Basic Information
| LncRNA/CircRNA Name | GAS5 |
| Synonyms | GAS5, NCRNA00030, SNHG2, ENST00000456293.5, GAS5-007 |
| Region | GRCh38_1:173863900-173868882 |
| Ensemble | ENSG00000234741 |
| Refseq | NR_002578 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | apoptosis;autophagy | Drug | Cisplatin | |
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | glioma |
| ICD-0-3 | NA |
| Methods | qPCR, Western blot, other |
| Sample | glioma cell lines (LN18and, U138MG) |
| Expression Pattern | down-regulated |
| Function Description | Functional assay confirmed that knockdown of GAS5 enhanced cell resistance to cisplatin in U87 cells, which had a relatively high expression of GAS5. Conversely, elevation of GAS5 increased cell sensitivity to cisplatin in U138 cells that had a relatively low expression of GAS5. Mechanistically, cisplatin exposure evoked excessive autophagy concomitant with an increase in autophagy-related LC3II expression and a decrease in autophagy substrate p62 expression, which was reversely muted after GAS5 overexpression. In addition, GAS5 restored cisplatin-inhibited mammalian target of rapamycin (mTOR) activation. Preconditioning with mTOR antagonist rapamycin engendered not only mTOR inhibition but also abrogated GAS5-mediated depression in cisplatin-evoked autophagy. Notably, blocking the mTOR pathway also attenuated GAS5-increased sensitivity to cisplatin in U138 cells. |
| Pubmed ID | 30317677 |
| Year | 2019 |
| Title | Long Noncoding RNA Growth Arrest-Specific 5 Facilitates Glioma Cell Sensitivity to Cisplatin by Suppressing Excessive Autophagy in an mTOR-dependent Manner |
External Links
| Links for GAS5 | GenBank HGNC NONCODE |
| Links for glioma | OMIM COSMIC |