External factors
| 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. |
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Regulatory relationship
| 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. |
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Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.
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