Gu Chang, Shi Xin, Dai Chenyang, Shen Feng, Rocco Gaetano, Chen Jiafei, Huang Zhengyu, Chen Chunji, He Chuan, Huang Tao, Chen Chang
Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China.
Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai 200030, China.
Innovation (Camb). 2020 Nov 4;1(3):100066. doi: 10.1016/j.xinn.2020.100066. eCollection 2020 Nov 25.
N-Methyladenosine (mA) RNA modification brings a new dawn for RNA modification researches in recent years. This posttranscriptional RNA modification is dynamic and reversible, and is regulated by methylases ("writers"), demethylases ("erasers"), and proteins that preferentially recognize mA modifications ("readers"). The change of RNA mA modification regulates RNA metabolism in eucaryon, including translation, splicing, exporting, decay, and processing. Thereby the dysregulation of mA may lead to tumorigenesis and progression. Given the tumorigenic role of abnormal mA expression, mA regulators may function as potential clinical therapeutic targets for cancers. In this review, we emphasize on the underlying mechanisms of mA modifications in tumorigenesis and further introduce the potential mA regulators-associated therapeutic targets for tumor therapy.
N-甲基腺苷(mA)RNA修饰近年来为RNA修饰研究带来了新的曙光。这种转录后RNA修饰是动态且可逆的,受甲基化酶(“书写者”)、去甲基化酶(“擦除者”)以及优先识别mA修饰的蛋白质(“阅读者”)调控。RNA mA修饰的变化在真核生物中调节RNA代谢,包括翻译、剪接、输出、衰变和加工。因此,mA失调可能导致肿瘤发生和进展。鉴于异常mA表达的致瘤作用,mA调节剂可能作为癌症潜在的临床治疗靶点。在本综述中,我们着重阐述mA修饰在肿瘤发生中的潜在机制,并进一步介绍与mA调节剂相关的肿瘤治疗潜在靶点。