| External factors: | Doxorubicin |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Flow cytometry |
| Description: | Flow cytometry：Flow cytometric examination of the cell cycle distribution of NCI-H292 cells showed a significant increase of cells with DNA content corresponding to G2/M at 80 nM of doxorubicin compared to the control and 20 nM (p<0.05), whereas the cells with DNA content corresponding to G0/G1 concurrently decreased (p<0.05). SA-β-gal activity assay：The number of β-gal-positive senescent cells was markedly increased in doxorubicin treated by comparison with untreated NCI-H292 cultures. |
| Target gene: | P53//γH2AX//P21 |
| R-EF-Target gene: | Upregulation//Activation//Upregulation |
| Official symbol(s): | P53//H2AX//P21 |
| Target gene experiment: | Western blot |
| Target gene description: | In order to determine the effect of doxorubicin on p53 protein levels western blotting analysis was performed.Doxorubicin at of 20, 40 and 80 nM induced a significant increase of p53 protein levels to 1.7 fold compared to the untreated condition (p<0.01). By using a specific antibody directed against phosphorylated H2AX, we observed that 40 and 80 nM doxorubicin promoted a significant phosphorylation of H2AX at the Ser139 residue (γH2AX) compared to 20 nM and UT, favoring its activation. Data reported, panels C-E also demonstrated that the increase of p53 was accompanied by a significant up-elevation of p21 at 80 nM doxorubicin compared to all other conditions (p<0.001). Moreover, p21 protein levels were significantly higher at 40 nM doxorubicin compared to UT and 20 nM (p<0.001). |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: