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 NAMA NAMA 100996569 ENSG00000271086 NR_102270 GRCh38_9:99355337-99377240 papillary thyroid cancer NA M8260/3 qPCR, RNAi, RIP, Flow cytometry assay etc. PTC tissues, cell line (IHH-4) down-regulated The expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. 26323637 2015 BRAF-activated Long Non-coding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor. CCAT2 CCAT2, LINC00873, NCCP1 101805488 ENSG00000280997 NR_109834 GRCh38_8:127400399-127402150 gastric cancer C16 NA qPCR, Western blot etc. cell lines (BGC-823) up-regulated CCAT2 was able to positively regulate the expression of POU5F1B gene. Furthermore, silencing of CCAT2 gene inhibited the proliferation of BGC-823 cells, as well as induced apoptosis and autophagy in BGC-823 cells, by suppression of the PI3K/mTOR signaling pathways.Recent studies confirmed that the lncRNA CCAT2, located at the 8q24 amplicon of the cancer risk-associated rs6983267 SNP, regulated the cancer metabolism in vitro and in vivo by directly interacting in an allele-specific manner with a protein complex. The chromosomal region 8q24 emerged as an important region for genetic susceptibility in various cancer types, thus DNA methylation or SNPs at this locus may contribute to cancer risk. RT-qPCR results revealed that CCAT2 gene expression was effectively suppressed by the transfection, while POU domain class 5 transcription factor 1B (POU5F1B) gene expression was significantly decreased. 29435046 2017 Effect of silencing colon cancer-associated transcript 2 on the proliferation,apoptosis and autophagy of gastric cancer BGC-823 cells. EZR-AS1 NA 101409257 ENSG00000233893 NR_102425 GRCh38_6:158818011-158820593 esophageal squamous cell cancer NA NA RNA-seq, qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP esophageal squamous cell carcinoma (ESCC) tissues and cell lines (KYSE150 and KYSE510) up-regulated Both in vivo and in vitro studies revealed that EZR-AS1 promoted cell migration through up-regulation of EZR expression. Mechanistically, antisense lncRNA EZR-AS1 formed a complex with RNA polymerase II to activate the transcription of EZR. Moreover, EZR-AS1 could recruit SMYD3 to a binding site, present in a GC-rich region downstream of the EZR promoter, causing the binding of SMYD3 and local enrichment of H3K4me3. Finally, the interaction of EZR-AS1 with SMYD3 further enhanced EZR transcription and expression. Our findings suggest that antisense lncRNA EZR-AS1, as a member of an RNA polymerase complex and through enhanced SMYD3-dependent H3K4 methylation, plays an important role in enhancing transcription of the EZR gene to promote the mobility and invasiveness of human cancer cells.EZR-AS1 regulates EZR transcriptional activity in ESCC cells by interacting with RNA polymerase II, but not by affecting the binding of SP1 and AP-1 transcription factors. the overexpression of EZR-AS1 accompanied the enhanced expression of EZR (variant 1), both at the mRNA and protein levels, in KYSE150 cells (Figure 1H and I). 29253179 2018 The interaction of lncRNA EZR-AS1 with SMYD3 maintains overexpression of EZR in ESCC cells. FAM99A FAM99A 387742 ENSG00000205866 NR_026643 GRCh38_11:1665597-1667856 hepatocellular carcinoma C22.0 M8170/3 RNA-seq, qPCR etc. HCC tissues down-regulated We found that LINC01093, FAM99A and CRNDE were differentially expressed in HCC compared with cirrhotic tissues, confirming the data we obtained in the RNA-Seq experiment. Moreover, we found that LINC01093 and FAM99A were already significantly downregulated in cirrhotic tissues compared with normal livers. 26887054 2016 Identification of novel long non-coding RNAs deregulated in hepatocellular carcinoma using RNA-sequencing. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 colon cancer C18 NA qPCR, Western blot, Luciferase reporter assay etc. cell lines (CCL228, HeLa, MCF7, SH-SY5Y) up-regulated Along with HIF1a, histone methylases MLL1 and histone acetylase p300 are enriched at the HOTAIR promoter under hypoxia. The levels of H3K4-trimethylation and histone acetylation are also enriched at the HOTAIR promoter. Furthermore, knockdown of MLL1 downregulated the hypoxia-induced HOTAIR expression, indicating key roles of MLL1 in hypoxia-induced HOTAIR expression. HIFs are transcription factors and regulate the expression of a variety of target genes under hypoxia and that contribute to the tumor growth and metastasis.Misregulation and mutations in lncRNAs are widely associated with a variety of human diseases. 28756022 2017 Histone methylase MLL1 coordinates with HIF and regulate lncRNA HOTAIR expression under hypoxia. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 pancreatic neuroendocrine tumor C25 M8246/3 microarray, qPCR, Luciferase reporter assay etc. pancreatic neuroendocrine tumors tissues, cell lines (MIN6 and MIN6-4N) down-regulated We found that Meg3 has tumor-suppressor activity in PNET cells because the overexpression of Meg3 in MIN6 cells (insulin-secreting mouse PNET cell line) blocked cell proliferation and delayed cell cycle progression. Gene expression microarray analysis showed that Meg3 overexpression in MIN6 mouse insulinoma cells down-regulated the expression of the protooncogene c-Met (hepatocyte growth factor receptor), and these cells showed significantly reduced cell migration/invasion. Compared with normal islets, mouse or human MEN1-associated PNETs expressed less MEG3 and more c-MET 25565142 2015 Epigenetic regulation of the lncRNA MEG3 and its target c-MET in pancreatic neuroendocrine tumors SAMMSON LINC01212 101927152 ENSG00000240405 NR_110000 GRCh38_3: 69999550-70518064 melanoma NA M8720/3 qPCR, RIP etc. cell lines (Mel501, SK-MEL-28), melanoma tissues up-regulated Our results indicate that silencing of the lineage addiction oncogene SAMMSON disrupts vital mitochondrial functions in a cancer-cell-specific manner; this silencing is therefore expected to deliver highly effective and tissue-restricted antimelanoma therapeutic responses. 27008969 2016 Melanoma addiction to the long non-coding RNA SAMMSON H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 colorectal cancer C19.9 NA microarray, qPCR, RIP, ChIP etc. cell lines (DLD1, HCT116, HT29 and SW480) differential expression H19 silencing blocked G1-S transition, reduced cell proliferation, and inhibited cell migration. Our experimental data showed that H19 affects phosphorylation of RB1 protein by regulating gene expression of CDK4 and CCND1. We further demonstrated that reduced CDK8 expression underlies changes of B-catenin activity, and identified that H19 interacts with macroH2A, an essential regulator of CDK8 gene transcription. 27789274 2016 H19 Noncoding RNA, an Independent Prognostic Factor, Regulates Essential Rb-E2F and CDK8-B-Catenin Signaling in Colorectal Cancer. LINC00210 LINC00210, NCRNA00210 100885798 ENSG00000231814 NR_048550 GRCh38_1:217892900-217920804 non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) up-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. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 glioma NA M9380/3 qPCR, Western blot etc. cell lines (U87 and U251) up-regulated we found that the expression of lncRNA MALAT1 was significantly increased in glioma tissues compared with that of paracancerous tissues. Meanwhile, the expression of MALAT1 was highly expressed in U98 and U251 cells. In order to explore the function of MALAT1, the expression of MALAT1 was greatly reduced in U87 and U251 cells transfected with siRNA specifically targeting MALAT1. Consequently, cell viability of U87 and U251 cells were drastically decreased after the knockdown of MALAT1. Concomitantly, the apoptosis rate of the two cell lines was dramatically increased. Furthermore, the expression levels of some tumor markers were reduced after the knockdown of MALAT1, such as CCND1 and MYC 27134488 2016 Silencing of Long Non-Coding RNA MALAT1 Promotes Apoptosis of Glioma Cells MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 lung cancer C34 NA qPCR, RIP, ChIP, Cell migration assay etc. cell lines (A549 and LC-2/ad) up-regulated The expression of MEG3 long noncoding RNA (lncRNA), which could interact with JARID2, was clearly increased during transforming growth factor-B (TGF-B)-induced EMT of human lung cancer cell lines. Knockdown of MEG3 inhibited TGF-B-mediated changes in cell morphology and cell motility characteristic of EMT and counteracted TGF-B-dependent changes in the expression of EMT-related genes such as CDH1, ZEB family, and the microRNA-200 family. Overexpression of MEG3 influenced the expression of these genes and enhanced the effects of TGF-B in their expressions. Chromatin immunoprecipitation (ChIP) revealed that MEG3 regulated the recruitment of JARID2 and EZH2 and histone H3 methylation on the regulatory regions of CDH1 and microRNA-200 family genes for transcriptional repression. 27852821 2017 MEG3 Long Noncoding RNA Contributes to the Epigenetic Regulation of Epithelial-Mesenchymal Transition in Lung Cancer Cell Lines. nc886 VTRNA2-1, CBL-3, CBL3, MIR886, MIRN886, VTRNA2, hsa-mir-886, hvg-5, nc886, svtRNA2-1a 100126299 ENSG00000270123 NR_030583 GRCh38_5:136080470-136080597 gastric cancer C16 NA RNA-seq, qPCR etc. gastric cancer tissues, gastric cell lines down-regulated Our real-time RT-PCR data (Fig 1A) indicated that the expression level of nc886 was lower in a subpopulation of tumor tissues than in normal tissues. nc886 inhibits cell proliferation when ectopically expressed in gastric cancer cells. 25003254 2014 nc886, a non-coding RNA of anti-proliferative role, is suppressed by CpG DNA methylation in human gastric cancer. ncSRPK1 SRPK1, SFRSK1 NA NA NA NA renal cell carcinoma C64.9 NA microarray, qPCR, Western blot etc. RCC tissues up-regulated Four lncRNAs mapping to intronic regions, namely ncC11orf49, ncHDAC5, ncRAB31 and ncSRPK1, showed a significant differential expression between tumor and nontumor paired samples as measured by qPCR. 24238219 2013 Expression analysis and in silico characterization of intronic long noncoding RNAs in renal cell carcinoma: emerging functional associations. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, RNAi etc. cell lines (MCF-7, MDA-MB-231) down-regulated we demonstrated that downregulating the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in breast cancer cells inhibited cell growth and induced cell apoptosis. In addition, the RNA-binding protein fused in sarcoma/translocated in liposarcoma (FUS/TLS) physically interacted with NEAT1, and reducing the expression of FUS/TLS also induced cell apoptosis. Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis 27147820 2016 NEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548 ECONEXIN NA NA NA NA NA glioma NA M9380/3 Western blot, Microarray, luciferase reporter assay. glioma tissue, glioma cell lines (U87,U251) up-regulated Our data demonstrated that ECONEXIN is a potential oncogene that regulates TOP2A by sponging miR-411-5p in glioma. In addition, our investigative approaches to identify conserved lncRNA and their molecular characterization by validation in mouse tumor models may be useful to functionally annotate novel lncRNAs, especially cancer-associated lncRNAs.which coordinately promotes self-renewal by sponging miR-145 in the cytoplasm and recruiting polycomb to repress differentiation genes by the locus-specific methylation of histone H3K27 in the nucleus.promoter region (~500 bp upstream of transcriptional start site). Transcriptional factor binding motif analysis using the JASPAR database revealed that 140 transcription factors may bind to the ECONEXIN and C130071C03Rik promoter regions.28 28368417 2017 Oncogenic effects of evolutionarily conserved noncoding RNA ECONEXIN on gliomagenesis. FEZF1-AS1 NR_036484 154860 ENSG00000230316 NR_036484 GRCh38_7:122303658-122310077 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP, ChIP, MTT assay etc. gastric cancer tissues, cell lines (MGC-803, SGC-7901, AGS) up-regulated FEZF1-AS1 was overexpressed in gastric cancer. Further experiments revealed that knockdown FEZF1-AS1 significantly inhibited gastric cancer cells proliferation by inducing G1 arrest and apoptosis, whereas endogenous expression FEZF1-AS1 promoted cell growth. Additionally, RIP assay and RNA-pulldown assay evidenced that FEZF1-AS1 could epigenetically repress the expression of P21 via binding with LSD1, the first discovered demethylase. 28209170 2017 LincRNAFEZF1-AS1 represses p21 expression to promote gastric cancer proliferation through LSD1-Mediated H3K4me2 demethylation. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot etc. NSCLC tissues, cell lines (A549, H1650, H1299, H1975, SK-MES etc.) down-regulated The results revealed that GAS5 expression was down-regulated in cancerous tissues compared to adjacent noncancerous tissues and was highly related to tumor size and TNM stage. This correlation between GAS5 and clinicopathological parameters indicates that GAS5 might function as a tumor suppressor. Furthermore, GAS5 overexpression increased tumor cell growth arrest and induced apoptosis in vitro and in vivo. 24357161 2013 A critical role for the long non-coding RNA GAS5 in proliferation and apoptosis in non-small-cell lung cancer. LINC00441 LINC00441, ncRNA-RB1 NA ENSG00000231473 NA GRCh38_13:48296513-48303661 hepatocellular carcinoma C22.0 M8170/3 qPCR, ChIP, Luciferase reporter assay, RNA pull-down assay etc. HCC tissues up-regulated We found that aberrant upregulated intranuclear Linc00441 was reversely correlated with RB1 expression in human HCC samples. The gain- and loss-of-function investigation revealed that Linc00441 could promote the proliferation of HCC cells in vitro and in vivo with an apoptosis suppression and cell cycle rearrangement. Furthermore, RNA pull-down assay indicated the decreased level of RB1 induced by Linc00441 was associated with the incidental methylation by DNMT3A recruited by Linc00441. On the contrary, the transcription factor (TCF-4) enhanced H3K27 acetylation and direct transcription factor for Linc00441 was responsible for the upregulation of Linc00441 in HCC. 28300839 2017 Bidirectional transcription of Linc00441 and RB1 via H3K27 modification-dependent way promotes hepatocellular carcinoma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 oral squamous cell carcinoma C06.9 M8070/3 qPCR, RNAi, Western blot etc. OSCC tissues, cell lines (Tscca, Tca8113P160, Tca8113, Hep-2) up-regulated We found that MALAT1 is overexpressed in OSCC tissues compared to normal oral mucosa by real-time PCR. MALAT1 served as a new prognostic factor in OSCC patients. When knockdown by small interfering RNA (siRNA) in OSCC cell lines TSCCA and Tca8113, MALAT1 was shown to be required for maintaining epithelial-mesenchymal transition (EMT) mediated cell migration and invasion. Western blot and immunofluorescence staining showed that MALAT1 knockdown significantly suppressed N-cadherin and Vimentin expression but induced E-cadherin expression in vitro. Meanwhile, both nucleus and cytoplasm levels of B-catenin and NF-B were attenuated, while elevated MALAT1 level triggered the expression of B-catenin and NF-B. More importantly, targeting MALAT1 inhibited TSCCA cell-induced xenograft tumor growth in vivo. 26522444 2015 Long Non Coding RNA MALAT1 Promotes Tumor Growth and Metastasis by inducing Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 multiple myeloma C42.1 M9732/3 qPCR etc. myeloma tissues up-regulated The upregulation of MALAT1 appeared associated in MM patients with molecular pathways involving cell cycle regulation, p53-mediated DNA damage response, and mRNA maturation processes. 26895470 2016 Distinct lncRNA transcriptional fingerprints characterize progressive stages of multiple myeloma. MALAT1 MALAT1, HCN, LINC00047, NCRNA00047, NEAT2, PRO2853 378938 ENSG00000251562 NR_002819 GRCh38_11:65497688-65506516 pancreatic cancer C25 NA qPCR, RNAi, Western blot, RIP, Flow cytometry assay, Cell proliferation assay etc. pancreatic cancer tissues, cell lines (CFPAC-1, SW1990, AsPC-1) up-regulated And knockdown of MALAT-1 upregulated E-cadherin mRNA expression in pancreatic cancer cell lines. Therefore, we hypothesized that EZH2 might be recruited by MALAT-1 to synergistically repress E-cadherin. To test this hypothesis, we first asked whether MALAT-1 bound to EZH2 using a RNA Immunoprecipitation (RIP) assay. There was an average of 14- and 18- fold enrichment for MALAT-1 in the AsPC-1 and CFPAC-1 cells over-expressing EZH2, respectively, as compared to the IgG group. These results suggest that MALAT-1 is physically associated with the EZH2, and silencing EZH2 could increase E-cadherin transcription. 26848980 2016 EZH2 promotes cell migration and invasion but not alters cell proliferation by suppressing E-cadherin, partly through association with MALAT-1 in pancreatic cancer. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 colon cancer C18 NA qPCR, Western blot, Northern blot, ChIP etc. cell lines (HCT116, U2OS) down-regulated We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter. Interestingly, MEG3 does not stimulate p21(CIP1) expression, suggesting that MEG3 can regulate the specificity of p53 transcriptional activation. p53 degradation is mainly mediated by the mouse double minute 2 homolog (MDM2). We found that MDM2 levels were down-regulated in cells transfected with MEG3, suggesting that MDM2 suppression contributes at least in part to p53 accumulation induced by MEG3. Finally, we found that MEG3 is able to inhibit cell proliferation in the absence of p53. 17569660 2007 Activation of p53 by MEG3 non-coding RNA. MEG3 MEG3, FP504, GTL2, LINC00023, NCRNA00023, PRO0518, PRO2160, onco-lncRNA-83, prebp1 55384 ENSG00000214548 NR_002766 GRCh38_14:100779410-100861031 osteosarcoma NA M9180/3 qPCR, Western blot, Northern blot, ChIP etc. cell lines (HCT116, U3OS) down-regulated We found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p53-dependent transcription from a p53-responsive promoter. We further found that MEG3 stimulates expression of the growth differentiation factor 15 (GDF15) by enhancing p53 binding to the GDF15 gene promoter. Interestingly, MEG3 does not stimulate p21(CIP1) expression, suggesting that MEG3 can regulate the specificity of p53 transcriptional activation. p53 degradation is mainly mediated by the mouse double minute 2 homolog (MDM2). We found that MDM2 levels were down-regulated in cells transfected with MEG3, suggesting that MDM2 suppression contributes at least in part to p53 accumulation induced by MEG3. 17569660 2007 Activation of p53 by MEG3 non-coding RNA. MIAT MIAT, C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-MIAT 440823 ENSG00000225783 NR_003491 GRCh38_22:26646428-26676475 chronic lymphocytic leukemia NA M9823/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. CLL tissues, leukemia/lymphoma cell lines up-regulated MIAT expression was upregulated in breast cancer cell lines and tissues.MIAT acted as a competing endogenous RNA (ceRNA) to regulate the expression of dual specificity phosphatase 7 (DUSP7) by taking up miR-155-5p in breast cancer. There were positive correlation between MIAT and DUSP7 expression in breast cancer patients.MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p in breast cancer. MIAT was specifically up-regulated in the plasma and aqueous humor of cataract patients. 27527866 2016 Upregulation of long noncoding RNA MIAT in aggressive form of chronic lymphocytic leukemias. MINCR MINCR, LINC01604 100507316 ENSG00000253716 NR_120682 GRCh38_8:143280161-143281690 B-cell lymphoma NA M9591/3 qPCR, RNAi, Lentiviral infection, ChIP etc. cell lines (hT-RPE-MycER) up-regulated We focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Differential gene expression analysis after RNAi showed a significant enrichment of cell cycle genes among the genes down-regulated after MINCR knockdown. Interestingly, these genes are enriched in MYC binding sites in their promoters, suggesting that MINCR acts as a modulator of the MYC transcriptional program. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. 26351698 2015 MINCR is a MYC-induced lncRNA able to modulate MYC's transcriptional network in Burkitt lymphoma cells. MIR22HG MIR22HG, C17orf91 84981 ENSG00000186594 NR_028502 GRCh38_17:1711493-1717174 lung squamous cell carcinoma C34 M8070/3 microarray, qPCR etc. LSCC tissues down-regulated Finally, to ensure that our results was not population and technical specific, we assessed the expression level of 6 lncRNAs using qRT-PCR in all 47 paired lung SQCC tumors and NTL tissues. These lncRNAs were randomly chosen from differentially expressed lncRNA transcripts. In consistent with microarray analysis, the results demonstrated that all the 6 lncRNAs were down-regulated in lung SQCC tissues vs. matched non-tumor tissues. 26159226 2015 Genome-scale long noncoding RNA expression pattern in squamous cell lung cancer. NBAT1 NBAT1, CASC14, NBAT-1 729177 ENSG00000260455 NR_034143 GRCh38_6:22134957-22147193 neuroblastoma NA M9500/3 qPCR etc. primary neuroblastoma tissues down-regulated We identified a lncRNA neuroblastoma associated transcript-1 (NBAT-1) as a biomarker significantly predicting clinical outcome of neuroblastoma. CpG methylation and a high-risk neuroblastoma associated SNP on chromosome 6p22 functionally contribute to NBAT-1 differential expression. Loss of NBAT-1 increases cellular proliferation and invasion. It controls these processes via epigenetic silencing of target genes. NBAT-1 loss affects neuronal differentiation through activation of the neuronal-specific transcription factor NRSF/REST. 25517750 2014 The risk-associated long noncoding RNA NBAT-1 controls neuroblastoma progression by regulating cell proliferation and neuronal differentiation. NEAT1 NEAT1, LINC00084, NCRNA00084, TncRNA, VINC 283131 ENSG00000245532 NR_028272 GRCh38_11:65422774-65445540 breast cancer C50 NA qPCR, ISH etc. cell lines (MCF-7, MDA-MB-231, MDAMB-468) up-regulated Induction of NEAT1 in hypoxia also leads to accelerated cellular proliferation, improved clonogenic survival and reduced apoptosis, all of which are hallmarks of increased tumorigenesis. Furthermore, in patients with breast cancer, high tumor NEAT1 expression correlates with poor survival, all of which are hallmarks of increased tumorigenesis. 25417700 2014 Tumor hypoxia induces nuclear paraspeckle formation through HIF-2a dependent transcriptional activation of NEAT1 leading to cancer cell survival. PACER PACERR, PACER, PTGS2-AS1 103752588 ENSG00000273129 NR_125801 GRCh38_1:186680622-186681446 osteosarcoma NA M9180/3 qPCR, RNAi, Western blot, Cell proliferation assay etc. osteosarcoma tissues, cell lines (143B, MG63, Saos-2, U2OS, hFOB1.19) up-regulated The results showed that PACER was overexpressed in osteosarcoma tissues and cell lines compared with normal tissues and osteoblasts, respectively. PACER knockdown inhibited the proliferation and invasion of human osteosarcoma cells. Downregulation of PACER significantly suppressed the expression of COX-2, and the effects of PACER on cell proliferation and invasion were rescued by COX-2 overexpression. 26476537 2016 P50-associated COX-2 extragenic RNA (PACER) overexpression promotes proliferation and metastasis of osteosarcoma cells by activating COX-2 gene. PCAT5 PCAT5, LINC01452, TPCAT-10-36067 102578074 ENSG00000280719 NR_110138 GRCh38_10:35778302-35800920 prostate cancer C61.9 NA RNA-seq, qPCR, RNAi etc. cell lines (PC-3, 22Rv1) up-regulated In vitro validation of these alterations revealed a complex integrated phenotype affecting cell growth, migration, invasion, colony-forming potential and apoptosis. Our findings reveal a key molecular determinant of differences between PC and CRPC at the level of the transcriptome. Further, they establish PCAT5 as a novel oncogenic lncRNA in ERG-positive prostate cancers, with implications for defining CRPC biomarkers and new therapeutic interventions. 26282172 2015 Transcriptome sequencing reveals PCAT5 as a novel ERG-regulated long non-coding RNA in prostate cancer. PCGEM1 PCGEM1, LINC00071, NCRNA00071, PCAT9 64002 ENSG00000227418 NR_002769 GRCh38_2:192749845-192776899 prostate cancer C61.9 NA qPCR, RIP etc. prostate cancer tissues,cell lines (LNCaP, LNCaP-cds1, LNCaP-cds2, CWR22Rv1 etc.), tissues (prostate tumour tissues) up-regulated Here we report that two lncRNAs highly overexpressed in aggressive prostate cancer, PRNCR1 (also known as PCAT8) and PCGEM1, bind successively to the androgen receptor and strongly enhance both ligand-dependent and ligand-independent androgen-receptor-mediated gene activation programs and proliferation in prostate cancer cells. 23945587 2013 lncRNA-dependent mechanisms of androgen-receptor-regulated gene activation programs. PRNCR1 PRNCR1, CARLo-3, PCAT8 101867536 ENSG00000282961 NR_109833 GRCh38_8:127079874-127092600 prostate cancer C61.9 NA qPCR, RIP etc. prostate cancer tissues, cell lines (LNCaP, LNCaP-cds1, LNCaP-cds2, CWR22Rv1 etc.) up-regulated Here we report that two lncRNAs highly overexpressed in aggressive prostate cancer, PRNCR1 (also known as PCAT8) and PCGEM1, bind successively to the androgen receptor and strongly enhance both ligand-dependent and ligand-independent androgen-receptor-mediated gene activation programs and proliferation in prostate cancer cells. 23945587 2013 lncRNA-dependent mechanisms of androgen-receptor-regulated gene activation programs. TRERNA1 TRERNA1, LINC00651, treRNA 100887755 ENSG00000231265 NR_051976 GRCh38_20:50040716-50041504 gastric cancer C16 NA qPCR, Western blot, RIP etc. gastric cancer tissues, gastric cancer cell lines (MKN-28, MKN-45, Bgastric cancer-823, AGS, Mgastric cancer-803) up-regulated In the present study, we demonstrate that lncRNA TRERNA1 acts like an enhancer of SNAI1 to promote cell invasion and migration and to contribute to metastasis of gastric cancer (GC). Further studies have shown that TRERNA1 not just inhibits the expression of CDH1 by enhancing SNAI1 expression, but also epigenetically silenced CDH1 by recruiting EZH2 to carry out histone methylation of its promoter region. lncRNA TRERNA1 was identified and located close to SNAI1, which is an epithelial-mesenchymal transition (EMT) master regulator transcription factor.It has been found that the expression of CDH1 is not only regulated by the transcription factor SNAI1, but also by epigenetic modification, such as microRNA (miRNA), DNA methylation, and histone modification. 28918030 2017 LncRNA TRERNA1 Function as an Enhancer of SNAI1 Promotes Gastric Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition. 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. AK123263 LOC100506974 NA NA NA GRCh38_17:13776832-13777349 non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. AK126698 NA NA NA NA NA non small cell lung cancer C34 M8046/3 microarray, qPCR, RNAi, Western blot etc. cell lines (A549, CDDP etc.) down-regulated For lncRNA, the results showed that AK123263, CES1P1-001, RP3-508I15.14, AK126698, TP53TG1, and AC090952.4.1 decreased, whereas uc003bgl.1 and NCRNA00210 increased in A549/CDDP. Cisplatin resistance in non-small-cell lung cancer cells may relate to the changes in noncoding RNAs. Among these, AK126698 appears to confer cisplatin resistance by targeting the Wnt pathway. 23741487 2013 The noncoding RNA expression profile and the effect of lncRNA AK126698 on cisplatin resistance in non-small-cell lung cancer cell. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 papillary thyroid cancer NA M8260/3 qPCR, Cell transfection, Western blot, Flow cytometry assay, Cell proliferation assay etc. PTC tissues, cell lines (TPC-1, K1, BCPAP and CGTH-W3) down-regulated BANCR levels are lower in PTC tumor tissues than control tissues. Decreased BANCR levels correlate with tumor size, the presence of multifocal lesions and advanced PTC stage. BANCR overexpression reduced PTC cell proliferation and promoted apoptosis, which inhibited metastasis. It also inactivated ERK1/2 and p38, and this effect was enhanced by treatment with the MEK inhibitor U0126. Finally, BANCR overexpression dramatically inhibited tumor growth from PTC cells in xenograft mouse models. 27462868 2016 BRAF-activated LncRNA functions as a tumor suppressor in papillary thyroid cancer. BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 papillary thyroid cancer NA M8260/3 qPCR, RNAi, RIP, Flow cytometry assay etc. PTC tissues, cell line (IHH-4) up-regulated The expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. BANCR-knockdown in a PTC-derived cell line (IHH-4) resulted in significant suppression of thyroid stimulating hormone receptor (TSHR). BANCR-knockdown also led to inhibition of cell growth and cell cycle arrest at G0/G1 phase through down-regulation of cyclin D1. In addition, BANCR was enriched by polycomb enhancer of zeste homolog 2 (EZH2), and silencing BANCR led to decreased chromatin recruitment of EZH2, which resulted significantly reduced expression of TSHR. 26323637 2015 BRAF-activated Long Non-coding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 astrocytoma NA M9400/3 qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell migration and invasion assay, ISH etc. astrocytoma tissues, cell lines (U251 and U87) up-regulated High CASC2c was positively correlated with astrocytoma progression, and an unfavorable prognosis factor for patients. Knockdown CASC2c inhibited proliferation and tumorgenesis. Overexpression of CASC2c promotes the malignant characteristic of astrocytoma cells.CASC2c directly bound miR-101 and mediated pre-miR-101 processing into mature miR-101, and functions as a competitor of miR-101 target genes such as CPEB1. 28252647 2017 CASC2c as an unfavorable prognosis factor interacts with miR-101 to mediate astrocytoma tumorigenesis. DLEU2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 10301 ENSG00000176124 NR_002605 GRCh38_13:50082171-50723236 chronic lymphocytic leukemia NA M9823/3 microarray, qPCR, RNAi, ChIP, Luciferase reporter assay etc. blood up-regulated In contrast, the lncRNA genes DLEU1 and variant DLEU2/Alt1 that display DNA-hypomethylation at their 5' ends are significantly upregulated in CLL cells. We found a significant inverse correlation of gene expression of the lncRNA genes DLEU1 and the DLEU2 variant Alt1 with DNA-methylation levels in regions D6 and E6 that are localized at their transcriptional start sites. 23593011 2013 Epigenetic upregulation of lncRNAs at 13q14.3 in leukemia is linked to the In Cis downregulation of a gene cluster that targets NF-kB. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 endometrial cancer NA M8380/3 qRT-PCR, Western blot, Luciferase reporter assay, in vitro knockdown, RIP Human EC cell lines (HEC-1-A and Ishikawa) up-regulated MiR-646 expression was significantly decreased both in human EC tissues and cell lines compared with the control.Moreover, miR-646 expression was negatively related to HOTAIR in human EC tissues.miR-646 overexpression considerably attenuated the E2-promoted viability, migration and invasion of Ishikawa and HEC-1-A cells in vitro.In addition, HOTAIR was confirmed to regulate the viability, migration and invasion of EC cells through negative regulating miR-646.More importantly, we also demonstrated that NPM1 was the target of miR-646,and HOTAIR promoted NPM1 expression through interacting with miR-646 in EC cells.HOTAIR was well documented in recruiting PRC2 components and subsequent chromosomal gene silencing via coordinated histone H3K27 methylation and H3K4 demethylation. 29466670 2018 Long non-coding RNA HOTAIR mediates the estrogen-induced metastasis of endometrial cancer cells via miR-646/NPM1 axis. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 neurofibromatosis type 1 NA M9540/1 microarray, qPCR etc. blood up-regulated Single-nucleotide polymorphism rs2151280 (located in ANRIL) was statistically significantly associated with the number of PNFs in NF1 patients. In addition, allele T of rs2151280 was statistically significantly associated with reduced ANRIL transcript levels, suggesting that modulation of ANRIL expression mediates PNF susceptibility. Identification of ANRIL as a modifier gene in NF1 may offer clues to the molecular pathogenesis of PNFs, particularly neurofibroma formation, and emphasizes the unanticipated role of large noncoding RNA in activation of critical regulators of tumor development. 22034633 2011 Role of noncoding RNA ANRIL in genesis of plexiform neurofibromas in neurofibromatosis type 1. CTBP1-AS CTBP1-AS, PCAT10 285463 ENSG00000280927 NR_104331 GRCh38_4:1210120-1218591 prostate cancer C61.9 NA qPCR, Western blot, Northern blot, RIP etc. prostate cancer tissues, cell lines (VCaP, LNCaP, DU145, RWPE etc.) up-regulated CTBP1-AS is predominantly localized in the nucleus and its expression is generally upregulated in prostate cancer. CTBP1-AS promotes both hormone-dependent and castration-resistant tumour growth. Mechanistically, CTBP1-AS directly represses CTBP1 expression by recruiting the RNA-binding transcriptional repressor PSF together with histone deacetylases. CTBP1-AS also exhibits global androgen-dependent functions by inhibiting tumour-suppressor genes via the PSF-dependent mechanism thus promoting cell cycle progression. 23644382 2013 Androgen-responsive long noncoding RNA CTBP1-AS promotes prostate cancer. DLEU2 DLEU1, BCMS, BCMS1, DLB1, DLEU2, LEU1, LEU2, LINC00021, NCRNA00021, XTP6 8847 ENSG00000231607 NR_002612 GRCh38_13:49982552-50125720 chronic lymphocytic leukemia NA M9823/3 microarray, qPCR, RNAi, ChIP, Luciferase reporter assay etc. blood up-regulated In contrast, the lncRNA genes DLEU1 and variant DLEU2/Alt1 that display DNA-hypomethylation at their 5' ends are significantly upregulated in CLL cells. We found a significant inverse correlation of gene expression of the lncRNA genes DLEU1 and the DLEU2 variant Alt1 with DNA-methylation levels in regions D6 and E6 that are localized at their transcriptional start sites. 23593011 2013 Epigenetic upregulation of lncRNAs at 13q14.3 in leukemia is linked to the In Cis downregulation of a gene cluster that targets NF-kB. GAS5 GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 60674 ENSG00000234741 NR_002578 GRCh38_1:173863900-173868882 gastric cancer C16 NA qPCR etc. GC tissues differential expression Genotype del/del was significantly associated with a higher survival rate. Patients with late tumor stage were found to have a significantly lower rate of genotype del/del than those with an early tumor stage . Patients with UICC III and IV were found to have a significantly lower rate of genotype del/del than those with UICC I and II. The variant rs145204276 of GAS5 is associated with the development and prognosis of GC.The allele del of rs145204276 is associated with a remarkably lower incidence of cancer progression and metastasis. Methylation percentage of the 7th CpG site significantly correlated with GAS5 expression in the tumor tissues 29557411 2018 The Variant rs145204276 of GAS5 is Associated with the Development and Prognosis of Gastric Cancer. GNG12-AS1 GNG12-AS1 100289178 ENSG00000232284 NR_040077 GRCh38_1:67832303-68202987 breast cancer C50 NA qPCR, RNAi, ChIP etc. cell lines (HB2, SUM159, MCF7, K562, Hs27, CAL51, MCF10A etc.) down-regulated We report that GNG12-AS1 is coexpressed with DIRAS3 in several tissues and coordinately downregulated with DIRAS3 in breast cancers. In breast cancer cell lines with loss of DIRAS3 imprinting, DIRAS3 and GNG12-AS1 are silenced in cis and the remaining GNG12-AS1 transcripts are predominantly monoallelic. 23871723 2013 Imprinted chromatin around DIRAS3 regulates alternative splicing of GNG12-AS1, a long noncoding RNA. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 acute myeloid leukemia NA M9861/3 qPCR etc. acute myeloid leukemia tissues, cell lines (HL60 and K562) up-regulated H19 expression was significantly increased in AML patients but not associated with embedded miR-675 expression. Moreover, H19 overexpression was not dependent on the methylation pattern in H19 differentially methylated region/imprinting control region. Strong association was observed between H19 overexpression and patients' characteristics including sex, higher white blood cells, older age, and intermediate karyotype, FLT3-ITD, and DNMT3A mutations. In addition, H19 overexpression correlated with lower complete remission (CR) rate and shorter overall survival, and further confirmed by multivariate analyses. Importantly, the prognostic effect of H19 expression was validated by TCGA and GEO data. In the follow-up of patients, H19 expression in CR phase was lower than diagnosis time and returned at relapse time. 29643943 2018 H19 overexpression promotes leukemogenesis and predicts unfavorable prognosis in acute myeloid leukemia. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 breast cancer C50 NA qPCR etc. cell line (MCF7) up-regulated When compared with MCF-7 cells, MCF-7-TNR cells exhibited an increase in the expression of HOTAIR, which correlated with characteristics of a luminal-like to basal-like transition as evidenced by dysregulated gene expression and accelerated growth. MCF-7-TNR cells exhibited reduced suppressive histone H3 lysine27 trimethylation on the HOTAIR promoter. Inhibition of HOTAIR and EZH2 attenuated the luminal-like to basal-like transition in terms of gene expression and growth in MCF-7-TNR cells. 25328122 2014 Elevated expression of long intergenic non-coding RNA HOTAIR in a basal-like variant of MCF-7 breast cancer cells. lincRNA-p21 TP53COR1, TRP53COR1, linc-p21, lincRNA-p21 102800311 NA NA NA colorectal cancer C19.9 NA qPCR, Western blot, RIP cancer tissues, human colorectal cancer cell lines (SW480, SW620) down-regulated In our study, we determined the anti-metastatic effect of EGb 761 on colorectal cancer cells and further explored the potential underlying regulatory mechanism.Plants have provided a rich source of therapeutic agents and bases for synthetic drugs. Previous studies indicated that LincRNA-p21 functioned as an tumor suppressor gene through participation in epigenetic regulation, such as histone methylation and/or CpG methylation at pluripotency gene promoters. Long intergenic non-coding RNA-p21 (LincRNA-p21) (3100 nt) is located on chromosome 6, approximately 15 kb upstream from the Cdkn1a (p21) gene. 29207671 2017 Ginkgo biloba extract EGb 761-induced upregulation of LincRNA-p21 inhibits colorectal cancer metastasis by associating with EZH2. MIR100HG MIR100HG, AGD1, linc-NeD125, lncRNA-N2 399959 ENSG00000255248 NR_024430 GRCh38_11:122028327-122556721 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Cell proliferation assay, Cell migration assay etc. cell lines (HepG2, SMMC-7721 and HCCLM9) differential expression Knockdown of seven of the ten candidate lncRNAs significantly affected cell migration in at least one cell line; knockdown of three lncRNAs produced accordant alterations in cell migration in at least two cell lines by suppressing or promoting cell migration 28194035 2017 Recurrently deregulated lncRNAs in hepatocellular carcinoma. 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. 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. PVT1 PVT1, LINC00079, MYC, NCRNA00079, onco-lncRNA-100 5820 ENSG00000249859 NR_003367 GRCh38_8:127794533-128101253 B-cell lymphoma NA M9591/3 qPCR, FISH, ISH etc. bone marrow, lymph node, pleural effusion differential expression In addition, not only MYC rearrangement but also PVT1 rearrangement may also be implicated in the disease development of HABCLs with 8q24 abnormalities. 23547836 2013 Deletion or methylation of CDKN2A/2B and PVT1 rearrangement occur frequently in highly aggressive B-cell lymphomas harboring 8q24 abnormality. RP1-153P14.5 RP1-153P14.5 NA NA NA GRCh38_6:37545145-37550860 hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Cell proliferation assay, Cell migration assay etc. cell lines (HepG2, SMMC-7721 and HCCLM9) differential expression Knockdown of seven of the ten candidate lncRNAs significantly affected cell migration in at least one cell line; knockdown of three lncRNAs produced accordant alterations in cell migration in at least two cell lines by suppressing or promoting cell migration 28194035 2017 Recurrently deregulated lncRNAs in hepatocellular carcinoma. XIST XIST, DXS1089, DXS399E, LINC00001, NCRNA00001, SXI1, swd66 7503 ENSG00000229807 NR_001564 GRCh38_X:73820651-73852753 glioma NA M9380/3 qPCR, Western blot, Luciferase assay, RIP etc. glioma tissues, PTBE tissues.Human glioma cell lines (U251, U373, LN229, U118, LN229) up-regulated Our data suggest that XIST can amplify the chemoresistance of glioma cell lines to TMZ through directly targetting miR-29c via SP1 and MGMT. XIST/miR-29c may be a potential therapeutic target for glioma treatment.Low XIST expression predicts drug response in PDXs associated with a significant reduction in the breast cancer stem cells population. Kaplan–Meier overall survival curves for 69 patients with glioma classified according to relative XIST expression level.Methylation damage can be reversed by MGMT. In addition, SP1 has been reported to regulate one of the key MMR proteins, MSH6. Recent evidence emphasizes the key regulatory roles of non-coding RNAs (lncRNAs and miRNAs) in tumor biology, including the chemoresistance of cancers.Additionally, the effect of miR-29c mimics or inhibitor on luciferase activity was offset by mutations in XIST. 28831025 2017 LncRNA-XIST interacts with miR-29c to modulate the chemoresistance of glioma cell to TMZ through DNA mismatch repair pathway. ZEB1-AS1 NR_024284 220930 ENSG00000237036 NR_024284 GRCh38_10:31206278-31320447 prostate cancer C61.9 NA Western blot, Luciferase reporter, RIP cell lines (PC3, DU145, NCI-H1299, A549, T98G, U251, A375, A875, HUVEC, HBE, SK-MES-1, HeLa, 293, LO2). up-regulated Collectively, ZEB1-AS1 functions as an oncogene in prostate cancer via epigenetically activating ZEB1 and indirectly regulating downstream molecules of ZEB1. Also, BMI1 promotes cell survival and attenuated chemosensitivity to docetaxelin prostate cancer. Work in mammalian H3K4 methylation has primarily focused on MLL1, the function of which depends on the participation of the helper proteins WDR5, RBBP5 and ASH2L. The discrepancies above might be explained by different cell lines used in different studies or different splicing variants of ZEB1-AS1.A construct with site-directed mutation of the corresponding seed sequence GTCATAT was prepared by overlapping PCR and designated as pGL3-BMI1-MUT. Dual reporter gene assay was performed as described. 28830551 2017 Long noncoding RNA ZEB1-AS1 epigenetically regulates the expressions of ZEB1 and downstream molecules in prostate cancer. 7SK RN7SK, 7SK 125050 ENSG00000283293 NR_001445 GRCh38_6:52995621-52995948 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues up-regulated The majority (14 out of 17) of these lncRNAs were confirmed to be dysregulated in HCC compared to the surrounding non-tumorous tissues, corroborating the reliability of our profiling data. 27894309 2016 Analysis of long noncoding RNA expression in hepatocellular carcinoma of different viral etiology. AB074278 NA NA NA NA GRCh38_17:63039470-63041178 urothelial cancer NA M8120/3 microarray, qPCR, RNAi, in vitro knockdown etc. urothelial carcinoma of the bladder tissues up-regulated AB074278 was chosen because it was significantly upregulated in all tumour phenotypes, strongly associated with tumour progression, and has a low protein coding potential score.AB074278 in apoptosis avoidance and the maintenance of a pro-proliferative state in cancer through a potential interaction with EMP1, a tumour suppressor and a negative regulator of cell proliferation. 25165097 2014 Identification of differentially expressed long noncoding RNAs in bladder cancer. AC026166.2-001 MTCO1P5 NA ENSG00000233026 NA GRCh38_3:12165299-12165642 laryngeal squamous cell cancer C32.3 NA microarray, qPCR etc. LSCC tissues down-regulated AC026166.2-001 and RP11-169D4.1-001 were distinctly dysregulated, with AC026166.2-001 exhibiting lower expression in cancer tissues and RP11-169D4.1-001 higher expression. We verified that both AC026166.2-001 and RP11-169D4.1-001 were expressed at a lower level in cervical lymph nodes compared with paired laryngeal cancer tissues and paired normal tissues. RP11-169D4.1-001 levels were positively correlated with lymph node metastasis. 25243407 2014 Long non-coding RNA profiling in laryngeal squamous cell carcinoma and its clinical significance: potential biomarkers for LSCC. 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). AGAP2-AS1 AGAP2-AS1, PUNISHER 100130776 ENSG00000255737 NR_027032 GRCh38_12:57726271-57728356 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot, Flow cytometry assay etc. NSCLC tissues, cell lines (A549, PC9, SPCA1, H1975 and H1299, H520, SK-MES-1 and H1703) up-regulated The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vitro loss- and gain-of-function assays revealed that AGAP2-AS1 knockdown inhibited cell proliferation, migration and invasion, and induced cell apoptosis. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription. Taken together, our findings indicate that AGAP2-AS1 may act as an oncogene by repressing tumor-suppressor LATS2 and KLF2 transcription. 27195672 2016 Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells. 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). AK129685 NA NA NA NA GRCh38_19:13837806-13840186 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). AK130275 PAX8-AS1 654433 ENSG00000189223 NR_015377 GRCh38_2:113211522-113276581 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). AK130977 NA NA NA NA GRCh38_20:36550794-36551444 malignant pleural mesothelioma NA M9050/3 microarray, qPCR etc. MPM tissues, cell lines (H28, H226, H2052, H2452, MSTO etc.) up-regulated AK130977 and AX746718 were both found to be down-regulated via both microarray and RT-qPCR (AK130977 Microarray (MA) = -5.207, RT-qPCR = -1.6; AX746718 MA = -3.37, RT-qPCR = -4.6), with AK130977 demonstrating fairly small changes using RT-qPCR. Similarly, BX648695, AK129685, EF177379, AK054908, AK130275, AF268386 and NR_003584 all demonstrated consistent up-regulation using both microarrays and RT-qPCR. 23976967 2013 Long non coding RNAs (lncRNAs) are dysregulated in Malignant Pleural Mesothelioma (MPM). ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 gastric cancer C16 NA qPCR, RNAi, Western blot, RIP etc. gastric cancer tissues, cell lines (SGC7901, BGC823, MGC803) up-regulated Higher expression of ANRIL was significantly correlated with a higher TNM stage and tumor size. Further experiments revealed that ANRIL knockdown significantly repressed the proliferation both in vitro and in vivo. We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation. 24810364 2014 Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a. ANRIL CDKN2B-AS1, ANRIL, CDKN2B-AS, CDKN2BAS, NCRNA00089, PCAT12, p15AS 100048912 ENSG00000240498 NR_003529 GRCh38_9:21994778-22121097 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues up-regulated The majority (14 out of 17) of these lncRNAs were confirmed to be dysregulated in HCC compared to the surrounding non-tumorous tissues, corroborating the reliability of our profiling data. 27894309 2016 Analysis of long noncoding RNA expression in hepatocellular carcinoma of different viral etiology. 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). BANCR BANCR, LINC00586 100885775 ENSG00000278910 NR_047671 GRCh38_9:69296682-69311111 non small cell lung cancer C34 M8046/3 qPCR, RNAi, Western blot etc. NSCLC tissues, cell lines (A549, SPC-A1, NCI-H1975, SK-MES-1 etc.) down-regulated BANCR expression was significantly decreased in 113 NSCLC tumor tissues compared with normal tissues. Additionally, reduced BANCR expression was associated with larger tumor size, advanced pathological stage, metastasis distance, and shorter overall survival of NSCLC patients. Reduced BANCR expression was found to be an independent prognostic factor for NSCLC. Histone deacetylation was involved in the downregulation of BANCR in NSCLC cells. Ectopic expression of BANCR impaired cell viability and invasion, leading to the inhibition of metastasis in vitro and in vivo. Overexpression of BANCR was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression. 24655544 2014 Downregulation of BRAF activated non-coding RNA is associated with poor prognosis for non-small cell lung cancer and promotes metastasis by affecting epithelial-mesenchymal transition. BC016831 LOC101926959 NA NA NA NA triple negative breast cancer C50 NA microarray, qPCR etc. primary breast cancer tissues, cell lines (MDA-MB-231, HCC-1937, MDA-MB-468, MDA-MB-453 etc.) down-regulated The qRT-PCR results showed that, compared with non-TNBC tissues, C17orf76-AS1 and CTC-338M12.3 were dominantly up-regulated in TNBC tissues; on the other hand, RP11-434D9.1, IGKV, LINC00052, BC016831, RP4-781K5.4, and LOC441242 were obviously down-regulated. However, there are some differences between the lncRNA expression patterns of tissues and cell lines. Briefly, compared with the non-TNBC cell group, only 4 lncRNAs (BC016831, IGKV, LINC00052, and RP11-434D9.1) were down-regulated congruously in all 4 TNBC cells. 26910840 2016 LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer. BC017743 NA NA NA NA GRCh38_3:78821184-78823458 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues up-regulated The majority (14 out of 17) of these lncRNAs were confirmed to be dysregulated in HCC compared to the surrounding non-tumorous tissues, corroborating the reliability of our profiling data. 27894309 2016 Analysis of long noncoding RNA expression in hepatocellular carcinoma of different viral etiology. BC043430 NA NA NA NA GRCh38_3:78920653-78922485 hepatocellular carcinoma C22.0 M8170/3 microarray, qPCR etc. HCC tissues up-regulated The majority (14 out of 17) of these lncRNAs were confirmed to be dysregulated in HCC compared to the surrounding non-tumorous tissues, corroborating the reliability of our profiling data. 27894309 2016 Analysis of long noncoding RNA expression in hepatocellular carcinoma of different viral etiology. BM742401 GATA6-AS1, BM742401, locus5689 100128893 ENSG00000266010 NR_102763 GRCh38_18:22166898-22168968 chronic lymphocytic leukemia NA M9823/3 qPCR, MSP-PCR, Western blot, in vitro knockdown etc. bone marrow, cell lines (MEC1 and CLL-AAT) up-regulated The promoter of BM742401 was unmethylated in normal controls including three each of normal bone marrow, peripheral blood buffy coats, and CD19-sorted peripheral B-cells, but methylated in four (57.1%) CLL cell lines. Functionally, stable overexpression of BM742401 resulted in inhibition of cellular proliferation and enhanced apoptosis through caspase-9-dependent intrinsic but not caspase-8-dependent extrinsic apoptosis pathway, suggesting a tumor suppressor role of BM742401 in CLL. In primary CLL samples, methylation of BM742401 was detected in 43/98 (43.9%) of patients. 27689399 2016 Epigenetic silencing of tumor suppressor long non-coding RNA BM742401 in chronic lymphocytic leukemia. CASC2 CASC2, C10orf5 255082 ENSG00000177640 NR_026939 GRCh38_10:118046279-118210153 renal cell carcinoma C64.9 NA qPCR, Cell transfection, Dual-luciferase reporter assay, Cell proliferation assay etc. RCC tissues, cell lines (786-O and A498) down-regulated The present study confirmed that CASC2 was downregulated in human RCC tissues and human RCC cell lines (786-O and A498). Restoration of CASC2 expression via transfection with a pcDNA3.1(+)-CASC2 vector was able to inhibit cell proliferation and migration in 786-O and A498 cells. Bioinformatics analysis and dual-luciferase reporter assays confirmed that CASC2 was a direct target gene of miR-21. miR-21 was able to decrease the expression of CASC2 in 786-O and A498 cells. Furthermore, overexpression of miR-21 partly abrogated CASC2-mediated inhibition of 786-O and A498 cell proliferation and migration. 27222255 2016 Downregulation of lncRNA CASC2 by microRNA-21 increases the proliferation and migration of renal cell carcinoma cells. CCAT1 CCAT1, CARLo-5, onco-lncRNA-40 100507056 ENSG00000247844 NR_108049 GRCh38_8:127207382-127219268 esophageal squamous cell cancer NA NA qPCR, RNAi, Western blot, Cell proliferation assay etc. ESCC tissues, cell lines (Eca-109 and TE-1) up-regulated We found that lncRNA CCAT1, whose expression is significantly increased and is correlated with outcomes in Esophageal Squamous Cell Carcinoma.Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo. In cytoplasm, CCAT1 regulates HOXB13 as a molecular decoy for miR-7, a microRNA that targets both CCAT1 and HOXB13, thus facilitating cell growth and migration. 27956498 2017 H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma. FAS-AS1 FAS-AS1, FAS-AS, FASAS, SAF 100302740 NA NR_028371 NA B-cell lymphoma NA M9591/3 qPCR, RIP, ChIP, ELISA etc. blood, cell lines (B-lymphocytes, Granta-519) down-regulated We found that the alternative splicing of Fas in lymphomas is tightly regulated by a long-noncoding RNA corresponding to an antisense transcript of Fas (FAS-AS1). Levels of FAS-AS1 correlate inversely with production of sFas, and FAS-AS1 binding to the RBM5 inhibits RBM5-mediated exon 6 skipping. EZH2, often mutated or overexpressed in lymphomas, hyper-methylates the FAS-AS1 promoter and represses the FAS-AS1 expression. EZH2-mediated repression of FAS-AS1 promoter can be released by DZNeP (3-Deazaneplanocin A) or overcome by ectopic expression of FAS-AS1, both of which increase levels of FAS-AS1 and correspondingly decrease expression of sFas. 24811343 2014 FAS-antisense 1 lncRNA and production of soluble versus membrane Fas in B-cell lymphoma. GIHCG NA NA NA NA NA hepatocellular carcinoma C22.0 M8170/3 qPCR, RNAi, Western blot, Northern blot, RIP, ChIP, RNA pull-down assay, Cell proliferation assay etc. HCC tissues, cell lines (L02, QSG7701, SMMC7721, Hep3B, Huh7, and HCCLM3) up-regulated Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression. 27380494 2016 Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 laryngeal squamous cell cancer C32.3 NA qPCR, Western blot, Luciferase reporter assay etc. LSCC tissues, cell line (Hep-2) up-regulated We identified microRNA miR-148a-3p as an inhibitory target for H19. Overexpression of miR-148a-3p reduced LSCC migration, invasion and proliferation cell, while inhibition of miR-148a-3p did the opposite. The inhibition of LSCC progression induced by H19 knockdown required the activity of miR-148a-3p. We also identified DNA methyltransferase enzyme DNMT1 as a target of miR-148a-3p. Cellular DNA methylation levels were inhibited by both miR-148a-3p overexpression and H19 knockdown 26872375 2016 Regulation of laryngeal squamous cell cancer progression by the lncRNA H19/miR-148a-3p/DNMT1 axis H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 liver cancer C22.0 NA qPCR, RNAi, Western blot, ChIP, Dual-luciferase reporter assay, Cell proliferation assay etc. cell lines (Hep3B and HepG2) up-regulated Herein, we demonstrate miR675 overexpression promotes and silencing miR675 attenuated liver cancer cell growth in vitro and in vivo. Mechanistically, miR675 inhibits the heterochromatin1 isoform HP1a expression in human liver cancer cells which causes a dramatically decrease of the total histone H3 lysine 9 trimethylation (H3K9me3), histone H3 lysine 27 trimethylation (H3K27me3) and a increase of histone H3 lysine 27 acetylation(H3K27Ac). Notably, a significant reduction of the H3K9me3 and H3K27me3 and the increment of H3K27Ac occupancy on the promoter region of EGR1 triggers EGR1 transcription, translation, sumoylation and activation which upregulates lincRNA H19. 26376677 2015 miR675 upregulates long noncoding RNA H19 through activating EGR1 in human liver cancer. H19 H19, ASM, ASM1, BWS, D11S813E, LINC00008, NCRNA00008, WT2 283120 ENSG00000130600 NR_002196 GRCh38_11:1995176-2001470 glioblastoma NA M9440/3 RT-qPCR, Western blot, in vitro knockdown, RIP glioblastoma tissues, cell lines (A172, LN229, U87MG, LN18 and T98G) up-regulated Most importantly,we provide a mechanistic perspective about the role of H19 in glioblastoma cells,by showing that its expression is inversely linked to that of NKD1,a negative regulator of Wnt pathway, suggesting that H19 might regulate NKD1 transcription via EZH2-induced H3K27 trimethylation of its promoter.Indeed, we showed that H19 binds EZH2 in glioblastoma cells,and that EZH2 binding to NKD1 and other promoters is impaired by H19 silencing.The molecular mechanisms described so far for an oncogenic role of H19 in GBM range from H19 processing to produce miR-675 to a function as sponge for miR-29a, in turn boosting tumor angiogenesis. 29643989 2018 The lncRNA H19 positively affects the tumorigenic properties of glioblastoma cells and contributes to NKD1 repression through the recruitment of EZH2 on its promoter. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 chondrosarcoma NA M9220/3 qPCR, RNAi, Western blot, Luciferase reporter assay, CCK-8 assay etc. chondrosarcoma tissues, cell lines (HC-a, SW1353, OUMS-27, HCS-2/8, JJ012) up-regulated HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. Functional experiments reveal that HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo. In addition to cycle arrest and apoptosis, knockdown of HOTAIR inhibits autophagy, which favors cell death. Mechanistically, we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions,which markedly silences miR-454-3p expression. Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p,initiate HOTAIR deficiency-induced apoptosis and reduce autophagy. 28182000 2017 Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth. HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 bladder cancer C67 NA qPCR, Western blot, Northern blot etc. cell lines (HCV29, 5637, T24, J82, SW780) up-regulated We have identified cyclin J (CCNJ) gene, which is involved in cell cycle regulation, as a novel target for miR-205. Furthermore, a long non-coding RNA HOTAIR (HOX transcript antisense RNA) was observed to participate in the silencing of miR-205 in bladder cancer cells by breaking the balance of histone modification between H3K4me3 (histone H3 at lysine 4 methylation) and H3K27me3 on miR-205 promoter. 26469956 2015 Long non-coding RNA HOTAIR regulates cyclin J via inhibition of microRNA-205 expression in bladder cancer HOTAIR HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 100124700 ENSG00000228630 NR_003716 GRCh38_12:53962308-53974956 pancreatic cancer C25 NA qPCR, RNAi, Western blot, Luciferase reporter assay etc. pancreatic cancer tissues, cell lines (BXPC3, CFPAC-1, Panc-1 and L3.6pl) up-regulated The long non-coding RNA, HOTAIR, was up-regulated in both pancreatic cancer cells and tissues, and HOTAIR suppressed the expression of miR-663b in pancreatic cancer by histone modification on H3K4me3 and H3K27me3 on miR-663b promoter. Further in vivo studies demonstrated that the stable overexpression of miR-663b or knock-down of HOTAIR inhibited tumor growth and was associated with IGF2 expression. 27895308 2016 Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2. HULC HULC, HCCAT1, LINC00078, NCRNA00078 728655 ENSG00000251164 NR_004855 GRCh38_6:8435568-9294133 hepatocellular carcinoma C22.0 M8170/3 qPCR etc. HCC tissues, cell lines (H7402, Huh7, HepG2, and HepG2.2.15) up-regulated HULC modulated the deregulation of lipid metabolism in HCC by activating the acyl-CoA synthetase subunit ACSL1. Moreover, HULC mRNA levels correlated positively with ACSL1 levels in 60 HCC cases according to real-time PCR analysis. Mechanistic investigations showed that HULC upregulated the transcriptional factor PPARA, which activated the ACSL1 promoter in hepatoma cells. HULC also suppressed miR-9 targeting of PPARA mRNA by eliciting methylation of CpG islands in the miR-9 promoter. We documented the ability of HULC to promote lipogenesis, thereby stimulating accumulation of intracellular triglycerides and cholesterol in vitro and in vivo. 25592151 2015 Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway. 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?