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 | apoptosis | Drug | ||
| Variant | Cell Growth | Circulating | |||
| MiRNA | EMT | Metastasis | |||
| Methylation | Coding Ability | Recurrence |
Cancer&Entry Information
| Cancer Name | lung cancer |
| ICD-0-3 | C34 |
| Methods | qPCR, Western blot, Luciferase reporter assay, RIP, etc. |
| Sample | A549 and PC9 cells and BEAS-2B cells |
| Expression Pattern | down-regulated |
| Function Description | SM inhib ited the growth of non small cell lung cancer (NSCLC) cells, which was enhanced in cells with silencing of long non coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR), while it overcame by overexpression of HOTAIR. In addition, SM increased the expression of miR 214 3p and inhibited 3 phosphoinositide dependent protein kinase 1 (PDPK1) gene expression, which was strengthened by miR 214 3p mimics. Intriguingly, HOTAIR could directly bind to miR 214 3p and sequestered miR 214 3p from the target gene PDPK1. HOTAIR effectively acted as a competing endogenous RNA (ceRNA) to stimulate the expression of target gene PDPK1. These complex interactions and feedback mechanisms contribute to the overall effect of SM. |
| Pubmed ID | 31475459 |
| Year | 2019 |
| Title | Novel reciprocal interaction of lncRNA HOTAIR and miR-214-3p contribute to the solamargine-inhibited PDPK1 gene expression in human lung cancer |
External Links
| Links for HOTAIR | GenBank HGNC NONCODE |
| Links for lung cancer | OMIM COSMIC |