摘要/Abstract

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
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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