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新型肿瘤发生中 mA RNA 甲基化的见解:一把双刃剑。

Novel insights on mA RNA methylation in tumorigenesis: a double-edged sword.

机构信息

Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, People's Republic of China.

出版信息

Mol Cancer. 2018 Jul 21;17(1):101. doi: 10.1186/s12943-018-0847-4.

DOI:10.1186/s12943-018-0847-4
PMID:30031372
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6054842/
Abstract

N6-methyladenosine (mA), the most prevalent modification of mammalian RNA, has received increasing attention. Although mA has been shown to be associated with biological activities, such as spermatogenesis modulation, cell spermatogenesis and pluripotency, Drosophila sex determination, and the control of T cell homeostasis and response to heat shock, little is known about its roles in cancer biology and cancer stem cells. Recent articles have noted that some genes have abnormal mA expression after tumorigenesis, including genes ABS2, RARA, MYB, MYC, ADAM19 and FOX1. Abnormal changes in the mA levels of these genes are closely related to tumour occurrence and development. In this review, we summarized the 'dual edge weapon' role of RNA methylation in the tumorigenesis. We discussed RNA methylation could lead to not only tumour progression but also tumour suppression. Moreover, we clarified that the abnormal changes in the mA enrichment of specific loci contribute to tumour occurrence and development, thereby representing a novel anti-cancer strategy by restoration to balanced RNA methylation in tumour cells.

摘要

N6-甲基腺苷(m6A)是哺乳动物 RNA 中最普遍的修饰物,受到了越来越多的关注。尽管已经表明 m6A 与生物活性有关,如精子发生调节、细胞精子发生和多能性、果蝇性别决定以及 T 细胞动态平衡和对热休克的反应的控制,但对于其在癌症生物学和癌症干细胞中的作用知之甚少。最近的文章指出,一些基因在癌变后出现异常的 m6A 表达,包括 ABS2、RARA、MYB、MYC、ADAM19 和 FOX1 基因。这些基因的 m6A 水平的异常变化与肿瘤的发生和发展密切相关。在这篇综述中,我们总结了 RNA 甲基化在肿瘤发生中的“双刃剑”作用。我们讨论了 RNA 甲基化不仅可以导致肿瘤进展,还可以抑制肿瘤。此外,我们阐明了特定基因座的 m6A 富集异常变化有助于肿瘤的发生和发展,从而通过恢复肿瘤细胞中平衡的 RNA 甲基化来代表一种新的抗癌策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d29/6054842/6a9090d6032d/12943_2018_847_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d29/6054842/51ebdc105ff6/12943_2018_847_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d29/6054842/6a9090d6032d/12943_2018_847_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d29/6054842/51ebdc105ff6/12943_2018_847_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d29/6054842/6a9090d6032d/12943_2018_847_Fig2_HTML.jpg

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