CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:The critical role of NAT10-mediated N4-acetylcytidine modification in tumor immunity.
The critical role of NAT10-mediated N4-acetylcytidine modification in tumor immunity.
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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。
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.
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