| Gene name: | TP53 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | EJ |
| Experiment: | Knockdown//SA-β-gal activity assay |
| Description: | The adenovirus-mediated expression of p53 in EJ p53-null human bladder cancer cells promoted remarkable morphological changes and senescence-associated β-galactosidase (SA-β-gal) activity, which are features of premature senescence phenotypes,within 6 days. Irreversible growth arrest, which is characteristic of cellular senescence, was also confirmed by a marked reduction in cell growth and decreased number of cells in the S-phase upon p53 expression. |
| Target gene: | P21//AKT |
| Official symbol(s): | P21//AKT |
| R-AG-Target gene: | --//Activation |
| Subcategory: | Unclear |
| Target gene experiment: | SA-β-gal activity assay//Western blot |
| Target gene description: | P53-mediated Akt activation and the inhibition of p53-induced SA-β-gal activity by LY294002 treatment were also observed in H1299 human lung cancer cells .Akt and p21 separately regulate p53-induced ROS increases and cell cycle arrest, respectively.suppression of the induction of p21 expression successfully inhibited the p53-induced increase in SA-β-gal activity and morphological changes. In addition, the p53-induced loss of proliferation and cell cycle arrest were inhibited by the suppression of p21 induction .We used a p21 shRNA retrovirus to specifically suppress the p53-mediated induction of p21 expression and cormnfied that its expression was effectively suppressed using Western blot analyses. |
| Regulatory pathway: | NF-κB-NOX4 |
| R-AG-Pathway: | -- |
| Official symbol(s): | NFKB1-NOX4 |
| Pathway experiment: | SA-β-gal activity assay//ChIP//RT-PCR |
| Pathway description: | NOX4 knockdown resulted in the significant suppression of p53-induced SA-β-gal activity but did not affect the loss of proliferation.Importantly, the chromatin immunoprecipitation (ChIP) assay results indicated that NF-kB binding to the putative binding site on the NOX4 promoter was enhanced by p53 expression, but this NF-kB binding was inhibited by BAY 11-7082 treatment. Furthermore, Akt inhibition by either LY294002 or Akt inhibitor IV treatment si gnificantly inhibited the increase in NF-kB binding in response to p53 expression, indicating that Akt activity is required for NF-kB binding to the NOX4 promoter. |
Annotation:
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