上海交通大学学报（医学版）

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2020 , Vol. 40 >Issue 3: 385

DOI: https://doi.org/10.3969/j.issn.1674-8115.2020.03.018

综述

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

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  • 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
朱正阳（1997—），男，本科生；电子信箱：Lennox@sjtu.edu.cn。王 成（1993—），男，硕士生；电子信箱：wang1313Ijj@163.com。*为共同第一作者。

网络出版日期: 2020-04-09

基金资助

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

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Aberrant RNA N6-methyladenosine modification causes tumorigenesis, progression and metastasis of malignant tumorsaffecting cancer stem cells

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  • 1. Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai 200080, China; 2. Clinical Medical College, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai 200080, China; 3. Department of Urology, Shanghai General Hospital of Nanjing Medical University, Shanghai 200080, China; 4. Department of Urology, Kashgar Prefecture Second People′s Hospital, Xinjiang, Kashgar 844000, China

Online published: 2020-04-09

Supported by

National Natural Science Foundation of China (81772746); Natural Science Foundation of Xinjiang Uygur Autonomous Region (2019D01C091).

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摘要

RNA N6-甲基腺嘌呤（N6-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 m6A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 m6A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 m6A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 m6A异常修饰通过影响肿瘤干细胞促进肿瘤进展的可能机制。

关键词： RNA甲基化; N6-甲基腺嘌呤; 恶性肿瘤; 肿瘤干细胞; 复发

本文引用格式

朱正阳1, 2*，王 成3*，姜辰一1，赵福军1, 3, 4 . 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[J]. 上海交通大学学报（医学版）, 2020 , 40(3) : 385 . DOI: 10.3969/j.issn.1674-8115.2020.03.018

Abstract

RNA N6-methyladenosine (m6A) modification is one of the most pervasive epigenetic modifications that correlate with gene , regulateda variety of methylases, demethylases and reader proteins. m6A 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 tumorsinducing 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 m6A modification and focus on recent advances in functions of dysregulated m6A 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.

Key words： RNA methylation; N6-methyladenosine (m6A); malignant tumor; cancer stem cells; recurrence

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