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 | T cell acute lymphoblastic leukemia |
| ICD-0-3 | NA |
| Methods | qRT-PCR , Luciferase reporter assay , Western blot , RIP , in vitro knockdown etc. |
| Sample | Human T-ALL cell lines(CCRF-CEM (CR)and Jurkat cells (JK)?) ,resistant cells ( CCRF-CEM/ADR (CR/A) and Jurkat/ADR (JK/A)) |
| Expression Pattern | up-regulated |
| Function Description | Elevated expression of ST6GAL1 has been detected. The altered level of ST6GAL1 was corresponding to the drug-resistant phenotype of T-ALL cell lines both in vitro and in vivo. ZFAS1/miR-150/ST6GAL1 axis was existed in T-ALL cell lines.MiR-150 was downregulated and inversely correlated to ST6GAL1 expression. ZFAS1 was a direct target of miR-150 and positively modulated ST6GAL1 level by binding miR-150. ZFAS1/miR-150/ST6GAL1 axis functioned to regulate ADR-resistant cell growth and apoptosis.Besides, EGFR was demonstrated to be a substrate of ST6GAL1, and the sialylated EGFR had an impact on the PI3K/Akt pathway. |
| Pubmed ID | 31096997 |
| Year | 2019 |
| Title | The regulatory ZFAS1/miR-150/ST6GAL1 crosstalk modulates sialylation of EGFR via PI3K/Akt pathway in T-cell acute lymphoblastic leukemia |
External Links
| Links for ZFAS1 | GenBank HGNC NONCODE |
| Links for T cell acute lymphoblastic leukemia | OMIM COSMIC |