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 | DZNEP | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | glioblastoma |
| ICD-0-3 | NA |
| Methods | CHIP-PCR etc. |
| Sample | GBM cell lines (U87, U87vIII), breast cancer cell line (MCF-7) |
| Expression Pattern | up-regulated |
| Function Description | The level of HOTAIR expression in GBM was higher than in other low grade gliomas and normal brain tissues. NLK (Nemo-like kinase), a negative regulator of the B-catenin pathway, was negatively correlated with HOTAIR expression. When the B-catenin pathway was inhibited, GBM cells became susceptible to cell cycle arrest and inhibition of invasion. Introduction of the HOTAIR 5' domain in human glioma-derived astrocytoma induced B-catenin. An intracranial animal model was used to confirm that HOTAIR depletion inhibited GBM cell migration/invasion. In the orthotopic model, HOTAIR was required for GBM formation in vivo. |
| Pubmed ID | 25823657 |
| Year | 2015 |
| Title | HOTAIR is a therapeutic target in glioblastoma. |
External Links
| Links for HOTAIR | GenBank HGNC NONCODE |
| Links for glioblastoma | OMIM COSMIC |