Basic Information
| LncRNA/CircRNA Name | ZFAS1 |
| Synonyms | NA |
| Region | GRCh38_20:49278178-49295738 |
| Ensemble | ENSG00000177410 |
| Refseq | NR_003604 |
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 | acute myeloid leukemia |
| ICD-0-3 | NA |
| Methods | qPCR, Western blot, Luciferase reporter assay, in vitro knockdown, etc. |
| Sample | Primary normal monocytes (Normal 1 and Normal 2), primary AML cells (primary AML 1 and primary AML 2), Kasumi-1 cells and NB4 cells |
| Expression Pattern | up-regulated |
| Function Description | RT-qPCR assay showed that ZFAS1 was highly expressed in bone marrow of acute leukemia patients and AML cell lines. Loss-of-function analyses revealed that ZFAS1 knockdown inhibited proliferation and promoted apoptosis in AML cells and curbed AML xenograft growth in vivo. Bioinformatics analysis and luciferase reporter assay unveiled that microRNA-150 (miR-150) could interact with ZFAS1, Myb 3 UTR and Sp1 3 UTR.Moreover, ZFAS1 acted as a molecular sponge of miR-150, giving rise to the downregulation of miR-150 level and upregulation of Myb and Sp1 levels. Moreover, miR-150 overexpression resulted in the reduction of AML cell proliferative ability and the increase of cell apoptotic rate. Additionally, the inhibition of miR-150 abrogated ZFAS1 loss-mediated anti-leukemia effects. |
| Pubmed ID | 30502345 |
| Year | 2018 |
| Title | Knockdown of ZFAS1 suppresses the progression of acute myeloid leukemia by regulating microRNA-150/Sp1 and microRNA-150/Myb pathways |
External Links
| Links for ZFAS1 | GenBank HGNC NONCODE |
| Links for acute myeloid leukemia | OMIM COSMIC |