摘要
N^(6)-甲基腺嘌呤(N6-methyladenine,m^(6)A)修饰作为信使RNA中广泛存在的一种甲基化修饰,它的动态变化在生命活动和疾病的发生发展中发挥着重要的作用。近年来研究发现,通过改变靶基因的m6A修饰水平可以调控肿瘤的进展,因此,通过小分子靶向干预m^(6)A去甲基化酶可作为抗肿瘤的新策略。本文重点讨论了m^(6)A去甲基化酶,包括脂肪含量与肥胖相关蛋白(fat mass and obesity-associated protein,FTO)和AlkB同源蛋白5(AlkB homlog5,ALKBH5)的作用方式以及它们在肿瘤中发挥的生物学功能,并总结了m^(6)A去甲基化酶小分子抑制剂的研究进展。
N^(6)-methyladenine(m^(6)A)modification,the most abundant and dynamic chemical modification on messenger RNA,plays an essential role in physiological and pathological progress.Recent studies have found that tumor progression can be affected by altering the m^(6)A modification level of target genes.Therefore,small molecule targeted m^(6)A demethylase can be used as a new anti-tumor strategy.This review focuses on the regulatory mechanism of m^(6)A demethylases,including fat mass and obesity-associated protein(FTO)and AlkB homlog 5(ALKBH5),as well as their biological functions in tumors,and summarizes the research progress of their small molecule inhibitors.
作者
高静
米雪
周琦
周君
GAO Jing;MI Xue;ZHOU Qi;ZHOU Jun(School of Life Science&Technology,China Pharmaceutical University,Nanjing 211198,China)
出处
《中国药科大学学报》
CAS
CSCD
北大核心
2022年第6期663-673,共11页
Journal of China Pharmaceutical University