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 | apoptosis | Drug | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | breast cancer |
| ICD-0-3 | C50 |
| Methods | RC-PCR, Western blot, Luciferase reporter assay |
| Sample | breast cancer cell lines (MDA-MB-231 and MCF-7) |
| Expression Pattern | up-regulated |
| Function Description | Paracrine TGF-B1 was essential for CAFs induced EMT and metastasis in breast cancer cells, which is a crucial mediator of the interaction between stromal and cancer cells. CAF-CM significantly enhanced the HOTAIR expression to promote EMT, whereas treatment with small-molecule inhibitors of TGF-B1 attenuated the activation of HOTAIR. Most importantly, SMAD2/3/4 directly bound the promoter site of HOTAIR, located between nucleotides -386 and -398, -440 and -452, suggesting that HOTAIR was a directly transcriptional target of SMAD2/3/4. Additionally, CAFs mediated EMT by targeting CDK5 signaling through H3K27 tri-methylation. |
| Pubmed ID | 29325547 |
| Year | 2018 |
| Title | Paracrine and epigenetic control of CAF-induced metastasis: the role of HOTAIR stimulated by TGF-1 secretion. |
External Links
| Links for HOTAIR | GenBank HGNC NONCODE |
| Links for breast cancer | OMIM COSMIC |