| Related LncRNAs | |||||||||
|---|---|---|---|---|---|---|---|---|---|
| ID | lncRNA Name | Disease | Method | Sample | Expression pattern | Dysfunction type | Description | PMID | Source |
| EL0016 | AB073614 | glioma | qRT-PCR | N/A | up-regulated | N/A | AB073614 expression was significantly up-regulated in cancerous tissues compared with normal brain tissues | 27104549 | |
| EL0032 | ADAMTS9-AS2 | glioma | qPCR, Western blot, knockdown etc. | glioma tumor tissue, cell lines (T98G, A172, SNB-19 etc.) | down-regulated | regulation | A new tumor suppressor?LncRNA?ADAMTS9-AS2 is regulated by DNMT1 and inhibits migration of glioma cells. | 24833086 | LncRNADisease Lnc2Cancer |
| EL0237 | BCYRN1 | glioma | qPCR etc. | cell lines(U251, U87) | down-regulated | expression | 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 | Lnc2Cancer |
| EL0265 | CADM1 | glioma | qPCR, knockdown etc. | glioma cancer tissue, cell lines ( U87, U251, SNB-19 etc.) | down-regulated | expression | The data showed that TSLC1-AS1 expression was down-regulated in tumor tissues compared with that in adjacent normal tissues, and negatively associated with the WHO criteria of the tumors. Overexpression of TSLC1-AS1 resulted in up-regulation of TSLC1 and significant inhibition of cell proliferation, migration and invasion in U87 cells, while knockdown of TSLC1-AS1 in SNB-19 cells showed the opposite effetc. The expression of TSLC1-AS1 was also positively correlated with other tumor suppressors NF1, VHL, PIK3R1 and negatively correlated with the oncogene BRAF. | 25031725 | Lnc2Cancer |
| EL0272 | CASC2 | glioma | qPCR, Luciferase reporter assay etc. | glioma tissue, cell lines (U251, U87) | down-regulated | regulation | In this study, we confirmed that CASC2 was lowly expressed in glioma tissues as well as in U251 and U87 glioma cell lines. Overexpression of CASC2 inhibited the malignancy of glioma cells, including proliferation, migration, and invasion, and promoted cell apoptosis.We found that up-regulated CASC2 decreased the expression of miR-21 significantly and there is a reciprocal repression between CASC2 and miR-21 in an Argonaute2-dependent manner. | 25446261 | Lnc2Cancer |
| EL0282 | CCDC26 | glioma | N/A | N/A | N/A | mutation | In the pooled analysis, the odds ratio for low-grade glioma associated with rs55705857 was 4.3 (P = 2.31 脳 10(-94)). rs55705857 maps to a highly evolutionarily conserved sequence within the long non-coding RNA CCDC26 raising the possibility of direct functionality. | 23399484 | LncRNADisease |
| EL0289 | CDKN2B-AS1 | glioma | N/A | N/A | N/A | mutation | Variants (rs1412829, C>T) in the CDKN2B and RTEL1 regions are associated with high-grade glioma susceptibility. | 19578366 | LncRNADisease |
| EL0289 | CDKN2B-AS1 | glioma | N/A | N/A | N/A | mutation | Association identified by GWAS. | 19578367 | LncRNADisease |
| EL0289 | CDKN2B-AS1 | glioma | N/A | N/A | N/A | mutation | More recent GWAS also identified ANRIL as a risk locus (rs3217992, A>G;rs1063192, C>T) for gliomas and basal cell carcinomas in accordance with the princeps observation. | 20956613 | LncRNADisease |
| EL0289 | CDKN2B-AS1 | glioma | N/A | N/A | N/A | locus | A genetic susceptibility locus. | 20956613 | LncRNADisease |
| EL0289 | CDKN2B-AS1 | glioma | N/A | N/A | N/A | mutation | Moreover, genome-wide association studies have demonstrated that the 9p21 genomic locus is a hotspot for the risk of stroke, glioma, plexiform neurofibroma and other disorders | 22814587 | LncRNADisease |
| EL0289 | CDKN2B-AS1 | glioma | N/A | N/A | N/A | mutation | Genetic variation in lncRNA genes causes disease and influences susceptibility | 23791884 | LncRNADisease |
| EL0289 | CDKN2B-AS1 | glioma | qPCR etc. | glioma tissue | differential expression | mutation | Risk SNPs (rs3217992, A>G;rs1063192, C>T) for coronary disease, stroke, diabetes, melanoma, and glioma were all associated with allelic expression of ANRIL. | 20386740 | LncRNADisease Lnc2Cancer |
| EL0305 | CRNDE | glioma | qPCR, Western blot, ChIP, Flow cytometry assay etc. | glioma tissue, cell lines(U87MG, U251) | up-regulated | expression | Overexpression of specific CRNDE transcript promotes cell growth and migration in vitro while knockdown of CRNDE expression manifests a repressive function during these cellular processes. Mechanistic studies further revealed that histone acetylation in the promoter region might account for the upregulation of CRNDE, and the level of CRNDE expression could be modulated by mammalian Target of Rapamycin (mTOR) signaling in glioma. | 25813405 | Lnc2Cancer |
| EL0556 | H19 | glioma | microarray, qPCR, Western blot, knockdown, Luciferase reporter assay etc. | glioma tissue, cell lines (U87, U251 etc.) | up-regulated | regulation | Long non-coding RNA H19 promotes glioma cell invasion by deriving miR-675. | 24466011 | LncRNADisease Lnc2Cancer |
| EL0556 | H19 | glioma | N/A | N/A | N/A | regulation | Epigenetic deregulation of lncRNAs genes is associated with disease | 23791884 | LncRNADisease |
| EL0578 | HOTAIR | glioma | microarray, Western blot etc. | glioblastoma tissue | up-regulated | N/A | HOTAIR expression was significantly higher in HGG than in low-grade glioma (LGG; P < .001). Moreover, as shown in Fig. 1A, GBM demonstrated a significant increase in HOTAIR transcript levels, compared with that observed in normal tissues (P = .093), LGGs (P < .001), or AGs (P = .011). Our data establish that HOTAIR serves as a prognostic factor for glioma patient survival, as well as a biomarker for identifying glioma molecular subtypes, a critical regulator of cell cycle progression. | 24203894 | Lnc2Cancer |
| EL0578 | HOTAIR | glioma | qRT-PCR, knock-down | glioma U87 and U251 cell lines | up-regulated | expression | knock-down of HOTAIR exerted tumor-suppressive function in glioma cells. Further, HOTAIR was confirmed to be the target of miR-326 and miR-326 mediated the tumor-suppressive effects of HOTAIR knock-down on glioma cell lines | 26183397 | |
| EL0600 | HULC | glioma | N/A | glioma patient tissues | up-regulated | N/A | positively correlated with grade dependency in glioma patient tissues | 26894862 | |
| EL0853 | MALAT1 | glioma | microarray, qPCR, Western blot, knockdown etc. | cell line SHG139S | down-regulated | interaction | Our results showed that downregulation of MALAT1 suppressed the expression of Sox2 and Nestin which are related to stemness, while downregulation of MALAT1 promoted the proliferation in SHG139S. Further research on the underlying mechanism showed that the effects of MALAT1 downregulation on SHG139S were through regulating ERK/MAPk signaling activity. And we also found that downregulation of MALAT1 could activate ERK/MAPK signaling and promoted proliferation in SHG139 cells. | 26649728 | Lnc2Cancer |
| EL0853 | MALAT1 | glioma | qPCR etc. | glioma tissue | up-regulated | expression | LncRNA MALAT1 expression was increased in glioma tissues compared with paired adjacent brain normal tissues. Furthermore, lncRNA MALAT1 was associated significantly with WHO grade (I-II vs. III-IV; P = 0.007) and tumor size. Moreover, the level of lncRNA MALAT1 expression was markedly correlated with the glioma patients' overall survival. Multivariate analysis suggested that increased lncRNA MALAT1 expression was a poor independent prognostic predictor for glioma patients. | 25613066 | Lnc2Cancer |
| EL0853 | MALAT1 | glioma | qPCR, Western blot, Luciferase reporter assays, RIP, ChIP etc. | glioma samples and normal brain tissues, cell lines (hCMEC/D3, ECs) | up-regulated | interaction | Our results proved that MALAT1 expression was up-regulated in brain microvessels of human glioma and glioma endothelial cells (GECs) which were obtained by co-culturing endothelial cells with glioma cells. Functionally, knockdown of MALAT1 resulted in an impairment and increased the permeability of BTB as well as decreased the expression of ZO-1, occludin and claudin-5 in GECs. Further, there was reciprocal repression between MALAT1 and miR-140, and miR-140 mediated the effects that MALAT1 knockdown exerted. Mechanistic investigations defined that nuclear factor YA (NFYA), a CCAAT box-binding transcription factor, was a direct and functional downstream target of miR-140, which was involved in the MALAT1 knockdown induced regulation of BTB function. Furthermore, NFYA could up-regulate the promoter activities and bind to the promoters of ZO-1, occludin and claudin-5 in GECs. | 26619802 | Lnc2Cancer |
| EL0861 | MEG3 | glioma | N/A | gliomas tissues | down-regulated | epigenetics | The downregulation of MEG3 expression due to hypermethylation of MEG3 was observed in gliomas tissues. Treatment of glioma cells with the DNA methylation inhibitor 5-Aza-2'-deoxycytidine (5-AzadC) decreased aberrant hypermethylation of the MEG3 promoter and prevented the loss of MEG3 expression. | 26676363 | |
| EL0861 | MEG3 | glioma | qPCR etc. | cell lines(U251, U87) | up-regulated | expression | 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 | Lnc2Cancer |
| EL0861 | MEG3 | glioma | qPCR, ISH etc. | neuroglioma tissue | down-regulated | expression | MEG3 expression is lost. | 14602737 | LncRNADisease Lnc2Cancer |
| EL0861 | MEG3 | glioma | qPCR, Luciferase reporter assay etc. | cell lines (U251, U87 etc.) | down-regulated | expression | Overexpression of the long non-coding RNA MEG3 impairs in vitro glioma cell proliferation. | 22234798 | LncRNADisease Lnc2Cancer |
| EL0877 | MIR155HG | glioma | qPCR etc. | cell lines(U251, U87) | down-regulated | expression | 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 | Lnc2Cancer |
| EL0973 | NEAT1 | glioma | qPCR etc. | glioma tissue | up-regulated | expression | In our results, the relative level of NEAT1 expression was higher in cancer tissues compared with adjacent noncancerous tissues (p < 0.001). High NEAT1 expression was observed to be closely correlated with larger tumor size (p = 0.023), higher WHO grade (p = 0.005), and recurrence (p = 0.011). | 26582084 | Lnc2Cancer |
| EL1077 | linc-POU3F3 | glioma | qPCR etc. | glioma tissue, cell lines (T98G, A172) | up-regulated | N/A | By using real-time PCR and gain-/loss-of-function studies,the authors revealed that linc-POU3F3 levels were extraordinarily associated with the tumor WHO grade.In related biochemical assays, overexpression of linc-POU3F3 promotes cell viability and proliferation in glioma cells, whereas knockdown of linc-POU3F3 showed the opposite effect. As expected, they also found that linc-POU3F3 expression was negatively correlated with the mRNA level of POU3F3. | 25445282 | LncRNADisease Lnc2Cancer |
| EL1240 | SPRY4-IT1 | glioma | qPCR, Western blot, knockdown etc. | glioma cell lines (U251, SF295) and the normal human astrocytes (NHA) | up-regulated | expression | We examined for the first time the expression and role of SPRY4-IT1 in glioma cells. The results of our study showed that SPRY4-IT1 was up-regulated in human glioma tissues and cell lines. Knockdown of SPRY4-IT1 could inhibit glioma cell growth and migration. Moreover, knockdown of SPRY4-IT1 could inhibit epithelial-mesenchymal transition (EMT) phenotype in glioma cells. | 26464658 | Lnc2Cancer |
| EL1246 | ST7-AS1 | glioma | qPCR etc. | cell lines(U251, U87) | up-regulated | expression | 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 | Lnc2Cancer |
| EL1399 | TUG1 | glioma | qPCR etc. | cell lines(U251, U87) | down-regulated | expression | 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 | Lnc2Cancer |
| EL1399 | TUG1 | glioma | quantitative RT-PCR, Annexin V/PI staining and cell counting kit-8 assays | glioma tissues | down-regulated | interaction | The dysregulation of taurine upregulated gene 1 affected the apoptosis and cell proliferation of glioma cells. Taurine upregulated gene 1 promoted cell apoptosis of glioma cells by activating caspase-3 and -9-mediated intrinsic pathways and inhibiting Bcl-2-mediated anti-apoptotic pathways, acting as a tumor suppressor in human glioma. | 26748401 | |
| EL1409 | uc.283-plus | glioma | microarray, qPCR etc. | glioma tissue | up-regulated | expression | Among the normal tissues, the uc.283 lncRNA was highly specific for pluripotent stem cells. Intriguingly, the uc.283-plus lncRNA was highly expressed in some solid cancers, particularly in one of the most untreatable types, glioma.uc.283-plus lncRNA might have a role in pluripotency of stem cells and in the biology of glioma. | 25352916 | Lnc2Cancer |