| External factors: | CGN |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Colorectal cancer |
| Experiment: | MTT assay//BrdU assay//Flow cytometry//SA-β-gal activity assay |
| Description: | CGN treatment markedly decreased cell viability in a dose- dependent manner in both HT- 29 and W480 cell lines, but had less cytotoxic effect in NCM460 cells.Consistently, BrdU assays showed that there were a significantly lower percentage of BrdU- positive cells in CGN- treated cells compared with controls.Colorectal cancer cells accumulated in the G2/M phase and de-creased in the G0/G1 phase upon CGN treatment, indicating that CGN induces G2/M arrest. SA- β- gal assays showed that CGN significantly enhanced senescence as indicated by a significant increase in the percentage of SA- β- gal- positive cells . |
| Target gene: | CDK4 |
| R-EF-Target gene: | Downregulation |
| Official symbol(s): | CDK4 |
| Target gene experiment: | Western blot |
| Target gene description: | CDK4 expression was significantly decreased, but CDK6 expression was not clearly affected upon CGN treatment (data not shown), suggesting that CGN selectively inhibits CDK4 by downregulation of CDK4 expression. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: