Basic Information
| LncRNA/CircRNA Name | MALAT1 |
| Synonyms | NA |
| Region | GRCh38_11:65497688-65506516 |
| Ensemble | ENSG00000251562 |
| Refseq | NR_002819 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | Drug | androgen | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | prostate cancer |
| ICD-0-3 | C61.9 |
| Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, etc. |
| Sample | Human prostate cancer cell lines DU145??C3??NCaP and 22Rv1 |
| Expression Pattern | up-regulated |
| Function Description | lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was increased in prostate cancer cells after androgen stimulation, as well as AR. The silencing of MALAT1 inhibited dihydrotestosterone (DHT) administration-induced acceleration of proliferation and cell cycle progression, and increase of AR expression in prostate cancer cells. MALAT1 bound to miR-320b and negatively regulated its expression, and vice versa. AR is a target of miR-320b. The phenotypic changes induced by silencing of MALAT1 were abolished by miR-320b inhibition or AR overexpression. Additionally, MALAT1 knockdown also suppressed the tumorigenesis of prostate cancer cells in nude mice. In summary, the silencing of MALAT1 inactivated AR signaling by sponging miR-320b, and inhibited proliferation and cell cycle progression in prostate cancer cells, suggesting that MALAT1 may be a new target in diagnosis and therapy of prostate cancer in clinic. |
| Pubmed ID | 30642743 |
| Year | 2019 |
| Title | Silencing of lncRNA MALAT1 inhibits cell cycle progression via androgen receptor signaling in prostate cancer cells |
External Links
| Links for MALAT1 | GenBank HGNC NONCODE |
| Links for prostate cancer | OMIM COSMIC |