| External factors: | KR12 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Colorectal cancer |
| Experiment: | SA-β-gal activity assay//Flow cytometry//Cell morphological analysis |
| Description: | After 48?h of 50?nM KR12 treatment, a flat cell morphology was displayed in LS180 cells, and SA-β-gal activity was strongly increased compared with DMSO- or #6-treated cells, suggesting that KR12 induced cellular senescence.Cell cycle arrest is a critical process in cellular senescence that is induced by the CDK inhibitor p21WAF1/CIP1 (ref. 17), and 48-h KR12 exposure significantly increased the proportion of G2/M-phase cells.Increased compared with DMSO- or #6-treated cells, suggesting that KR12 induced cellular senescence. |
| Target gene: | P53//γH2AX |
| R-EF-Target gene: | --//-- |
| Official symbol(s): | P53//H2AX |
| Target gene experiment: | Western blot |
| Target gene description: | KR12 markedly induced phosphorylation of p53 at Ser-15, p21WAF1/CIP1 and phosphorylated histone variant H2AX (γH2AX), whereas KR12-mediated cleavage of PARP at the 48-h time point was not observed . Phospho-p53 (Ser-15) and γH2AX inductions in KR12-treated cells were also visually confirmed by indirect immunofluorescence staining. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: