N6-甲基腺苷修饰在肿瘤程序性细胞死亡中的作用
Role of the N6-methyladenosine modification in programmed cell death in tumors
谈元郡 1王霞 2黄静 1张百红3
作者信息
- 1. 甘肃中医药大学第一临床医学院(兰州市 730000);中国人民解放军联勤保障部队第九四〇医院肿瘤科
- 2. 甘肃中医药大学第一临床医学院(兰州市 730000)
- 3. 中国人民解放军联勤保障部队第九四〇医院肿瘤科
- 折叠
摘要
非突变表观遗传重编程是肿瘤的关键特征之一,抵抗程序性细胞死亡是肿瘤的另一关键特征.作为体内最丰富的转录后表观遗传修饰方式,N6-甲基腺苷(N6-methyladenosine,m6A)通过靶向调节程序性细胞死亡关键因子在肿瘤细胞凋亡、自噬、焦亡、铁死亡、坏死性凋亡、铜死亡中发挥重要作用.现已有靶向异常DNA甲基化、组蛋白修饰的表观遗传调节剂应用于临床,靶向m6A修饰调控药物仍待探索.本文阐述了m6A修饰调控肿瘤细胞程序性死亡的机制,旨在为通过调节m6A修饰水平介导肿瘤细胞死亡这一潜在肿瘤治疗策略提供理论基础.
Abstract
Non-mutational epigenetic reprogramming and resistance to programmed cell death are key characteristics of tumors.N6-methyladenosine(m6A)is the most abundant post-transcriptional epigenetic modification in vivo.It plays important roles in apoptosis,auto-phagy,pyroptosis,necroptosis,andiron(Fe)-induced(ferroptosis)and copper(Cu)-induced(cuproptosis)death of tumor cells by targeting and regulating the key factors of programmed cell death.Epigenetic modulators targeting aberrant DNA methylation and histone modifica-tion are being used in clinical applications;however,drugs specifically targeting m6A modification regulation remain to be explored.In this review,the mechanisms of m6A modification regulating tumor cell programmed death is discussed with the aim of providing a theoretical basis for mediating tumor cell death by regulating the level of m6A modification as a potential tumor therapeutic strategy.
关键词
N6-甲基腺苷修饰/程序性细胞死亡/凋亡/自噬/焦亡/铁死亡/坏死性凋亡/铜死亡Key words
N6-methyladenosine(m6A)/programmed cell death/apoptosis/autophagy/pyroptosis/ferroptosis/necroptosis/cuproptosis引用本文复制引用
基金项目
甘肃省自然科学基金(22JR5RA007)
出版年
2024
NETL
NSTL
万方数据