Colorectal carcinoma (CRC), the third most commonly diagnosed cancer, accounts for 9.7% of all newly diagnosed cancer cases and 9.4% of cancer-related deaths globally. Recent studies have demonstrated that post-transcriptional RNA modifications, such as N⁶-methyladenosine, N -methylcytosine, and N⁷-methylguanosine, play critical roles in the regulation of mRNA stability and translation, primary microRNA processing, and lncRNA-protein complex that contributes to the progression of human cancer. Here, we found that the expression of the member of methyltransferase-like (METTL) family-METTL1, the m⁷G "writers", was remarkably up-regulated in colorectal cancer tissue and positively correlated with poor prognosis. METTL1 knockdown suppressed colorectal cancer cell growth and G1/S phase transition. Further functional experiments indicate that METTL1 could directly interact with checkpoint kinase 2 (CHEK2) and suppress its protein expression, which was abrogated by BML-277, the CHEK2 inhibitor. Our data uncover that METTL1 plays an important supportive role in colorectal cancer proliferation and progression, providing a potential therapeutic target for colorectal cancer.