Methylation of
adenosine in
RNA to
N6-methyladenosine (m6A) is widespread in eukaryotic cells with his integral
RNA regulation. This dynamic process is regulated by methylases (editors/writers), demethylases (remover/erasers), and
proteins that recognize methylation (effectors/readers). It is now evident that
m6A is involved in the proliferation and
metastasis of
cancer cells, for instance, altering
cancer cell metabolism. Thus, determining how
m6A dysregulates metabolic pathways could provide potential targets for
cancer therapy or early diagnosis. This review focuses on the link between the
m6A modification and the reprogramming of metabolism in
cancer. We hypothesize that
m6A modification could dysregulate the expression of
glucose,
lipid,
amino acid metabolism, and other metabolites or building blocks of cells by adaptation to the hypoxic tumor microenvironment, an increase in glycolysis,
mitochondrial dysfunction, and abnormal expression of metabolic
enzymes, metabolic receptors,
transcription factors as well as oncogenic signaling pathways in both
hematological malignancies and solid
tumors. These metabolism abnormalities caused by
m6A's modification may affect the metabolic reprogramming of
cancer cells and then increase cell proliferation,
tumor initiation, and
metastasis. We conclude that focusing on
m6A could provide new directions in searching for novel therapeutic and diagnostic targets for the early detection and treatment of many
cancers.