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 | TRAIL | ||
Variant | Cell Growth | Circulating | |||
MiRNA | EMT | Metastasis | |||
Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
Cancer Name | pancreatic cancer |
ICD-0-3 | C25 |
Methods | qPCR etc. |
Sample | cell lines (MiaPaCa-2, BxPC3, Suit2 and PANC-1) |
Expression Pattern | down-regulated |
Function Description | We observed that TRAIL-resistant pancreatic cancer cells had higher levels of HOTAIR expression, whereas TRAIL-sensitive pancreatic cancer cells had lower HOTAIR levels. Overexpressing HOTAIR in TRAIL-sensitive cells attenuated TRAIL-induced apoptosis, and shRNA-mediated HOTAIR knockdown in TRAIL-resistant PANC-1 cells sensitized them to TRAIL-induced apoptosis. These results support a causative effect of HOTAIR on TRAIL sensitivity. Mechanistically, we found that increased HOTAIR expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increased DR5 expression. We further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of zeste homolog 2 (EZH2) and that EZH2 controls histone H3 lysine 27 trimethylation on the DR5 gene. Taken together, these results demonstrate that high HOTAIR levels increase the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via epigenetic regulation of DR5 expression. |
Pubmed ID | 28476883 |
Year | 2017 |
Title | The long non-coding RNA HOTAIR enhances pancreatic cancer resistance to TNF-related apoptosis-inducing ligand. |
External Links
Links for HOTAIR | GenBank HGNC NONCODE |
Links for pancreatic cancer | OMIM COSMIC |