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解析癌症中外转录组调控的分子机制。

Deciphering the molecular mechanisms of epitranscriptome regulation in cancer.

机构信息

Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 04763; Research Institute for Natural Sciences, Hanyang University, Seoul 04763; Research Institute for Convergence of Basic Sciences, Hanyang University, Seoul 04763, Korea.

出版信息

BMB Rep. 2021 Feb;54(2):89-97. doi: 10.5483/BMBRep.2021.54.2.212.

DOI:10.5483/BMBRep.2021.54.2.212
PMID:33298243
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7907739/
Abstract

Post-transcriptional regulation is an indispensable cellular mechanism of gene expression control that dictates various cellular functions and cell fate decisions. Recently, various chemical RNA modifications, termed the "epitranscriptome," have been proposed to play crucial roles in the regulation of post-transcriptional gene expression. To date, more than 170 RNA modifications have been identified in almost all types of RNA. As with DNA modification-mediated control of gene expression, regulation of gene expression via RNA modification is also accomplished by three groups of proteins: writers, readers, and erasers. Several emerging studies have revealed that dysregulation in RNA modification is closely associated with tumorigenesis. Notably, the molecular outcomes of specific RNA modifications often have opposite cellular consequences. In this review, we highlight the current progress in the elucidation of the mechanisms of cancer development due to chemical modifications of various RNA species. [BMB Reports 2021; 54(2): 89-97].

摘要

转录后调控是基因表达调控中不可或缺的细胞机制,决定着各种细胞功能和细胞命运决定。最近,各种化学 RNA 修饰被称为“转录后组”,被认为在调节转录后基因表达中起着关键作用。迄今为止,几乎所有类型的 RNA 中已经鉴定出超过 170 种 RNA 修饰。与 DNA 修饰介导的基因表达调控一样,通过 RNA 修饰调节基因表达也是由三组蛋白完成的:写入器、读取器和橡皮擦。一些新出现的研究表明,RNA 修饰的失调与肿瘤发生密切相关。值得注意的是,特定 RNA 修饰的分子结果通常具有相反的细胞后果。在这篇综述中,我们强调了由于各种 RNA 种类的化学修饰而导致癌症发展的机制的最新进展。[BMB 报告 2021;54(2):89-97]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff28/7907739/30d037f1d039/bmb-54-2-89-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff28/7907739/30d037f1d039/bmb-54-2-89-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff28/7907739/30d037f1d039/bmb-54-2-89-f1.jpg

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本文引用的文献

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METTL14-mediated N6-methyladenosine modification of SOX4 mRNA inhibits tumor metastasis in colorectal cancer.METTL14 通过介导 SOX4 mRNA 的 N6-甲基腺苷修饰抑制结直肠癌的肿瘤转移。
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m6A修饰介导钙化性主动脉瓣疾病中的组织免疫微环境。
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Theranostics. 2020 Feb 10;10(7):3164-3189. doi: 10.7150/thno.41687. eCollection 2020.
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RETRACTED: Methyltransferase-like 1 (METTL1) served as a tumor suppressor in colon cancer by activating 7-methyguanosine (m7G) regulated let-7e miRNA/HMGA2 axis.撤回:甲基转移酶样蛋白 1(METTL1)通过激活 7-甲基鸟苷(m7G)调节的 let-7e miRNA/HMGA2 轴,在结肠癌中作为肿瘤抑制因子发挥作用。
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M6A-mediated upregulation of LINC00958 increases lipogenesis and acts as a nanotherapeutic target in hepatocellular carcinoma.M6A 介导的 LINC00958 上调促进脂肪生成,并作为肝细胞癌的一种纳米治疗靶点。
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YTHDF2 Recognition of N-Methyladenosine (mA)-Modified RNA Is Associated with Transcript Destabilization.YTHDF2 通过识别 N6-甲基腺苷(m6A)修饰的 RNA 参与转录本的不稳定性。
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