| External factors: | Arctigenin |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Gallbladder cancer |
| Experiment: | Flow cytometry//SA-β-gal activity assay |
| Description: | We also evaluated whether ATG was responsible for cellular senescence in GBC cells. Flow cytometric analysis of the cell cycle distribution indicated that the ATGtreated GBC cells were primarily arrested in the G1/G0 phase. SA-β-gal staining revealed that ATG treatment significantly increased the percentage of SA-βgal-positive cells, starting at 24 h after treatment with ATG.Apparently, cellular senescence occurs before cell apoptosis in ATG-treated cells, which is consistent with the cell cycle distribution analysis. |
| Regulatory pathway: | Raf-MEK-ERK |
| R-EF-Pathway: | Downregulation |
| Official symbol(s): | ZHX2-MAP2K7-MAPK1 |
| Pathway experiment: | Western blot//qRT-PCR//Immunofluorescence |
| Pathway description: | Immunofluorescence staining and western blot showed that the EGFR protein level significantly decreased in the ATG-treated group compared with the control group. Moreover, we observed a significant reduction in the level of the phosphorylated form of Raf (c-Raf and b-Raf), MEK, and ERK. The in vivo assay showed that the gene expression of EGFR was remarkably diminished by ATG treatment in ATG-treated subcutaneous mouse tumors. |
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