N6-methyladenosine (m6A) is the most abundant internal modification on eukaryotic mRNA, playing a critical role in regulating gene expression and various cellular processes, including cell self-renewal, differentiation, invasion, and apoptosis. m6A is added by methyltransferases, removed by demethylases, and recognized by reader proteins, which regulate RNA metabolism, including translation, splicing, export, degradation, and microRNA processing. Alterations in m6A levels are involved in cancer pathogenesis and progression by regulating the expression of tumor-related genes such as BRD4, MYC, SOCS2, and EGFR. This review summarizes recent advances in m6A enzyme research, highlights the mechanisms of m6A in cancer pathogenesis and progression, and reviews potential therapeutic targets in cancer treatment. m6A regulators are categorized into writers, erasers, and readers. Writers, such as METTL3, METTL14, WTAP, VIRMA, RBM15, and ZC3H13, catalyze m6A modification. Erasers, like FTO and ALKBH5, remove m6A. Readers, including YTHDF1, YTHDF2, YTHDF3, YTHDC1, YTHDC2, and IGF2BPs, recognize m6A and influence RNA fate. The interplay among these regulators is involved in cancer progression. m6A promotes oncogene expression and inhibits tumor suppressor gene expression, contributing to cancer progression. METTL3 enhances oncogene expression and promotes tumor growth, while METTL14 and ALKBH5 regulate cancer stem cells and tumor progression. m6A also influences cancer by modulating target gene expression, with different effects depending on whether the target gene is an oncogene or a tumor suppressor gene. The dual role of m6A in cancer is influenced by m6A levels, enzyme expression, and post-modification regulation. m6A modification affects cancer progression by modulating target gene expression and post-modification regulation. Therapeutic strategies targeting m6A, such as inhibitors of FTO and METTL3, are being explored for cancer treatment. Overall, m6A plays a significant role in cancer development and progression, and understanding its mechanisms is crucial for developing new therapeutic approaches.N6-methyladenosine (m6A) is the most abundant internal modification on eukaryotic mRNA, playing a critical role in regulating gene expression and various cellular processes, including cell self-renewal, differentiation, invasion, and apoptosis. m6A is added by methyltransferases, removed by demethylases, and recognized by reader proteins, which regulate RNA metabolism, including translation, splicing, export, degradation, and microRNA processing. Alterations in m6A levels are involved in cancer pathogenesis and progression by regulating the expression of tumor-related genes such as BRD4, MYC, SOCS2, and EGFR. This review summarizes recent advances in m6A enzyme research, highlights the mechanisms of m6A in cancer pathogenesis and progression, and reviews potential therapeutic targets in cancer treatment. m6A regulators are categorized into writers, erasers, and readers. Writers, such as METTL3, METTL14, WTAP, VIRMA, RBM15, and ZC3H13, catalyze m6A modification. Erasers, like FTO and ALKBH5, remove m6A. Readers, including YTHDF1, YTHDF2, YTHDF3, YTHDC1, YTHDC2, and IGF2BPs, recognize m6A and influence RNA fate. The interplay among these regulators is involved in cancer progression. m6A promotes oncogene expression and inhibits tumor suppressor gene expression, contributing to cancer progression. METTL3 enhances oncogene expression and promotes tumor growth, while METTL14 and ALKBH5 regulate cancer stem cells and tumor progression. m6A also influences cancer by modulating target gene expression, with different effects depending on whether the target gene is an oncogene or a tumor suppressor gene. The dual role of m6A in cancer is influenced by m6A levels, enzyme expression, and post-modification regulation. m6A modification affects cancer progression by modulating target gene expression and post-modification regulation. Therapeutic strategies targeting m6A, such as inhibitors of FTO and METTL3, are being explored for cancer treatment. Overall, m6A plays a significant role in cancer development and progression, and understanding its mechanisms is crucial for developing new therapeutic approaches.