RNA N6-甲基腺嘌呤异常修饰影响肿瘤干细胞促进恶性肿瘤发生、发展的研究进展  

Aberrant RNA N^6-methyladenosine modification causes tumorigenesis, progression and metastasis of malignant tumors by affecting cancer stem cells

作　　者：朱正阳 王成 姜辰一 赵福军[1,3,4] ZHU Zheng-yang;WANG Cheng;JIANG Chen-yi;ZHAO Fu-jun(Department of Urology,Shanghai General Hospital,Shanghai Jiao Tong University,Shanghai 200080,China;Clinical Medical College,Shanghai General Hospital,Shanghai Jiao Tong University,Shanghai 200080,China;Department of Urology,Shanghai General Hospital of Nanjing Medical University,Shanghai 200080,China;Department of Urology,Kashgar Prefecture Second People′s Hospital,Xinjiang,Kashgar 844000,China)

机构地区：[1]上海交通大学附属第一人民医院泌尿外科,上海200080 [2]上海交通大学附属第一人民医院临床医学院,上海200080 [3]南京医科大学附属上海市第一人民医院临床医学院泌尿外科,上海200080 [4]新疆维吾尔自治区喀什地区第二人民医院泌尿外科,喀什844000

出　　处：《上海交通大学学报（医学版）》2020年第3期385-390,共6页Journal of Shanghai Jiao tong University:Medical Science

基　　金：国家自然科学基金(81772746);新疆维吾尔自治区自然科学基金(2019D01C091)。

摘　　要：RNA N6-甲基腺嘌呤(N^6-methyladenosine,m6A)修饰是RNA较常见的表观遗传修饰形式,受到甲基化酶、去甲基化酶以及多种识别蛋白调节,与基因的表达调控密切相关。近年来研究发现RNA m^6A异常修饰在恶性肿瘤发生、进展及转移中起到重要作用。深入研究提示RNA m^6A异常修饰可能诱导肿瘤干细胞形成,提高肿瘤细胞对治疗后损伤的抗性,促进恶性肿瘤放射治疗和化学治疗抵抗的产生,从而导致恶性肿瘤进展或复发。该文回顾RNA m^6A修饰的调节机制,及其在恶性肿瘤进展、复发中的作用机制研究进展,同时结合肿瘤干细胞对放射治疗和化学治疗产生抵抗的机制,以探讨RNA m^6A异常修饰通过影响肿瘤干细胞促进肿瘤进展的可能机制。RNA N^6-methyladenosine(m^6A) modification is one of the most pervasive epigenetic modifications that correlate with gene expression, regulated by a variety of methylases, demethylases and reader proteins. m^6A has been found crucial during cancer progression, aberrant changes of which contribute to tumorigenesis and metastasis. It’s also been reported to be influential on chemotherapy and radiotherapy resistance of malignant tumors by inducing cancer stem cells(CSC) generation and enhancing post-therapy damage resistance, thus causing the progression or recurrence. In this review, we review the regulation of RNA m^6A modification and focus on recent advances in functions of dysregulated m^6A modification in the pathogenesis of cancer progression and recurrence. In addition, we also discuss the possible participation of CSC in this process combining current perspectives on the chemotherapy and radiotherapy resistance mechanism of CSC.

关 键 词：RNA甲基化 N^6-甲基腺嘌呤 恶性肿瘤 肿瘤干细胞 复发 

分 类 号：R73[医药卫生—肿瘤]