Basic Information
| LncRNA/CircRNA Name | MALAT1 |
| Synonyms | Metastasis-associated lung adenocarcinoma transcript 1 |
| Region | GRCh38_11:65497688-65506516 |
| Ensemble | ENSG00000251562 |
| Refseq | NR_002819 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | autophagy/apoptosis | Drug | Propofol/Cisplatin | |
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | gastric cancer |
| ICD-0-3 | C16 |
| Methods | qRT-PCR, western blot analysis, Dual luciferase reporter assay |
| Sample | GC cell line SGC7901 |
| Expression Pattern | up-regulated |
| Function Description | Chemoresistant GC cells presented higher IC50 of cisplatin, increased autophagy activity and stronger expression of MALAT1. The application of propofol promoted cell apoptosis and reduced the activity of autophagy through downregulating MALAT1. Silencing of MALAT1 inhibited chemo-induced autophagy, whereas MALAT1 overexpression promoted autophagy in GC cells. Mechanistic researches demonstrated that MALAT1 could bind with miR-30e to regulate ATG5 expression, thus causing the suppression of autophagy. |
| Pubmed ID | 31926239 |
| Year | 2020 |
| Title | Propofol Facilitates Cisplatin Sensitivity via lncRNA MALAT1/miR-30e/ATG5 Axis Through Suppressing Autophagy in Gastric Cancer |
External Links
| Links for MALAT1 | GenBank HGNC NONCODE |
| Links for gastric cancer | OMIM COSMIC |