期刊
MOLECULAR CANCER
卷 21, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12943-022-01652-3
关键词
N-6-methyladenosine (m(6)A); cancer; Tumor; Immunotherapy; Tumor immune escape (TIE)
资金
- Harbin Medical University Cancer Hospital [Nn102017-02]
- National Natural Science Foundation of China [81972706, 82173235, 82072904, 81872149]
- Outstanding Youth Project of Heilongjiang Provincial Natural Science Foundation [YQ2019H027]
- Distinguished Young Scholars of Harbin Medical University Cancer Hospital [JCQN2018-03]
- Yong Elite Training Foundation Grant of Harbin Medical University Cancer Hospital [JY2016-02]
- Heilongjiang Health and Family Planning Commission Foundation [2019-056]
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.
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.
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