| External factors: | PTC-209 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//Western blot//EdU assay |
| Description: | The stained cells were counted and plotted. We also examined the expression of senescence-associated proteins such as p21, p53, pRB and p16. The results showed that the PTC-209 strongly induced expression of p53, p21 and p16, and increased expression of hypo-phosphorylated pRB in MRC5 cells. Furthermore, PTC-209 strongly induced premature senescence in these cells as indicated by increase in SA-β-gal positive cells and corresponding decrease in EdU positive cells. PTC-209 also strongly induced premature senescence in MDA-MB-231 and MCF7 breast cancer cells. |
| Target gene: | MIR-200C//MIR-141 |
| R-EF-Target gene: | Upregulation//Upregulation |
| Official symbol(s): | MIR-200C//MIR-141 |
| Target gene experiment: | qRT-PCR//Luciferase reporter assay//EdU assay//Western blot//SA-β-gal activity assay |
| Target gene description: | PTC-209 treatment resulted in upregulation of both miR-200c and miR-141 . The results of qRT-PCR were further confirmed by promoter-reporter assays, which showed that the PTC-209 upregulated miR-200c/141 promoter activity in a dose-dependent manner .The results showed that the PTC-209 strongly induced p21 in control IH cells and that inhibition of either miR-200c or miR-141 could suppress p21 induction by PTC-209. The results indicated that the PTC-209 treatment led to the induction of premature senescence in control IH cells but not in cells expressing inhibitors of either miR-200c or miR-141. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: