MINI REVIEW article
Front. Immunol.
Sec. Cancer Immunity and Immunotherapy
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1695495
The critical role of NAT10-mediated N4-acetylcytidine modification in tumor immunity
Provisionally accepted
- 1Suining Central Hospital, Suining, China
- 2City of Hope, Duarte, United States
- 3Department of Gastroenterology, Suining Central Hospital, Suining, China
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NAT10, a conserved RNA acetyltransferase, installs N4-acetylcytidine (ac4C) on RNA, thereby regulating stability and translation. Beyond tumor cell proliferation, DNA repair, and chromatin remodeling, NAT10 shapes the tumor immune microenvironment, influencing immune evasion, immune cell infiltration, and responses to immunotherapy. Preclinical studies highlight NAT10 inhibition, such as with Remodelin, as a strategy to enhance cancer treatment-alone or combined with checkpoint blockade, adoptive cell transfer, or chemoradiotherapy. Remaining challenges include in vivo validation, greater inhibitor specificity, and biomarker development. This mini-review synthesizes emerging evidence on NAT10 mechanistic roles in tumor immunity and its promise as a therapeutic target.
Keywords: NAT10, RNA acetylation, N4-acetylcytidine (ac4C), tumor immunity, Immune Regulation, immune checkpoints, cancer immunotherapy
Received: 02 Sep 2025; Accepted: 22 Sep 2025.
Copyright: © 2025 Li, Jiang, Jia, Zhou, Yuan and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Qiang Wang, wangqiang902497@126.com
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