast cancer cells, but not in ERa-negative breast cancer cells. LncRNA H19 attenuated cell apoptosis in response to PTX treatment by inhibiting transcription of pro-apoptotic genes BIK and NOXA. H19 was further confirmed to suppress the promoter activity of BIK by recruiting EZH2 and by trimethylating the histone H3 at lysine 27. 27845892 2016 LncRNA H19 confers chemoresistance in ERa-positive breast cancer through epigenetic silencing of the pro-apoptotic gene BIK. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, Northern blot etc. cell line (MCF-7) up-regulated We discovered that the mRNA of the H19 gene is overexpressed in MCF-7/AdrVp cells relative to parental MCF-7 cells or drug-sensitive MCF-7/AdrVp revertant cells. H19 is an imprinted gene with an important role in fetal differentiation, as well as a postulated function as a tumor suppressor gene. Another p95-overexpressing multidrug-resistant cell line, human lung carcinoma NCI-H1688, also displays high levels of H19 mRNA. 8674037 1996 H19 gene overexpression in atypical multidrug-resistant cells associated with expression of a 95-kilodalton membrane glycoprotein. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot etc. hepatocellular carcinoma tissues, cell line Huh 7 down-regulated The study provides evidence that downregulation of H19 may induce OS and reverse chemotherapy resistance of CD133 cancer stem cells by blocking the MAPK/ERK signaling pathway in HCC. 29800569 2018 Effect of long non-coding RNA H19 on oxidative stress and chemotherapy resistance of CD133+ cancer stem cells via the MAPK/ERK signaling pathway in hepatocellular carcinoma 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 hepatocellular carcinoma C22.0 M8170/3 qPCR, Western blot, e luciferase reporter assay, etc. Human HCC cell lines (ie, Bel-7402, HepG2, Hep3b, QGY7703, SMMC-7721). HCC tissues. up-regulated In conclusion, the miR-193a-3p targeted by lncRNA H19 tended to master the chemo- and radio- resistances of HCC by modulation of PSEN1, which might assist in supplying novel biomarkers to improve the treatment efficacy for HCC for that chemo- and radio-resistances themselves could make the efficacies be poor. The following drugs were taken into application, including docetaxel (DT) (Sanofi-Aventis, Paris, France), paclitaxel (Pt) (Taijipharmaceutical Co. Xi'an, China), vinorelbine (Vb) (Pierre Fabre, Castres, France), and 5-fluorouracil (5-Fu) (Macklin, Shanghai, China). The restrained lncRNA H19 and over-expressed miR-193a-3p expressions tended to significantly elevate the survival rate and proliferation of Bel-7402 cells, when they were exposed to radiation and subject to chemo-therapies. PSEN1 appeared to be subject to the modification of lncRNA H19 and miR-193a-3p in its acting on the survival rates and proliferative abilities of HCC cells. The lncRNA H19/miR-193a-3p/PSEN1 axis could be regarded as the treatment targets for HCC, so as to further improve the treatment efficacy of chemo- and radio-therapies for HCC. 29968942 2018 The LncRNA H19/miR-193a-3p axis modifies the radio-resistance and chemotherapeutic tolerance of hepatocellular carcinoma cells by targeting PSEN1. 1 H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 breast cancer C50 NA qPCR, etc. breast cancer cell line, breast cancer tumor tissues. down-regulation Our results suggest that the combined let-7a and H19 signature is a novel prognostic factor for breast cancer patients treated with neoadjuvant chemotherapy.H19 is associated with drug-resistance in breast cancer cells.Univariate and multivariate survival analyses were conducted using the Cox proportional hazards regression method. As determined using X-tile, the optimal cutoff value for the risk score to assess progression-free survival (PFS) based on the combined signature was -0.1. Several miRNAs and lncRNAs, including let-7a and H19, provide prognostic information for many cancers. 29963109 2018 Combined Let-7a and H19 Signature: A Prognostic Index of Progression-Free Survival in Primary Breast Cancer Patients. 1 HAND2-AS1 HAND2-AS1, DEIN, NBLA00301, UPH 79804 ENSG00000237125 NR_136192 GRCh38_4:173527270-173659696 osteosarcoma NA M9180/3 RNA-seq, qPCR, Western blot, in vitro knockdown, RNAi etc. cell lines (MG-63, SAOS-2, U-2OS, HOS, SW1353) up-regulated Mechanistic investigations indicated that knockdown of HAND2-AS1 abrogated the energy stress-induced effect on cell apoptosis and proliferation, and promoted osteosarcoma progression. Moreover, knockdown of HAND2-AS1 promoted glucose uptake, lactate production, and the expression level of a serious of enzymes that involved in energy metabolism.HAND2-AS1 regulated osteosarcoma metabolism through sequestering FBP1 from binding to HIF1a, thereby releasing HIF1a expression and promoting the protein level. T 29637006 2017 Energy stress-induced lncRNA HAND2-AS1 represses HIF1a-mediated energy metabolism and inhibits osteosarcoma progression. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, ChIP, Luciferase reporter assay etc. primary breast tumor tissues, cell lines (MCF-7, T47D, BT474, MDA-MB-468, MDA-MB-231, ZR-75-1 etc.) up-regulated We show that expression of HOTAIR is regulated by B-catenin through a LEF1/TCF4-binding site. The dual treatment blocks nuclear expression of B-catenin and prevents its recruitment to the HOTAIR promoter. Consistently, forced expression of B-catenin rescued HOTAIR expression and cell viability in the presence of both drugs. Upregulation of HOTAIR is associated with TNBC in cell lines and a cohort of primary tumors. 25883211 2015 Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 chronic myeloid leukemia NA M9863/3 qPCR, RNAi, Western blot etc. bone marrow, cell line (K562) up-regulated Our results showed that lncRNA HOTAIR was greatly upregulated in the MRP1-high patients as well as in the K562-imatinib-resistant cells compared with control. Knockdown of HOTAIR expression downregulated the MRP1 expression levels in the K562-imatinib cells and resulted in higher sensitivity to the imatinib treatment. In addition, the activation of PI3K/Akt was greatly attenuated when HOTAIR was knocked down in K562-imatinib cells. 27875938 2016 The role of long noncoding RNA HOTAIR in the acquired multidrug resistance to imatinib in chronic myeloid leukemia cells. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 small cell lung cancer C56.9 M8441/3 qPCR, RNAi, Western blot, RIP, Flow cytometry assay etc. cell lines (NCI-H446 and NCI-H69) up-regulated The results showed that downregulation of HOTAIR increased cell sensitivity to anticancer drugs through increasing cell apoptosis and cell cycle arrest, and suppressed tumor growth in vivo. Moreover, HOXA1 methylation increased in the resistant cells using bisulfite sequencing PCR. Depletion of HOTAIR reduced HOXA1 methylation by decreasing DNMT1 and DNMT3b expression. 26707824 2016 Long noncoding RNA-HOTAIR affects chemoresistance by regulating HOXA1 methylation in small cell lung cancer cells. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 glioblastoma NA M9440/3 qPCR, Lentiviral infection, Western blot etc. cell lines (U87 and LN229) up-regulated These results suggest that HOTAIR might regulate cell cycle progression through EZH2. Our intracranial mice model also revealed delayed tumor growth in HOTAIR siRNA- and EZH2 inhibitor-treated groups. Moreover, in HOTAIR knock-down cell lines, the expression of the PRC2-binding domain of HOTAIR (5' domain) but not of the LSD1-binding domain of HOTAIR (3' domain) resulted in accelerated cell cycle progression. In conclusion, HOTAIR promotes cell cycle progression in glioma as a result of the binding of its 5' domain to the PRC2 complex. 25428914 2015 Long non-coding RNA HOTAIR promotes glioblastoma cell cycle progression in an EZH2 dependent manner. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 laryngeal squamous cell cancer C32.3 NA qPCR etc. LSCC tissues up-regulated We discovered that five lncRNAs were differentially expressed between primary LSCC samples and adjacent normal tissues. Among them, three lncRNAs were up-expressed in tumor specimens, including CDKN2B-AS1, HOTAIR and MALAT1. More, two lncRNAs had significant down-expression, which were lncRNA RRP1B and SRA1. Cisplatin and paclitaxel have target function on significant lncRNAs in LSCC, which presents novel molecular targets to cure LSCC patients and also leads an orientation for developing new drugs. 25257554 2014 Cisplatin and paclitaxel target significant long noncoding RNAs in laryngeal squamous cell carcinoma. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 prostate cancer C61.9 NA qPCR, Western blot, ChIP, Luciferase reporter assay etc. cell lines (LNCaP, CWR22Rv1, C4-2, C4-2B, HMC-1) up-regulated Mechanism dissection revealed infiltrating mast cells could decrease AR transcription via modulation of the PRC2 complex with LncRNA-HOTAIR at the AR 5' promoter region in PCa cells. The consequences of suppressing AR may then increase PCa cell invasion via increased MMP9 expression and/or increased stem/progenitor cell population. The in vivo mouse model with orthotopically xenografted PCa CWR22Rv1 cells with/without mast cells also confirmed that infiltrating mast cells could increase PCa cell invasion via suppression of AR signals. 25895025 2015 Infiltrating mast cells enhance prostate cancer invasion via altering LncRNA-HOTAIR/PRC2-androgen receptor (AR)-MMP9 signals and increased stem/progenitor cell population. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 prostate cancer C61.9 NA qPCR, RIP, ChIP, RNA pull-down assay etc. prostate cancer tissues up-regulated Here, we report HOTAIR as an androgen-repressed lncRNA, and, as such, it is markedly upregulated following androgen deprivation therapies and in CRPC. Functionally, HOTAIR overexpression increases, whereas HOTAIR knockdown decreases, prostate cancer cell growth and invasion. Taken together, our results provide compelling evidence of lncRNAs as drivers of androgen-independent AR activity and CRPC progression, and they support the potential of lncRNAs as therapeutic targets. 26411689 2015 LncRNA HOTAIR Enhances the Androgen-Receptor-Mediated Transcriptional Program and Drives Castration-Resistant Prostate Cancer 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 head and neck squamous cell carcinoma C76.0 M8070/3 in vitro knockdown, Luciferase reporter assay, qPCR,Western blot, RNA-seq etc. cell lines (SCC25, Cal27,UM-SCC1,SCC15, Tscca, Tca8113,Hep-2,Tb3.1), HNSCC tumor tissues up-regulated STAT3 inhibition with WP1066 decreased HOTAIR level and sensitized HNSCC to cisplatin or cetuximab. STAT3 promoted HOTAIR transcription and its interaction with pEZH2-S21, resulting in enhanced growth of HNSCC cells.STAT3 signaling promotes HNSCC progression via regulating HOTAIR and pEZH2-S21 in HNSCC with PI3K overexpression/activation. 29540490 2018 STAT3/HOTAIR Signaling Axis Regulates HNSCC Growth in an EZH2-dependent Manner. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. cell lines (A549, H460, H1299, NCI-H460, HCC-827,HBEC) up-regulated HOTAIR was overexpressed in NSCLC cell lines. Silencing of HOTAIR decreased cell proliferation and increased apoptosis of NSCLC cells (A549).Silencing of HOTAIR decreased drug resistance of NSCLC cells might through inhibiting autophagy via the ULK1 pathway.Silencing of HOTAIR decreased drug resistance of NSCLC cells to Crizotinib through inhibition of autophagy via suppressing phosphorylation of ULK1. 29470986 2018 Silencing of LncRNA-HOTAIR decreases drug resistance of Non-Small Cell Lung Cancer cells by inactivating autophagy via suppressing the phosphorylation of ULK1. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, Luciferase reporter assay etc. cell lines (A2780, A2780_CR5, SKOV3, HEYC2, OV90, IOSE, IGROV etc.) up-regulated In this study, we show that upregulation of HOTAIR induced platinum resistance in ovarian cancer, and increased HOTAIR levels were observed in recurrent platinum-resistant ovarian tumors vs primary ovarian tumors. To investigate the role of HOTAIR during DNA damage induced by platinum, we monitored double-strand breaks and show that HOTAIR expression results in sustained activation of DNA damage response (DDR) after platinum treatment. We demonstrate that ectopic expression of HOTAIR induces NF-kB activation during DDR and interleukin-6 and interleukin-6 expression, both key NF-kB target genes. 27041570 2016 NF-kB-HOTAIR axis links DNA damage response, chemoresistance and cellular senescence in ovarian cancer 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 esophageal squamous cell cancer NA NA qPCR, MTT assay etc. ESCC tissues, cell lines (KYSE30, KYSE70, KYSE150, KYSE450, KYSE510, and TE10) up-regulated Three lncRNAs (AFAP1-AS1, UCA1, HOTAIR) were found to be deregulated in cisplatin-resistant cells compared with their parent cells. AFAP1-AS1 was significantly up-regulated in tumor tissues compared with adjacent normal tissues. Furthermore, overexpression of AFAP1-AS1 was closely associated with lymph node metastasis, distant metastasis, advanced clinical stage, and response to dCRT. 26756568 2016 High expression of long non-coding RNA AFAP1-AS1 predicts chemoradioresistance and poor prognosis in patients with esophageal squamous cell carcinoma treated with definitive chemoradiotherapy. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR etc. cervical cancer tissues differential expression Compared with the CC genotype, TT genotype was significantly correlated with the elevated expression of HOTAIR; however, the CT genotype did not associate with the HOTAIR upregulation. In addition, we also found that the TT genotype of rs920778 was correlated with advanced tumor stage, highly histological grade, lympho node metastasis and positive infection of high risk HPV. Among the patients who underwent concurrent chemo-radiotherapy, TT genotype carriers present notably resistance to the combination of EBRT + ICBT + cisplatin. 27229487 2016 Analysis of the association of HOTAIR single nucleotide polymorphism (rs920778) and risk of cervical cancer. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 ovarian cancer C56.9 NA qPCR, RNAi, Western blot, MTT assay etc. ovarian cancer tissues, cell lines (A2780, 3AO, OVCAR3, SKOV3, HO-8910) up-regulated HOTAIR overexpression promoted cell cycle progression (and thus cell proliferation) by activating the Wnt/B-Catenin signaling pathway. Likewise, knockdown of HOTAIR suppressed cell proliferation and arrested cell cycle at G1 phase via inhibition of Wnt/B-Catenin signaling. Moreover, the results of primary culture demonstrated that elevated HOTAIR expression correlated positively with chemoresistance in ovarian cancer. 26341496 2015 Overexpression of long non-coding RNA HOTAIR leads to chemoresistance by activating the Wnt/B-Catenin pathway in human ovarian cancer. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, RNAi, Luciferase reporter assay cell lines (MCF-7, MDA-MB-231 and SKBR3) differential expression Treatment of mice harboring platinum-resistant ovarian tumor xenografts with pHLIP-PNA constructs suppressed HOTAIR activity, reduced tumor formation and improved survival. 28420874 2017 Therapeutic targeting using tumor specific peptides inhibits long non-coding RNA HOTAIR activity in ovarian and breast cancer 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. cell lines (MCF7, T47D, ZR-751, MDA-MB-453 and MDA-MB-468) up-regulated HOTAIR expression is negatively regulated by oestrogen, positively regulated by FOXA1 and FOXM1, and is inversely correlated with oestrogen receptor and directly correlated with FOXM1 in breast tumours. The combination of HOTAIR and FOXM1 enables greater discrimination of endocrine therapy responders and non-responders in patients with oestrogen receptor positive breast cancer. Consistent with this, HOTAIR expression is increased in cell-line models of endocrine resistance. 27378691 2016 Long-range regulators of the lncRNA HOTAIR enhance its prognostic potential in breast cancer. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR, Western blot, Cell proliferation assay etc. cell line (MCF-7) down-regulated Both calycosin and genistein inhibited proliferation and induced apoptosis in MCF-7 breast cancer cells, especially after treatment with calycosin. Treatment of MCF-7 cells with calycosin or genistein resulted in decreased phosphorylation of Akt, and decreased expression of its downstream target, HOTAIR. 25613518 2015 Calycosin and genistein induce apoptosis by inactivation of HOTAIR/p-Akt signaling pathway in human breast cancer MCF-7 cells. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi etc. HCC tissues, cell lines (SMMC-7721, HepG2, Hep3B etc.) up-regulated The expression level of HOTAIR in cancer tissues was higher than in adjacent noncancerous tissues. High expression level of HOTAIR was an independent prognostic factor for predicting HCC recurrence in LT patients. Furthermore, in patients exceeding the Milan criteria, those with a high expression level of HOTAIR revealed a significantly shorter recurrence-free survival. 21327457 2011 Overexpression of long non-coding RNA HOTAIR predicts tumor recurrence in hepatocellular carcinoma patients following liver transplantation. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 gastric cancer C16 NA qPCR, RNAi, Western blot, Luciferase reporter assay, 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. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 cervical cancer C53 NA qPCR, Western blot etc. cervical cancer tissues, cell lines (HeLa, SiHa, C33A, CaSki) differential expression Stable knockdown of HOTAIR significantly suppressed tumor growth and sensitized cervical cancer to radiotherapy in vivo. 25547435 2014 HOTAIR enhanced aggressive biological behaviors and induced radio-resistance via inhibiting p21 in cervical cancer. 1 HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 non small cell lung cancer C34 M8046/3 qPCR, Western blot etc. non small cell lung cancer tissues, cell lines up-regulated The mRNA level of lncRNA-HOTAIR in cancer tissues was significantly higher than that in cancer-adjacent tissues (P<0.05), and the high expression of lncRNA-HOTAIR indicated that the OS of patients was shortened (P<0.05). The IC50 of NCI-H1299/DDP cells inhibiting DDP was 127.82 uM, which was significantly higher than that of parental NCI-H1299 cells (IC50=8.40 uM) (P<0.05). 29805510 2018 The action mechanism of lncRNA-HOTAIR on the drug resistance of non-small cell lung cancer by regulating Wnt signaling pathway 1 HOTAIRM1 HOTAIRM1, HOXA-AS1, HOXA1-AS1, NCRNA00179 100506311 ENSG00000233429 NA GRCh38_7:27095647-27100265 pancreatic ductal adenocarcinoma C25.3 M8500/3 microarray, qPCR etc. PDAC tissues up-regulated We found that ASHGA5P022276, ASHGA5P029774, ASHGA5P028603, ASHGA5P014632, ASHGA5P043753, ASHGA5P036884, ASHGA5P016768, ASHGA5P032173, ASHGA5P051732 and ASHGA5P014130 were upregulated, and ASHGA5P055771, ASHGA5P044524, ASHGA5P039672, ASHGA5P017734 and ASHGA5P018902 were downregulated in the PDAC samples compared with adjacent non-tumor samples. Thus, the results from the qRT-PCR analysis and the microarray data analysis were consistent. 26676849 2016 Microarray expression profile analysis of long non-coding RNAs in pancreatic ductal adenocarcinoma. 1 KCNQ1OT1 KCNQ1OT1, KCNQ1-AS2, KCNQ10T1, Kncq1, KvDMR1, KvLQT1-AS, LIT1, NCRNA00012 10984 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 lung adenocarcinoma C34 M8140/3 qPCR, Western blot etc. LAD tissues, cell line (A549) up-regulated the expression of KCNQ1OT1 was confrmed to be highly expressed in LAD tissues and cells contrast to control tissues and cells, and high KCNQ1OT1 expression correlated to malignant behaviors of LAD, including big tumor size, poor differentiation, positive lymphatic metastasis and high TNM stages. The transfection of si-KCNQ1OT1 could effectually knockdown the expression of KCNQ1OT1 in A549 and A549/PA cells. 28600629 2017 Knockdown of long non-coding RNA KCNQ1OT1 depressed chemoresistance to paclitaxel in lung adenocarcinoma. 1 KCNQ1OT1 KCNQ1OT1,KCNQ1-AS2,KCNQ10T1,Kncq1,KvDMR1,KvLQT1-AS,LIT1,NCRNA00012 10984 ENSG00000269821 NR_002728 GRCh38_11:2608328-2699994 hypopharyngeal squamous cell carcinoma C13 M8070/3 Microarray,qPCR,Western blot,Cell proliferation assay,Luciferase reporter assay,RIP,etc. TSCC samples and cell lines(CAL27,SCC9),normal tissues,chemo-sensitive samples and chemo-insensitive TSCC tissues. up-regulated Finally, miR-211-5p inhibition in sh-KCNQ1OT1-expressing TSCC cells rescued the suppressed cell proliferation and cisplatin resistance induced by KCNQ1OT1 knockdown. In summary, our study has elucidated the role of the oncogenic lncRNA KCNQ1OT1 in TSCC growth and chemo-resistance, which may serve as a new target for TSCC therapy.he stable cisplatin-resistant cell lines, CAL27-res and SCC9-res, were established by the selection of CAL27 or SCC9 colonies treated with 10?7 to 10?5?M cisplatin (Sigma, Carlsbad, CA, USA) as described previously.Kaplan-Meier survival analysis indicated that increased KCNQ1OT1 expression in TSCC tissues was significantly associated with a lower rate of overall survival (p?