| External factors: | 4,5-diphenyl-2-methyl picolinate |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Gastric cancer |
| Experiment: | SA-β-gal activity assay//SAHF//Western blot |
| Description: | DMP treatment resulted in significantly enhanced number of SA-β-gal positive cells and SAHF positive cells when compared with untreated ones. H3K9me3 protein, a core element of SAHF, was accumulated in nuclear and co-localized with SAHF. Western blot results suggested that expression levels of H3K9me3, as well as another SAHF protein marker HP1γ, were dramatically increased after DMP treatment. |
| Regulatory pathway: | p53-p21//p16-Rb |
| R-EF-Pathway: | Activation//Activation |
| Official symbol(s): | TP53-CDKN1A//CDKN2A-RB1 |
| Pathway experiment: | Western blot |
| Pathway description: | Furthermore, some key proteins in p53/p21 and p16/Rb signaling pathways were greatly changed in DMP-treated gastric cancer cells. Compared with vehicle-treated cells, expression levels of p-AKT were dramatically reduced; expression levels of p-p38, p-p53, p21, and p16 were greatly increased; while expression levels of p27 remained unchanged, indicating that DMP induced gastric cancer cell senescence by activating p53/p21 and p16 signaling pathways. |
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