Basic Information
| LncRNA/CircRNA Name | MLK7-AS1 |
| Synonyms | MAP3K20-AS1 |
| Region | NA |
| Ensemble | NA |
| Refseq | NA |
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 | ovarian cancer |
| ICD-0-3 | C56.9 |
| Methods | qPCR, Western blot, Luciferase reporter assay, RIP, other |
| Sample | ovarian cancer tissues and cell lines (SKOV3, OVCAR3,PEO1, A2780, 3AO, CAOV3) |
| Expression Pattern | up-regulated |
| Function Description | Knockdown of MLK7-AS1 inhibited the ability of cell migration, invasion, proliferation, colony formation and wound healing, whereas promoted cell apoptosis in vitro. By using online tools and mechanistic analysis, we demonstrated that MLK7-AS1 could directly bind to miR-375 and downregulate its expression. Besides, MLK7-AS1 reversed the inhibitory effect of miR-375 on the growth of ovarian cancer cells, which might be involved in the upregulation of Yes-associated protein 1 (YAP1) expression. Moreover, knockdown MLK7-AS1 expression inhibited primary tumor growth in ovary and metastatic tumors in multiple peritoneal organs including liver and spleen in vivo, which were partly abolished by miR-375 inhibition. Mechanically, we found that MLK7-AS1 modulated the epithelial-mesenchymal transition (EMT) process by interacting with miR-375/YAP1 both in vivo and vitro, which promoted the expression of Slug. |
| Pubmed ID | 30249278 |
| Year | 2018 |
| Title | Long Noncoding RNA MLK7-AS1 Promotes Ovarian Cancer Cells Progression by Modulating miR-375/YAP1 Axis |
External Links
| Links for MLK7-AS1 | GenBank HGNC NONCODE |
| Links for ovarian cancer | OMIM COSMIC |