Objective To investigate the effects of m6A methylation modification and changes in oxidative stress levels on the progression of colorectal cancer (CRC) in Apc ^{min/ +}mice with normal and high-fat diets. Methods C57BL / 6J mice and Apc ^{min/ +} mice were fed with a normal or high-fat diet (60% fat) for 2 (S group), 6 (M group),or 12 weeks (L group), respectively. Food intake, body mass, and the size, number, and volume of small intestinal polyps and colon tumors were then measured. Protein expression levels of the cancer markers Ki-67 and proliferating cell nuclear antigen in colon tissues were detected by immunohistochemical staining and the serum levels or activities of the antioxidant enzymes catalase, reduced glutathione, and lipid peroxide malondialdehyde were detected using appropriate kits. mRNA expression levels of m6A methylation-related enzymes in colon tissues were detected by RTqPCR and total levels of m6A methylation modification in colon tissues were detected. Results (1) Apc ^{min/ +} mice showed rapid tumor growth from the early to middle stages of cancer. Tumor proliferation from the middle to late stages of cancer was slowed in mice fed a normal diet, while a high-fat diet promoted the further development of cancer. (2) Decreased m6A methylation levels and enhanced antioxidant capacity may have delayed advanced tumor development in Apc ^{min/ +}mice fed a normal diet. (3)In contrast, a high-fat diet may have promoted the sustainable development of CRC by increasing the total level of m6A methylation, while the enhanced antioxidant capacity may have been insufficient to resist the promoting effect of m6A methylation on CRC. Conclusions A high-fat diet may promote the advancement of CRC compared with a normal diet by affecting m6A methylation modification. Both normal and highfat diets enhanced the antioxidant capacity,suggesting that antioxidant effects may initiate self-protection mechanisms during cancer progression.