Epitranscriptomic Regulation by m6A in Metabolic Reprogramming and Cellular Plasticity during Cancer Progression

N6-methyladenosine (m 6 A) RNA modification has recently emerged as a key epigenetic regulator that profoundly influences cancer biology.In particular, m 6 A plays a central role in metabolic reprogramming, enabling cancer cells to sustain rapid proliferation and adapt to stress conditions such as nutrient deprivation and hypoxia.This review summarizes current advances in understanding how m 6 A modification regulates cancer metabolism.By modulating the stability and translation of mRNAs encoding metabolic enzymes and signaling regulators, m 6 A writers, erasers, and readers coordinate glucose metabolism, glutamine utilization, lipid synthesis, and redox homeostasis.These regulatory networks confer metabolic plasticity, allowing tumor cells to flexibly switch energy sources and biosynthetic pathways in response to dynamic microenvironments.Finally, we highlight the therapeutic significance of targeting m 6 A machinery in cancer.Disrupting m 6 A-mediated metabolic flexibility may overcome drug resistance and enhance the efficacy of conventional treatments.Future efforts should focus on elucidating context-specific functions of m 6 A across cancer types, developing selective modulators, and integrating m 6 A-targeted strategies into combination therapies.Collectively, these insights provide a foundation for more effective and personalized cancer treatments.