Basic Information
| LncRNA/CircRNA Name | HOTAIR |
| Synonyms | HOTAIR, HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 |
| Region | GRCh38_12:53962308-53974956 |
| Ensemble | ENSG00000228630 |
| Refseq | NR_003716 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | Drug | Delphinidin-3-glucoside | ||
| 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 etc. |
| Sample | cell line (MCF10A) |
| Expression Pattern | up-regulated |
| Function Description | The level of HOTAIR significantly increases in a time-dependent manner during chronic breast carcinogenesis. Dp treatment down-regulates HOTAIR expression in breast carcinogenesis and breast cancer cells. Furthermore, Dp administration inhibits the growth of xenografted breast tumors in athymic mice, and decreases HOTAIR in vivo. Further studies showed that Dp represses Akt activation, promotes IRF1 expression and increases IRF1 binding to the HOTAIR promoter. Silence of IRF1 expression via transfecting cells with IRF1 siRNAs significantly reduced the effects of Dp on HOTAIR, resulting in decreased cytotoxic effects of Dp on breast cancer cells. |
| Pubmed ID | 27388461 |
| Year | 2016 |
| Title | Delphinidin-3-glucoside suppresses breast carcinogenesis by inactivating the Akt/HOTAIR signaling pathway. |
External Links
| Links for HOTAIR | GenBank HGNC NONCODE |
| Links for breast cancer | OMIM COSMIC |