Basic Information
| LncRNA/CircRNA Name | MALAT1 |
| Synonyms | NEAT2 |
| Region | GRCh38_11:65497688-65506516 |
| Ensemble | ENSG00000251562 |
| Refseq | NR_002819 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | apoptosis | Drug | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | gastric adenocarcinoma |
| ICD-0-3 | C16 |
| Methods | qPCR, Western blot, Luciferase reporter assay, etc. |
| Sample | gastric adenocarcinoma tissues, gastric adenocarcinoma cell line MGC-803 and immortalized normal gastric epithelial cell line GES-1 |
| Expression Pattern | up-regulated |
| Function Description | MALAT1 was highly expressed in the serum of patients with gastric adenocarcinoma and in cell lines. Downregulating MALAT1 inhibited proliferation and promoted apoptosis of MGC-803 cells. In addition, MALAT1 directly targeted and decreased the expression of miR-181a-5p, which in turn upregulated the expression of AKT3. Further, overexpressing miR-181a-5p or directly inhibiting the AKT pathway with the inhibitor ipatasertib exhibited similar effects to MALAT1 knockdown. Our research proposes a novel mechanism where the role of MALAT1 is dependent on the MALAT1/miR-181a5p/AKT3 axis. MALAT1 competes with AKT3 for miR-181a-5p binding, thereby upregulating the AKT3 protein level and ultimately promoting the growth of gastric adenocarcinoma. |
| Pubmed ID | 31480991 |
| Year | 2019 |
| Title | MALAT1 promotes gastric adenocarcinoma through the MALAT1/miR-181a-5p/AKT3 axis |
External Links
| Links for MALAT1 | GenBank HGNC NONCODE |
| Links for gastric adenocarcinoma | OMIM COSMIC |