N6-Methyladenosine in Cancer Immunotherapy: An Undervalued Therapeutic Target
Chao Quan, Belaydi Othmane, Jiao Hu, Huihuang Li, Anze Yu, Peihua Liu, Zhenglin Yi, Dongxu Qiu, Wenbiao Ren, Hongzhi Ma, Guanghui Gong, Zhenyu Ou, Minfeng Chen, Yin Sun, Jinbo Chen, Xiongbing Zu
Abstract
N 6 -methylation of adenosine (m 6 A), a post-transcriptional regulatory mechanism, is the most abundant nucleotide modification in almost all types of RNAs. The biological function of m 6 A in regulating the expression of oncogenes or tumor suppressor genes has been widely investigated in various cancers. However, recent studies have addressed a new role of m 6 A modification in the anti-tumor immune response. By modulating the fate of targeted RNA, m 6 A affects tumor-associated immune cell activation and infiltration in the tumor microenvironment (TME). In addition, m 6 A-targeting is found to affect the efficacy of classical immunotherapy, which makes m 6 A a potential target for immunotherapy. Although m 6 A modification together with its regulators may play the exact opposite role in different tumor types, targeting m 6 A regulators has been shown to have wide implications in several cancers. In this review, we discussed the link between m 6 A modification and tumor with an emphasis on the importance of m 6 A in anti-tumor immune response and immunotherapy.