m6A methyltransferase METTL3 promotes non-small-cell lung carcinoma progression by inhibiting the RIG-I-MAVS innate immune pathway

IF 5 2区 医学 Q2 Medicine Translational Oncology Pub Date : 2025-01-01 Epub Date: 2024-12-02 DOI:10.1016/j.tranon.2024.102230
Tinghui Huang , Xudong Ao , Jie Liu , Chuancheng Sun , Yunfei Dong , Xuechen Yin , Yan Zhang , Xinping Wang , Wenying Li , Jiujiu Cao , Feiyan Pan , Zhigang Hu , Zhigang Guo , Lingfeng He
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Abstract

Our experimental study showed that METTL3 was highly expressed in NSCLC cells and promoted the growth of tumor cells. METTL3 takes N6-methyladenosine (m6A) as the main means of mRNA modification to control the expression and function of RIG-I-MAVS signalling pathway. RIG-I-MAVS constitute the first line frontier in the innate immune defense of human cells. Activation of RIG-I-MAVS signaling can inhibit tumor cell growth and activate the immune microenvironment. Our experimental data reveal that lung cancer cells utilize METTL3-mediated methylation modifications to inhibit the activation of RIG-I-MAVS signaling pathway and immune responses. Our work provides new ideas for biotherapy and immunotherapy.

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m6A甲基转移酶METTL3通过抑制RIG-I-MAVS先天免疫途径促进非小细胞肺癌的进展。
我们的实验研究表明,METTL3在NSCLC细胞中高表达,促进肿瘤细胞的生长。METTL3以n6 -甲基腺苷(m6A)为主要的mRNA修饰手段,控制RIG-I-MAVS信号通路的表达和功能。RIG-I-MAVS构成了人类细胞先天免疫防御的第一线前沿。RIG-I-MAVS信号的激活可以抑制肿瘤细胞生长,激活免疫微环境。我们的实验数据表明,肺癌细胞利用mettl3介导的甲基化修饰来抑制RIG-I-MAVS信号通路的激活和免疫反应。我们的工作为生物治疗和免疫治疗提供了新的思路。
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来源期刊
CiteScore
8.40
自引率
2.00%
发文量
314
审稿时长
54 days
期刊介绍: Translational Oncology publishes the results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of oncology patients. Translational Oncology will publish laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer. Peer reviewed manuscript types include Original Reports, Reviews and Editorials.
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