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 | Adriamycin | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | acute myeloid leukemia |
| ICD-0-3 | NA |
| Methods | qPCR, Western blot, Luciferase reporter assay, RIP etc. |
| Sample | acute myeloid leukemia tissues, cell lines (HL60 and HS-5) |
| Expression Pattern | up-regulated |
| Function Description | UCA1 expression was upregulated following ADR-based chemotherapy.Knockdown of UCA1 increased the cytotoxic effect of ADR and inhibited HIF-1a-dependent glycolysis in ADR-resistant AML cells.Additionally, UCA1 functioned as a ceRNA of miR-125a by directly binding to miR-125a. HK2, a target of miR-125a, was positively regulated by UCA1 in HL60 and HL60/ADR cells.More notably, UCA1 overexpression overturned miR-125-mediated inhibition on HIF-1a-dependent glycolysis in HL60 and HL60/ADR cells.Furthermore, 2-deoxy-glucose (2-DG) exposure inhibited HIF-1a-dependent glycolysis,and attenuated UCA1-induced increase of chemoresistance in HL60 and HL60/ADR cells. |
| Pubmed ID | 29663500 |
| Year | 2018 |
| Title | Knockdown of LncRNA-UCA1 suppresses chemoresistance of pediatric AML by inhibiting glycolysis through the microRNA-125a/hexokinase 2 pathway. |
External Links
| Links for UCA1 | GenBank HGNC NONCODE |
| Links for acute myeloid leukemia | OMIM COSMIC |