External factors: | BI-D1870 |
Aging type: | Accelerate |
Aging characteristic: |
Category: | Chemical compounds |
Phenotype: | Cancer |
Experiment: | SA-β-gal activity assay//Knockdown |
Description: | BI-D1870 almost completely prevented γIR-induced apoptosis of p53-deficient HCT116 cells and, similar to U0126, produced the senescent phenotype in both wild-type and p53-deficient cells regardless of whether or not they were irradiated. BI-D1870 also induced senescence in MCF-7/casp3 breast carcinoma cells, indicating a more general response to this compound . |
Target gene: | P21 |
R-EF-Target gene: | Upregulation |
Official symbol(s): | P21 |
Target gene experiment: | Western blot |
Target gene description: | Therefore, we analyzed p21 expression in BI-D1870-treated cells and found that this compound induced a substantial p21 accumulation in HCT116 wild-type cells albeit to a lesser extent compared with γIR .Interestingly, BI-D1870-mediated p21 accumulation appears to occur independently of p53 that was only stabilized following γIR, but not in response to BI-D1870.Consistent with our observation that BI-D1870 was able to induce senescence in MCF-7/casp3 cells as well, this event was also accompanied by p21 upregulation. |
Regulatory pathway: | -- |
R-EF-Pathway: | -- |
Pathway experiment: | -- |
Pathway description: | -- |
Annotation: