Basic Information
LncRNA/CircRNA Name | HCP5 |
Synonyms | NA |
Region | GRCh38_6:31400702-31477506 |
Ensemble | ENSG00000206337 |
Refseq | NR_040662 |
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 | anaplastic thyroid cancer |
ICD-0-3 | C73 |
Methods | qRT-PCR, RIP assay etc. |
Sample | human thyroid follicular cell line Nthy-ori 3-1 ,the human ATC cell lines (FRO, ARO, SW1736, and 8305C) |
Expression Pattern | up-regulated |
Function Description | Compared with human thyroid follicular cell line Nthy-ori 3-1 cells, HCP5 expression level was significantly increased in ATC cell lines. Besides, HCP5 expression level was increased in ATC tissues when compared with adjacent normal tissues. Knockdown of HCP5 reduced cell viability, while elevated apoptotic rate and caspase-3/7 activity in ARO and SW1736 cells. MiR-128-3p was predicted to be a target gene of HCP5. The expression level of miR-128-3p was significantly decreased in ATC cells and tissues, as compared to Nthy-ori 3-1 cells and adjacent normal tissues, respectively. MiR-128-3p overexpression reduced ATC cell viability, and induced cell apoptosis. HCP5 directly bound to miR-128-3p and regulated the expression of miR-128-3p in ARO and SW1736 cells. Furthermore, the effects of HCP5 knockdown on ATC cell viability and apoptosis were attenuated by the inhibitor of miR-128-3p. |
Pubmed ID | 31102936 |
Year | 2019 |
Title | Knockdown of HCP5 exerts tumor-suppressive functions by up-regulating tumor suppressor miR-128-3p in anaplastic thyroid cancer |
External Links
Links for HCP5 | GenBank HGNC NONCODE |
Links for anaplastic thyroid cancer | OMIM COSMIC |