| External factors: | Berberine |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Glioblastoma |
| Experiment: | SA-β-gal activity assay//EdU assay |
| Description: | We therefore tracked the fates of U87 and U251 cells treated with berberine using SA-β-gal staining assay. Berberine treatment led to a significant increase in the percentage of senescent cells. After being treated with berberine (15 μM) for seven days, over 70% U87 and 40% U251 cells became senescent. Consistent with the emergence of a high percentage of SA-β-gal positive cells, EdU incorporation assay showed that the percentages of EdU-positive cells were greatly reduced seven days after treatment with berberine, suggesting that very few of the berberine-treated cells were in S phase. |
| Regulatory pathway: | EGFR-MEK-ERK |
| R-EF-Pathway: | Downregulation |
| Official symbol(s): | EGFR-MAP2K7-MAPK1 |
| Pathway experiment: | Western blot |
| Pathway description: | We therefore tested whether EGFR-initiated pathways are altered in glioblastoma cells treated with berberine. Interestingly, in both U87 and U251 cells treated with berberine, we observed a significant reduction in the level of EGFR. Furthermore, the levels of phosphorylated (Activate) form of RAF, MEK and ERK were all decreased .This result indicated that accompanying the declined level of EGFR, the RAF-MEK-ERK pathways was significantly downregulated in berberine-treated glioma cells. |
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