The emerging roles of the interaction between m6A modification and c‐Myc in driving tumorigenesis and development

N6‐methyladenosine (m6A) is an extremely common and conservative posttranscriptional modification, that can specifically target and regulate the expression or stability of a series of tumor‐related genes, thus playing critical roles in the occurrence and development of tumors. c‐Myc is an important tumorigenic transcription factor that promotes tumorigenesis and development by mainly regulating the expression of downstream target genes. Increasing evidence shows that m6A modification, as well as abnormal expression and regulation of c‐Myc, is critical molecular mechanisms driving tumorigenesis and development. Although more evidence has been uncovered about the individual roles of m6A modification or c‐Myc in tumors, the interaction between m6A modification and c‐Myc in tumorigenesis and development has not been systematically summarized. Therefore, this review is focused on the mutual regulation between m6A modification and c‐Myc expression and stability as well as its roles in tumorigenesis and development. We also summarized the potential value of the interaction between m6A modification and m6A expression and stability in tumor diagnosis and treatment, which provides a specific reference for revealing the mechanism of tumor occurrence and development as well as clinical diagnosis and treatment. N6‐methyladenosine (m6A) regulators including writers, erasers, and readers affect the transcription, stability, and translation efficiency of c‐Myc. c‐Myc regulates the expression of m6A regulators in the transcriptional levels. The interaction between m6A regulators and c‐Myc forms a double positive feedback loop, driving the occurrence and development of tumors.