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MA修饰在肿瘤相关长链非编码RNA调控中的作用。

The role of MA modification in the regulation of tumor-related lncRNAs.

作者信息

Lan Yufei, Liu Boyang, Guo Hongbo

机构信息

Neurosurgery Center, The National Key Clinical Specialty, The Engineering Technology Research Center of Education Ministry of China on Diagnosis and Treatment of Cerebrovascular Disease, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.

出版信息

Mol Ther Nucleic Acids. 2021 Apr 9;24:768-779. doi: 10.1016/j.omtn.2021.04.002. eCollection 2021 Jun 4.

Abstract

-methyladenosine (mA) is the most abundant modification in eukaryotic cells, and it regulates RNA transcription, processing, splicing, degradation, and translation. Long non-coding RNAs (lncRNAs), as transcriptional products with no or limited protein coding ability more than 200 nt in length, play an important role in epigenetic modification, mRNA transcription, splicing, stability, translation, and other biological functions. Extensive studies have shown that both mA modification and lncRNAs are involved in the pathogenesis of various diseases, such as kinds of cancers, heart failure, Alzheimer's disease, periodontitis, human abdominal aortic aneurysm, and obesity. To date, mA modification has been identified as an important biological function in enrichment and regulation of lncRNAs. In this review, we summarize the role of mA modification in the regulation and function of tumor-related lncRNAs. Moreover, we discuss the potential applications and possible future directions in the field.

摘要

N6-甲基腺苷(m⁶A)是真核细胞中最丰富的修饰,它调控RNA转录、加工、剪接、降解及翻译。长链非编码RNA(lncRNA)作为长度超过200 nt、无蛋白质编码能力或蛋白质编码能力有限的转录产物,在表观遗传修饰、mRNA转录、剪接、稳定性、翻译及其他生物学功能中发挥重要作用。大量研究表明,m⁶A修饰和lncRNA均参与多种疾病的发病机制,如各类癌症、心力衰竭、阿尔茨海默病、牙周炎、人类腹主动脉瘤及肥胖症。迄今为止,m⁶A修饰已被确定为lncRNA富集和调控中的一项重要生物学功能。在本综述中,我们总结了m⁶A修饰在肿瘤相关lncRNA调控及功能中的作用。此外,我们还讨论了该领域的潜在应用及可能的未来发展方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9261/8094576/f976cf830694/fx1.jpg

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