The m6A modification in cancer: roles, implications, and its potential in therapy

Abstract N 6 -methyladenosine (m 6 A) serves as the dominant epitranscriptomic mark within eukaryotic mRNA transcripts, exerting pivotal regulatory functions in modulating mRNA structural integrity, translational efficiency, and splicing, thereby influencing gene expression patterns in cancer cells. m 6 A modification is recognized as a principal epigenetic determinant in driving malignant progression and fostering therapeutic resistance, making it crucial for advancing precision oncology. This review begins with a brief introduction to m 6 A modification, with a particular focus on its dynamic variability in distinct malignancies and clinical staging scenarios. Moreover, we underscore the critical functions of m 6 A methylation in cancer biology, including cancer-related molecular networks, cancer hallmarks, cancer stem cells, and the tumor microenvironment. We further outline the implications of m 6 A dysregulation in cancer, emphasizing the diagnostic potential of m 6 A regulators, the prognostic value of m 6 A, and the role of m 6 A in treatment resistance. Additionally, we analyze the potential of m 6 A modification in cancer therapy, encompassing the use of m 6 A inhibitors, combinations with existing cancer therapies, and personalized medicine approaches. Finally, we dissect the current limitations and future directions in m 6 A modification research, directing resources toward the development of high-throughput platforms for the dynamic monitoring of m 6 A modification in living systems. Overall, this review reinforces the central significance of m 6 A modification in cancer biology, emphasizing its transformative capacity to reshape cancer diagnostic paradigms and therapeutic intervention strategies.