| External factors: | As2O3 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Glioblastoma |
| Experiment: | Immunostaining//SA-β-gal activity assay//Telomere length assay//Flow cytometry//Western blot |
| Description: | Immunofluorescent labeling showed that ATR, 53BP1, γ-H2 AX and Mer11 accumulated in the nucleus of cells exposed to 4 μM As2 O3 for 48h .In addition,obvious dose-related increases in p-ATM, ATR, γ-H2 AX,53BP1, Mer11, and p21 were detected by immunoblotting. As2O3 significantly reduced the telomeric G-overhang length after 48 h of treatment (P < 0.01), though the total telomere length did not change. Most of the cells in the control group are in G0-G1 phase. By contrast, As2O3 induced G2-M phase arrest, which is in agreement with the reported effect of As2O3 on Burkitt’s lymphoma cells .Using aging staining we also observed that As2O3 treatment for 2 weeks increased the incidence of cellular senescence marked by cell swelling and blue staining. Dose-related effects were seen with all of four cell types tested . |
| Target gene: | P53//P21 |
| R-EF-Target gene: | Upregulation//Upregulation |
| Official symbol(s): | P53//P21 |
| Target gene experiment: | Western blot |
| Target gene description: | In addition, obvious dose-related increases in p-A TM, A TR, γ-H2AX, 53BP1, Mer11, and p21 were detected by immunoblotting . Moreover, immunoblotting revealed dose- and time-dependent up-regulation of the pro-apoptotic proteins p53, p-p53 and Bax and down-regulation of anti-apoptotic protein Bcl-2 in U87 cells. We also observed elevation of PARP and Caspase-3 cleavage, which is consistent with increased incidence of apoptosis. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: