Basic Information
| LncRNA/CircRNA Name | circMYLK |
| Synonyms | |
| Region | |
| Ensemble | |
| Refseq |
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 | bladder cancer |
| ICD-0-3 | C67 |
| Methods | RNA immunoprecipitation (RIP), Luciferase reporter assay, Fluorescence in situ hybridization (FISH) |
| Sample | Bladder cancer cell lines EJ, T24, 5673 and BIU-87, 293T cells, BC tissues and matched adjacent non-tumor tissues |
| Expression Pattern | up-regulated |
| Function Description | We found that circRNA-MYLK and VEGFA were significantly up-regulated and co-expressed in BC. Importantly, circRNA-MYLK levels were related to the progression of stage and grade of BC. Mechanistically, we demonstrated that circRNA-MYLK could directly bind to miR-29a and relieve suppression for target VEGFA, which activated VEGFA/VEGFR2 signaling pathway. Functionally, we found that ectopically expressing circRNA-MYLK accelerated cell proliferation, migration, tube formation of HUVEC and rearranged cytoskeleton. Moreover, up-regulating circRNA-MYLK promoted epithelial-mesenchymal transition (EMT). Whereas circRNA-MYLK knockdown decreased cell proliferation, motility, and induced apoptosis. Finally, up-regulating circRNA-MYLK promoted the growth, angiogenesis and metastasis of BC xenografts. |
| Pubmed ID | 28687357 |
| Year | 2017 |
| Title | Circular RNA MYLK as a competing endogenous RNA promotes bladder cancer progression through modulating VEGFA/VEGFR2 signaling pathway |
External Links
| Links for circMYLK | GenBank HGNC NONCODE |
| Links for bladder cancer | OMIM COSMIC |