Basic Information
| LncRNA/CircRNA Name | HOTAIR |
| Synonyms | NA |
| Region | GRCh38_12:53962308-53974956 |
| Ensemble | ENSG00000228630 |
| Refseq | NR_003716 |
Classification Information
| Regulatory Mechanism | Biological Function | Clinical Application | |||
|---|---|---|---|---|---|
| TF | Immune | Survival | |||
| Enhancer | Apoptosis | Drug | AC1Q3QWB (AQB) | ||
| 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 |
| Sample | glioblastoma cells, N5 and N33, Cal51 breast cancer cells, SGC-7901 and MGC-803 gastric cancer cells, glioblastoma tumor and adjacent tissue |
| Expression Pattern | differential expression |
| Function Description | Tumor cells highly expressing HOTAIR and EZH2 were sensitive to AQB. APC2, as one of the target genes, was significantly up-regulated by AQB and led to degradation of ?-catenin resulting in suppression of Wnt/?-catenin signaling which may contribute to inhibition of tumor growth and metastasis in vitro and in orthotopic breast cancer models. Remarkably, AQB enhanced the toxicity of DZNep in vitro. In orthotopic breast cancer and glioblastoma patient-derived xenografts (PDX) models, the combination of low doses of AQB and DZNep realized much better killing than DZNep treatment alone. |
| Pubmed ID | 31367244 |
| Year | 2019 |
| Title | A Compound AC1Q3QWB Selectively Disrupts HOTAIR-Mediated Recruitment of PRC2 and Enhances Cancer Therapy of DZNep |
External Links
| Links for HOTAIR | GenBank HGNC NONCODE |
| Links for breast cancer | OMIM COSMIC |