| Gene name: | HOTAIR |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | A2780_CR5 |
| Gene ID: | 100124700 |
| Category: | ncRNA |
| Phenotype: | Ovarian cancer |
| Experimental category: | HL |
| PMID: | 27041570 |
| Experiment: | SA-β-gal activity assay//PI staining//Flow cytometry//Knockdown |
| Description: | In addition, IL-6 secretion, an established marker for cell senescence was increased by CDDP in A2780 p overexpressing HOTAIR compared with vector-transfected cells .DsiRNA knockdown of HOTAIR in A2780_CR5 cells reduced the number of senescent cells.We observe a decrease in S1 and an increase in G2 phase 48 h post CDDP treatment in HOTAIR expressing cells and a reversal of this effect in A2780_CR5 cells, suggesting that a subpopulation of cells undergo HOTAIR-dependent cell senescence. |
| Regulatory pathway: | NF-κB//CHK1-P53-P21 |
| R-AG-Pathway: | --//-- |
| Official symbol(s): | NFKB1//CHEK1-TP53-CDKN1A |
| Pathway experiment: | Western blot//SA-β-gal activity assay//MTT assay |
| Pathway description: | In HOTAIR overexpressing A2780p cells, SA-β-Gal-positive cell numbers were increased by high vs low evels of CDDP , and NF-κB inhibitor Bay-11 reduced the number of senescent cells,ctopic expression of HOTAIR in NF-κB knockdown cells rescued (Po0.05) proliferation and increased clonogenic survival.In HOTAIR overexpressing vs vector control cells, decreased p-p53 levels were observed and the level of p-Chk1 was essentially unchanged , suggesting ATR dependent activation of p53 by HOTAIR. Activation of p53 and p21 by HOTAIR was observed only during high CDDP treatment, indicated by p53 phosphorylation and p21 expression . |
Annotation:
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