| External factors: | PBA |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | Cell morphological analysis//Immunoblotting//SA-β-gal activity assay |
| Description: | Interestingly, we observed a drastic morphological change in the MCF-7 cells treated with PBA at concentrations higher .These treated cells appeared flattened and enlarged.Since PBA-induced growth inhibition was not accompanied with apoptosis,the possibility that PBA-induced growth inhibition may result in cellular senescence was assessed.Also,an increase in senescence-associated-β-galactosi-dase (SA-β-gal) activity was also observed in these cells, which is a marker of senescence. |
| Regulatory pathway: | Akt-p21 |
| R-EF-Pathway: | -- |
| Official symbol(s): | AKT1-CDKN1A |
| Pathway experiment: | Immunoblotting |
| Pathway description: | Interestingly, a recent study showed that insulin receptor substrate (IRS), which is an upstream signaling molecule of both MAPKs and Akt/PKB, is activated in PBA treated mouse liver tissue. To confirm this, we investigated various signaling molecules in cells treated with 100–300 lM PBA.We only detected Akt activation, but neither JNK nor p38,in PBA treated MCF-7cells. Furthermore, we observed induction of p21WAF1and no effect on the level of p53 in a dose-dependent manner . |
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