Background
Colon cancer is one of the most prevalent digestive cancers worldwide.
Conclusions
These results indicate that aspirin induces G1 arrest and apoptosis in colorectal cancer cells via the p53-CDK1 pathway. Aspirin may be a promising drug candidate for colon cancer prevention.
Methods
We determined the global protein expression profiles of colorectal cancer and aspirin-treated cells using quantitative proteomic analysis. We analyzed the proteomic
Results
We found that 552 proteins were significantly dysregulated, of which 208 and 334 were upregulated and downregulated, respectively, in colon cancer cells exposed to 10 mmol/L of aspirin (95% confidence interval [CI]: -1.269 to -0.106, P < 0.05). Further gene enrichment analysis revealed that cell cycle-related proteins, such as p53 and CDK1, were significantly differentially expressed. Proteomic analysis showed that after 24 h of aspirin exposure, the level of p53 increased by 2.52-fold and CDK1 was downregulated to half that of the controls in HT29 cells (95% CI: -0.619 to -0.364, P < 0.05). Real-time PCR and Western blotting results showed that p53 was upregulated (95%CI: -3.088 to -1.912, P < 0.001) and CDK1 was significantly downregulated after aspirin exposure in colon cancer cells (95% CI: 0.576 to 1.045, P < 0.05). We observed that aspirin promoted G1/S cell cycle arrest in HT29 cells. We confirmed that aspirin induces apoptosis in human HT29 colon cancer cells in a concentration-dependent manner. Conclusions: These results indicate that aspirin induces G1 arrest and apoptosis in colorectal cancer cells via the p53-CDK1 pathway. Aspirin may be a promising drug candidate for colon cancer prevention.