Objective To observe the effects of advanced glycation end products (AGEs) on the oxidative stress of HCT116 colorectal cancer cells. Methods HCT116 cells were cultured by the reactive oxygen species (ROS) capture agent. The ROS level of AGEs-treated HCT116 cells was detected by the flow cytometry and fluorescent microscopy. The oxidative stress status was intervened by the N-acetyl cysteine (NAC) and its effects on ROS increase and cell proliferation induced by AGEs were observed. Results ROS level increased after HCT116 cells were treated by AGEs. ROS increase and cell proliferation induced by AGEs were significantly inhibited after HCT116 cells were treated by NAC. The differences were statistically significant (P<0.05). Conclusion AGEs enhances the proliferation of HCT116 colorectal cancer cells by activating the oxidative stress response.