Basic Information
| LncRNA/CircRNA Name | TUG1 |
| Synonyms | NA |
| Region | GRCh38_22:30969245-30979395 |
| Ensemble | ENSG00000253352 |
| Refseq | NR_002323 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | 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, Luciferase reporter assay, RIP, etc. |
| Sample | AML tissues, Human bone marrow stromal cell line HS-5 and human AML cell line HL60 |
| Expression Pattern | up-regulated |
| Function Description | TUG1 was up-regulated in ADR-resistant AML tissues and cells. High TUG1 expression was correlated with poor prognosis of AML patients. TUG1 knockdown improved the sensitivity of HL60/ADR cells to ADR. Moreover, TUG1 could epigenetically suppress miR-34a expression via recruiting Enhancer of zeste homolog 2 (EZH2). miR-34a overexpression could mimic the functional role of down-regulated TUG1 in ADR resistance. miR-34a knockdown counteracted the inductive effect of TUG1 inhibition on ADR sensitivity of HL60/ADR cells. Furthermore, TUG1 knockdown facilitated ADR sensitivity of ADR-resistant AML cells in vivo. |
| Pubmed ID | 30551433 |
| Year | 2019 |
| Title | TUG1 confers Adriamycin resistance in acute myeloid leukemia by epigenetically suppressing miR-34a expression via EZH2 |
External Links
| Links for TUG1 | GenBank HGNC NONCODE |
| Links for Acute myeloid leukemia | OMIM COSMIC |