| External factors: | Sirtinol |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Cancer |
| Experiment: | BrdU assay//SA-β-gal activity assay//Western blot//Colony formation assay |
| Description: | Treatment with Sirtinol inhibited cell growth in both MCF-7 and H1299 cells；This was supported by reduced incorporation of BrdU in Sirtinol-treated MCF-7 and H1299 cells at 10 days after the addition of Sirtinol, as compared with untreated cells；Sirtinol treatment increased SA-β-gal-positive cells in a dose-dependent manner 10 days after the addition of Sirtinol in both MCF-7 and H1299 cells；Sirtinol treatment also resulted in increased expression of PAI-1 in both MCF-7 and H1299 cells.Colony formation assay also revealed that both Sirtinol and Splitomicin elicited antiproliferative effects in MCF-7 and H1299 cells in a dose-dependent manner. |
| Target gene: | SIRT1 |
| R-EF-Target gene: | Downregulation |
| Official symbol(s): | SIRT1 |
| Target gene experiment: | Cell morphological analysis//SA-β-gal activity assay |
| Target gene description: | Sirt1 inhibition by Sirtinol, Splitomicin or siRNA also induced senescence-like phenotype in human diploid fibroblasts, WI-38 and IMR-90 cells, reflected by induction of SA-β-gal staining, and enlarged and flattened cell morphology. |
| Regulatory pathway: | Ras-MAPK |
| R-EF-Pathway: | -- |
| Official symbol(s): | MAPK |
| Pathway experiment: | Western blot |
| Pathway description: | By contrast, in Sirtinol-treated senescent MCF-7 and H1299 cells at 10 days after the addition of Sirtinol (100mM), basal (unstimu-lated) phosphorylation of ERK, JNK/SAPK and p38 MAPK was reduced compared with untreated cells. |
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