Basic Information
| LncRNA/CircRNA Name | UCA1 |
| Synonyms | UCA1, CUDR, LINC00178, NCRNA00178, UCAT1, onco-lncRNA-36 |
| Region | GRCh38_19:15828206-15836326 |
| Ensemble | ENSG00000214049 |
| Refseq | NR_015379 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | autophagy | Drug | MRP1, LRP, GST, and TOPO-II | |
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | bladder cancer |
| ICD-0-3 | C67 |
| Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, etc. |
| Sample | Bladder cancer tissues, human bladder cancer cell lines (SV-HUC-1, HT-1376, T24, J82, 5637, EJ cells) |
| Expression Pattern | up-regulated |
| Function Description | UCA1 expression was upregulated in bladder cancer tissues and cells, while the depletion of UCA1 by shRNA resulted in the suppression of cell proliferation, invasion, migration, and drug resistance. Further studies demonstrated that UCA1 could directly interact with miR-582-5p, and that there was an inverse correlation between miR-582-5p and UCA1. In addition, we found that ATG7 is a target of miR-582-5p and can be downregulated by either miR-582-5p overexpression or UCA1 knockdown. In particular, the autophagy is reduced when UCA1 shRNA is introduced. Moreover, the in vivo experiment further demonstrated the contribution of UCA1 in bladder cancer including tumor growth, invasion, and migration, and UCA1 knockdown can inhibit the aforementioned activities |
| Pubmed ID | 30666128 |
| Year | 2019 |
| Title | Long noncoding RNA UCA1 targets miR-582-5p and contributes to the progression and drug resistance of bladder cancer cells through ATG7-mediated autophagy inhibition |
External Links
| Links for UCA1 | GenBank HGNC NONCODE |
| Links for bladder cancer | OMIM COSMIC |