Basic Information
| LncRNA/CircRNA Name | LINC00672 |
| Synonyms | LINC00672 |
| Region | GRCh38_17:38925168-38929384 |
| Ensemble | ENSG00000263874 |
| Refseq | NR_038847 |
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 | endometrial cancer |
| ICD-0-3 | NA |
| Methods | qPCR, Western blot, Northern blot, RIP, Luciferase reporter assay, CCK-8 assay etc. |
| Sample | cell lines (HEC-1A, Ishikawa, 293T) |
| Expression Pattern | down-regulated |
| Function Description | LINC00672 is aberrantly down-regulated during the development of EC. Nevertheless, LINC00672 is a p53-targeting lincRNA acting along with heterogeneous nuclear ribonucleoproteins as a suppressive cofactor, which locally reinforces p53-mediated suppression of LASP1, an evolutionarily conserved neighboring gene of LINC00672 and putatively associated with increased tumor aggressiveness, during anti-tumor processes. LINC00672 overexpression could lower the levels of LASP1 and slow the development of malignant phenotypes of EC both in vitro and in vivo. Moreover, LINC00672 significantly increased the 50% inhibitory concentration of paclitaxel in EC cells and increased the sensitivity of xenograft mice to paclitaxel. |
| Pubmed ID | 28232485 |
| Year | 2017 |
| Title | Long non-coding RNA LINC00672 contributes to p53 protein-mediated gene suppression and promotes endometrial cancer chemosensitivity. |
External Links
| Links for LINC00672 | GenBank HGNC NONCODE |
| Links for endometrial cancer | OMIM COSMIC |