Basic Information
| LncRNA/CircRNA Name | ZFAS1 |
| Synonyms | ZFAS1, C20orf199, HSUP1, HSUP2, NCRNA00275, ZNFX1-AS1 |
| Region | GRCh38_20:49278178-49295738 |
| Ensemble | ENSG00000177410 |
| Refseq | NR_003604 |
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 | colorectal cancer |
| ICD-0-3 | C19.9 |
| Methods | qPCR, Western blot, Luciferase reporter assay, RIP, RNAi, other |
| Sample | CRC tissues and cell lines (HCT116, HCT8, HT29, SW620, SW480 and DLD-1) |
| Expression Pattern | up-regulated |
| Function Description | We found that ZFAS1 expression was higher in CRC tissues, where it was associated with poor overall survival (OS), we also showed that ZFAS1 upregulation was induced by nuclear transcription factor SP1. Moreover, ZFAS1 and VEGFA are both targets of miR-150-5p, while ZFAS1 binds to miR-150-5p in an AGO2-dependent manner. Additionally, ZFAS1 upregulation markedly promoted as well as ZFAS1 knockdown significantly suppressed CRC cell proliferation, migration, invasion and angiogenesis, and the inhibitory effect caused by ZFAS1 knockdown could be reversed by antagomiR-150-5p. Lastly, we demonstrated that ZFAS1 knockdown inhibited EMT process and inactivated VEGFA/VEGFR2 and downstream Akt/mTOR signaling pathway in CRC. |
| Pubmed ID | 30250022 |
| Year | 2018 |
| Title | SP1-induced lncRNA-ZFAS1 Contributes to Colorectal Cancer Progression via the miR-150-5p/VEGFA Axis |
External Links
| Links for ZFAS1 | GenBank HGNC NONCODE |
| Links for colorectal cancer | OMIM COSMIC |