Targeting RNA N6-methyladenosine modification: a precise weapon in overcoming tumor immune escape

Immunotherapy, especially immune checkpoint inhibitors (ICIs), has revolutionized the treatment of many types of cancer, particularly advanced-stage cancers. Nevertheless, although a subset of patients experiences dramatic and long-term disease regression in response to ICIs, most patients do not benefit from these treatments. Some may even experience cancer progression. Immune escape by tumor cells may be a key reason for this low response rate. N-6-methyladenosine (m(6)A) is the most common type of RNA methylation and has been recognized as a critical regulator of tumors and the immune system. Therefore, m(6)A modification and related regulators are promising targets for improving the efficacy of tumor immunotherapy. However, the association between m(6)A modification and tumor immune escape (TIE) has not been comprehensively summarized. Therefore, this review summarizes the existing knowledge regarding m(6)A modifications involved in TIE and their potential mechanisms of action. Moreover, we provide an overview of currently available agents targeting m(6)A regulators that have been tested for their elevated effects on TIE. This review establishes the association between m(6)A modifications and TIE and provides new insights and strategies for maximizing the efficacy of immunotherapy by specifically targeting m(6)A modifications involved in TIE.

Automated summary

This review summarizes the existing knowledge on N-6-methyladenosine (m(6)A) modifications involved in tumor immune escape (TIE), explores their potential mechanisms, and provides an overview of available drugs targeting m(6)A modifications.