Quantitative Proteomic Analysis of Preventive Potential of Aspirin for Colon Cancer Cells

Abstract Objective: To further systematically understand the molecular mechanisms that aspirin prevents colon carcinogenesis.Methods: We detected the global protein expression profiles of colorectal cancer along with the treatment of aspirin by a quantitative proteomic approach. We analyzed the proteomic results using bioinformatics（including differential proteins, protein annotation, Kegg Pathways and protein-protein interaction network ）. Cell viability of HT29 cells treated with aspirin was determined by CCK8 assay. The expression of differential proteins p53 and CDK1 were quantified by real-time PCR and Western blot. We measured cell cycle distribution and cell apoptosis of H1299 cells exposed to aspirin by flow cytometric analysis. Results: We found 552 proteins that were significantly dysregulated after10mM aspirin treatment of colon cancer cells. Further enrichment analysis of the dysregulated proteins suggested that cell cycle-related proteins are the most differential proteins such as p53, CDK1, CyclinB, Chk1, Chk2 and CyclinD. The results of real-time PCR and Western blot showed that p53 and CDK1 obvious upregulation after aspirin exposed to colon cancer cells. We also detected that aspirin promoted the G1/S arrest of cell cycle in HT29 cells. We confirmed aspirin induced cell apoptosis in human HT29 colon cancer cells with concentration-dependent increase. Conclusions: The result indicated that aspirin induced colorectal cancer cells G1 arrest and cell apoptosis by p53-CDK1 pathway. Accordingly, aspirin may represent a promising preventive candidate for colon cancer.