| External factors: | Metformin |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Hepatocellular carcinoma |
| Experiment: | SA-β-gal activity assay//Western blot//BrdU assay//Flow cytometry |
| Description: | Low concentration of metformin induced HepG2 cell senescence in a dose-dependent manner, as evident by increased SA-β-gal activity, a universal marker of cellular senescence .Protein expression level of Dec1, one of he established markers for senescence (18) was enhanced in response to metformin compared with controls.HepG2 cells treated with 1 mM metformin exhibited a marked decrease in BrdU incorporation, a marker of cell proliferation.The results indicated that the percentage of G0/G1 phase cells was significantly increased in metformin treated cells and correspondingly, the cell population of G2/M was declined compared with the controls. |
| Target gene: | P53 |
| R-EF-Target gene: | -- |
| Official symbol(s): | P53 |
| Target gene experiment: | Western blot |
| Target gene description: | The acetylation of p53 (Ac-p53) and p21 were increased in metformin-treated HepG2 cells. |
| Regulatory pathway: | AMPK |
| R-EF-Pathway: | Activation |
| Official symbol(s): | AMPK |
| Pathway experiment: | Western blot |
| Pathway description: | In metformin-treated senescent HepG2 cells, robust phosphorylation of AMPK and ACC was observed compared with untreated cells, indicating that activation of AMPK signaling cascade are relevant to the senescence in HepG2 cells. |
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