| External factors: | SAHA |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Glioma |
| Experiment: | Colony formation assay//Flow cytometry//SA-β-gal activity assay |
| Description: | As expected, SAHA was found to suppress colony formation of cells from dissociated GSCs in a dose-dependent manner. We assessed the cell cycle of GSCs by flow cytometry, and the results indicated that low doses (1 μM and 2.5 μM) of SAHA caused a decrease in the proportion of S and G2/M cells and a corresponding increase in cells with a DNA content greater than 4 N.We found that GSCs displayed high SA-β-gal activity upon SAHA treatment. |
| Regulatory pathway: | p38-p53 |
| R-EF-Pathway: | Activation |
| Official symbol(s): | MAPK14-TP53 |
| Pathway experiment: | Western blot |
| Pathway description: | We verified that levels of p53 protein and p38 phosphorylation were up-regulated 7 days after SAHA treatment in a dose-dependent manner Low-dose SAHA-elicited phosphorylation of p38 at Thr180/Tyr182, phosphorylation of p53 at Ser33, and p53 protein levels were also significantly attenuated by SB203580 . |
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