The role of m6A-mediated PD-1/PD-L1 in antitumor immunity

N6-methyladenosine (m6A) is the most prevalent, abundant and conserved type of internal posttranscriptional RNA modification in eukaryotic cells. Emerging evidence suggests that m6A modifications perform important functions that affect antitumor immunity. Programmed death 1 (PD-1) and programmed cell death-ligand 1 (PD-L1) are the two most well-studied immune checkpoint pathways. The interaction of PD-L1 with its receptor PD-1 inhibits cytotoxic T-cell-mediated tumor responses, and blockade of this interaction has proven to be an effective immunotherapy strategy in various cancers. Unfortunately, few cancer patients benefit from the two tools due to uncertain resistance. m6A plays an important role in affecting RNA biogenesis and process in various cancers. Understanding the molecular mechanism of drug resistance will promote the development of personalized clinical management. In this review, we systematically discussed the mechanisms by which m6A regulates PD-1 and PD-L1 expression and further their functions in the process of tumor immunotherapy and the potential application prospects of m6A-associated molecules. Moreover, mounting m6Ascore is established to evaluate the prognosis of cancer.