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 | cervical cancer |
| ICD-0-3 | C53 |
| Methods | qPCR, Western blot, Luciferase reporter assay, RIP etc. |
| Sample | cervical cancer tissues, cell lines (SiHa, HeLa, Caski, c4-1 and HaCaT) |
| Expression Pattern | up-regulated |
| Function Description | HOTAIR expression was elevated while miR-143-3p expression was reduced in cervical cancer tissues and cell lines.HOTAIR knockdown suppressed proliferation and enhanced apoptosis in cervical cancer cells.Moreover, HOTAIR could function as a sponge for miR-143-3p.The inhibitory effect of HOTAIR knockdown on cervical cancer cells growth was abolished following decrease of miR-143-3p expression.Furthermore, HOTAIR promoted BCL2 expression by modulating miR-143-3p.BCL2 overexpression attenuated the tumor-suppressive effect of miR-143-3p in cervical cancer.Finally, the carcinogenicity of HOTAIR was validated in mice.HOTAIR acted as a ceRNA to modulate BCL2 expression via competitively binding to miR-143-3p. |
| Pubmed ID | 29336659 |
| Year | 2018 |
| Title | Long non-coding RNA HOTAIR promotes cervical cancer progression through regulating BCL2 via targeting miR-143-3p. |
External Links
| Links for HOTAIR | GenBank HGNC NONCODE |
| Links for cervical cancer | OMIM COSMIC |