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NAT10 介导的 N4-乙酰胞苷修饰在肿瘤免疫中的关键作用

英文原题:The critical role of NAT10-mediated N4-acetylcytidine modification in tumor immunity.

查看英文原题

The critical role of NAT10-mediated N4-acetylcytidine modification in tumor immunity.

PubMed 2025/10/02(内容时间) Front Immunol Q1 · IF 7(JCR 2025)

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中文摘要

NAT10是一种保守的RNA乙酰转移酶,可在RNA上添加N4-乙酰胞苷(ac4C),从而调节RNA稳定性和翻译。除影响肿瘤细胞增殖、DNA修复和染色质重塑外,NAT10还塑造肿瘤免疫微环境,影响免疫逃逸、免疫细胞浸润和免疫治疗应答。临床前研究强调,抑制NAT10(例如使用Remodelin)可作为增强癌症治疗的策略,无论单独使用还是与检查点阻断、过继细胞转移或放化疗联用。当前挑战包括体内验证不足、抑制剂特异性有待提高,以及生物标志物开发仍不充分。本综述总结了NAT10在肿瘤免疫中的新兴机制证据及其作为治疗靶点的前景。

展开英文摘要原文

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.

论文信息

作者
Li C、Jiang X、Jia Y、Zhou Q、Yuan Y、Wang Q
第一作者单位
Department of Oncology, Suining Central Hospital, Suining, Sichuan, China.China
通讯作者单位
Department of Gastrointestinal Surgical Unit, Suining Central Hospital, Suining, Sichuan, China.China
文献类型
综述
期刊
Frontiers in immunology2025
原文标识
PubMed 41112236 · DOI 10.3389/fimmu.2025.1695495