Basic Information
| LncRNA/CircRNA Name | GHET1 |
| Synonyms | Gastric carcinoma proliferation enhancing transcript 1 |
| Region | GRCh38_7:148987527-148989432 |
| Ensemble | ENSG00000281189 |
| Refseq | NR_130107 |
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 | cervical cancer |
| ICD-0-3 | C53 |
| Methods | qRT-PCR, Western blot, RIP |
| Sample | tumor tissues,CC cell lines (C33A, HeLa, C4-1 and SiHa) and the normal cervical cell line (Crl-2614) |
| Expression Pattern | up-regulated |
| Function Description | We proposed to examine the biological role of GHET1 in CC and the underlying mechanism and validated the up-regulated expression of GHET1 in CC cell lines. Loss-of-function assays demonstrated that down-regulation of GHET1 inhibited cell growth, migration and epithelial-to-mesenchymal transition (EMT) in CC.GHET1 down-regulation could inactivate AKT/mTOR and Wnt/?-catenin pathways, and that respective activation of these two pathways abrogated the inhibitive effect of GHET1 knockdown on CC cell growth, migration and EMT. |
| Pubmed ID | 31682716 |
| Year | 2020 |
| Title | LncRNA GHET1 Promotes Cervical Cancer Progression Through Regulating AKT/mTOR and Wnt/?-catenin Signaling Pathways |
External Links
| Links for GHET1 | GenBank HGNC NONCODE |
| Links for cervical cancer | OMIM COSMIC |