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向METTL3重新编程瘤微环境以改善癌症免疫疗法

Haisheng Yu¹, Jing Liu², Xia Bu³

¹Department of Radiation and Medical Oncology, Medical Research Institute, Frontier Science Center of Immunology and Metabolism, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan 430071, China.

Cell chemical biology

|September 26, 2023

概括

在非小细胞肺癌 (NSCLC) 中准METTL3重新编程瘤微环境 (TME),以增强抗PD-1免疫疗法. 低METTL3表达与免疫治疗期间患者预后更好相关.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

瘤微环境 (TME) 极大地影响瘤的进展和免疫治疗反应.
甲基转移酶样3 (METTL3) 是RNA m⁶A修饰中的一个关键酶,参与各种细胞过程.
METTL3在非小细胞肺癌 (NSCLC) TME和抗瘤免疫力中的作用基本上是未知的.

研究的目的:

研究METTL3在调节NSCLCTME和抗瘤免疫中的功能.
确定METTL3抑制是否可以提高NSCLC中抗PD-1疗法的疗效.

主要方法:

研究了METTL3对化学激素表达 (CXCL1,CXCL5,CCL20) 和PD-L1mRNA稳定性的影响.
利用小鼠肺瘤模型来评估METTL3抑制对TME炎症和抗PD-1治疗反应的影响.
分析了与METTL3表达水平相关的抗PD-1治疗的NSCLC患者的临床数据.

主要成果:

METTL3促进了亲瘤源的化学因子,并以m-A依赖的方式破坏了PD-L1mRNA的稳定,从而产生了非炎症的TME.
抑制METTL3将TME重新编程为更炎症的状态,从而增加了临床前模型中抗PD-1疗法的有效性.
在NSCLC患者中,低METTL3表达与治疗抗PD-1疗法时的改善结果有关.

结论:

METTL3在塑造非炎症TME和抑制NSCLC中抗瘤免疫力方面发挥着重要作用.
向METTL3代表了一种有希望的策略,以提高抗PD-1免疫治疗在NSCLC患者的疗效.
在NSCLC中,METTL3可以作为抗PD-1治疗反应的预测生物标志物.

关键词:

在METTL3中,METTL3是METTL3的第一个类型.在PD-L1中.癌症免疫疗法免疫疗法化学物质 (chemokines) 是一种化学物质.瘤微环境是一个微环境.

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