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解析异常 RNA 可变剪接在肝细胞癌中的作用:一篇全面的综述。

Decoding the role of aberrant RNA alternative splicing in hepatocellular carcinoma: a comprehensive review.

机构信息

School of Basic Medical Sciences, Anhui Medical University, Hefei, China.

Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA, USA.

出版信息

J Cancer Res Clin Oncol. 2023 Dec;149(19):17691-17708. doi: 10.1007/s00432-023-05474-8. Epub 2023 Oct 29.

DOI:10.1007/s00432-023-05474-8
PMID:37898981
Abstract

During eukaryotic gene expression, alternative splicing of messenger RNA precursors is critical in increasing protein diversity and regulatory complexity. Multiple transcript isoforms could be produced by alternative splicing from a single gene; they could eventually be translated into protein isoforms with deleted, added, or altered domains or produce transcripts containing premature termination codons that could be targeted by nonsense-mediated mRNA decay. Alternative splicing can generate proteins with similar, different, or even opposite functions. Increasingly strong evidence indicates that abnormal RNA splicing is a prevalent and crucial occurrence in cellular differentiation, tissue advancement, and the development and progression of cancer. Aberrant alternative splicing could affect cancer cell activities such as growth, apoptosis, invasiveness, drug resistance, angiogenesis, and metabolism. This systematic review provides a comprehensive overview of the impact of abnormal RNA alternative splicing on the development and progression of hepatocellular carcinoma.

摘要

在真核生物基因表达过程中,信使 RNA 前体的选择性剪接对于增加蛋白质多样性和调控复杂性至关重要。多个转录本异构体可以由单个基因的选择性剪接产生;它们最终可能被翻译成具有缺失、添加或改变的结构域的蛋白质异构体,或者产生含有终止密码子的转录本,这些转录本可以被无意义介导的 mRNA 降解靶向。选择性剪接可以产生具有相似、不同甚至相反功能的蛋白质。越来越多的证据表明,异常的 RNA 剪接是细胞分化、组织发育以及癌症的发生和发展过程中的一种普遍而关键的现象。异常的选择性剪接可能会影响癌细胞的活动,如生长、凋亡、侵袭、耐药性、血管生成和代谢。本系统综述全面概述了异常 RNA 选择性剪接对肝细胞癌发生和发展的影响。

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Hepatology. 2024 Apr 1;79(4):E121-E122. doi: 10.1097/HEP.0000000000000677. Epub 2023 Nov 8.
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Hepatology. 2023 Nov 1;78(5):1506-1524. doi: 10.1097/HEP.0000000000000433. Epub 2023 May 3.
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