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 | Drug | |||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | glioma |
| ICD-0-3 | NA |
| Methods | qPCR, Western blot, RNAi, Luciferase reporter assay, RIP, other |
| Sample | glioma tissues and cell lines(U87 and U251) |
| Expression Pattern | up-regulated |
| Function Description | Here, we report that the expression of UCA1 is significantly increased by transforming growth factor-? (TGF-?) treatment in glioma cells and is greater in glioma tissues than in normal adjacent tissues. Additionally, TGF-? induced EMT and the stemness of glioma cells, whereas knockdown of lncRNA UCA1 attenuated these two processes and their enhancement by TGF-?. Mechanistically, knockdown of UCA1 decreased Slug expression by acting as a competitive endogenous RNA (ceRNA) through competitive binding with miR-1 and miR-203a; this effect was further evidenced by the fact that transfection with miR-1 or miR-203a inhibitors abrogated the effects of UCA1 knockdown on Slug expression, and UCA1 colocalized with miR-1 and miR-203a in glioma tissues. |
| Pubmed ID | 30410864 |
| Year | 2018 |
| Title | LncRNA UCA1 Is Necessary for TGF-?-induced Epithelial-Mesenchymal Transition and Stemness via Acting as a ceRNA for Slug in Glioma Cells |
External Links
| Links for UCA1 | GenBank HGNC NONCODE |
| Links for glioma | OMIM COSMIC |