m^(6)A甲基化修饰在肿瘤耐药中的作用机制研究进展  

Research Progress in Action of Mechanism of m^(6)A Methylation Modification in Drug Resistance of Tumors

作　　者：陈珊珊 伍燕 颜新建 李高峰 CHEN Shanshan;WU Yan;YAN Xinjian;LI Gaofeng(School of Medicine,Jishou University,Jishou 416099,China;Department of Medical Oncology,Zhuzhou Central Hospital,Xiangya Medical College,Central South University,Zhuzhou 412007,China)

机构地区：[1]吉首大学医学院,湖南吉首416099 [2]中南大学湘雅医学院附属株洲市中心医院肿瘤内科,湖南株洲412007

出　　处：《医学综述》2024年第2期177-181,共5页Medical Recapitulate

基　　金：湖南省自然科学基金(2022JJ50101);吉首大学校级科研项目(Jdzd22038)。

摘　　要：N^(6)-甲基腺嘌呤(m^(6)A)甲基化是哺乳动物体内最常见、规模最大的一类RNA修饰过程,属于表观遗传学修饰之一,在甲基化酶、去甲基化酶、识别酶等调控下参与RNA转录、核输出、翻译和微RNA的加工处理等,因此m^(6)A甲基化修饰可调控基因的表达。肿瘤耐药性是肿瘤临床治疗的主要障碍,在细胞癌变过程中,m^(6)A甲基化修饰可通过调控基因的表达、激活或抑制信号转导通路等引发相应信使RNA翻译改变,促进肿瘤进展,导致再次使用靶向药物时产生耐药性。因此,深入研究m^(6)A甲基化修饰在肿瘤耐药中的作用机制,可以为肿瘤的治疗提供新思路。N^(6)-methyladenine(m^(6)A)methylation is one of the most common and large-scale RNA modification processes in mammals.It is one of the epigenetic modifications and is involved in RNA transcription,nuclear output,translation and microRNAs processing under the regulation of methylase,demethylase and recognition enzymes,therefore,m^(6)A methylation can regulate gene expression.Drug resistance is a major obstacle in the clinical treatment of tumor.In the process of cell carcinogenesis,m^(6)A methylation modification can induce the translation changes of corresponding messenger RNA by regulating gene expression,activating or inhibiting signal transduction pathways,etc.,promoting tumor progression,and resulting in drug resistance when targeted drugs are used again.Therefore,in-depth studies of the mechanism of m^(6)A methylation modification in tumor drug resistance can provide new ideas for the treatment of tumors.

关 键 词：肿瘤耐药 N^(6)-甲基腺嘌呤甲基化 甲基化酶 去甲基化酶 识别酶 

分 类 号：R73[医药卫生—肿瘤]