Basic Information
| LncRNA/CircRNA Name | LINC-ROR |
| Synonyms | LINC-ROR, ROR, lincRNA-RoR |
| Region | GRCh38_18:57054558-57072119 |
| Ensemble | ENSG00000258609 |
| Refseq | NR_048536 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | apoptosis | Drug | Tamoxifen | |
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | breast cancer |
| ICD-0-3 | C50 |
| Methods | qPCR, Western blot, RIP etc. |
| Sample | cell line MCF-7 |
| Expression Pattern | up-regulated |
| Function Description | linc-RoR functions as an onco-lncRNA to promote estrogen-independent growth of ER+ breast cancer. Under estrogen deprivation, linc-RoR causes the upregulation of phosphorylated MAPK/ERK pathway which in turn activates ER signaling. Knockout of linc-RoR abrogates estrogen deprivation-induced ERK activation as well as ER phosphorylation, whereas re-expression of linc-RoR restores all above phenotypes. Moreover, we show that the ERK-specific phosphatase Dual Specificity Phosphatase 7 (DUSP7), also known as MKP-X, is involved in linc-RoR KOinduced repression of MAPK/ERK signaling. Interestingly, linc-RoR KO increases the protein stability of DUSP7, resulting in repression of ERK phosphorylation. Clinical data analysis reveal that DUSP7 expression is lower in ER+ breast cancer samples than that in ER- breast cancer. Moreover, downregulation of DUSP7 expression is associated with poor patient survival. |
| Pubmed ID | 29041978 |
| Year | 2017 |
| Title | Linc-RoR promotes MAPK/ERK signaling and confers estrogen-independent growth of breast cancer |
External Links
| Links for LINC-ROR | GenBank HGNC NONCODE |
| Links for breast cancer | OMIM COSMIC |