Objective The aim of this study was to investigate the effects of m6A methylation modification and changes in oxidative stress levels in Apcmin/+ ^{mice in the early, middle, and a}dvanced stages of cancer on the progression of Colorectal cancer (CRC) with normal and high-fat diets. Methods C57BL/6J mice and Apc^min/+ mice were given normal maintenance feed and diet type high fat feed (60% fat) for 2 weeks (S group), 6 weeks (M group) and 12 weeks (L group), respectively. After intervention, food intake, body weight, size, number and volume of small intestinal polyps and colon tumors were measured. The expression levels of cancer markers Ki-67 and PCNA protein in colon tissues of mice were detected by immunohistochemical staining. The activity or concentration of antioxidant enzymes CAT, GSH and lipid peroxide MDA in serum were detected by the kit. RT-qPCR was used to detect the mRNA expression of m6A methylation-related enzymes in colon tissues of mice. The total level of m6A methylation modification in mouse colon tissue was detected by the kit. Results (1) Rapid tumor growth in Apc^min/+ mice from early to middle stage of cancer; In the middle to late stage of cancer, normal diet slowed down the tumor proliferation, while high-fat diet promoted the further development of cancer. (2) The decrease of m6A methylation level and the enhancement of antioxidant capacity in Apc^min/+ mice under normal diet may delay the advanced development of tumor. (3) High-fat diet may promote the sustainable development of CRC by increasing the total level of m6A methylation in Apc^min/+ mice, while the enhanced antioxidant capacity may not be enough to resist the promoting effect of m6A methylation on CRC. Conclusions The difference between normal diet and high fat diet on CRC is mainly due to the difference of m6A methylation modification. Antioxidant capacity was enhanced in both diets, suggesting that the body may use antioxidant effects to initiate self-protection mechanisms during cancer progression.