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m6A 修饰与 c-Myc 相互作用在驱动肿瘤发生和发展中的新兴作用。

The emerging roles of the interaction between m6A modification and c-Myc in driving tumorigenesis and development.

机构信息

NHC Key Laboratory of Carcinogenesis, Hunan Key Laboratory of Oncotarget Gene, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.

Cancer Research Institute, School of Basic Medical Sciences, Central South University, Changsha, China.

出版信息

J Cell Physiol. 2022 Jul;237(7):2758-2769. doi: 10.1002/jcp.30733. Epub 2022 Apr 6.

DOI:10.1002/jcp.30733
PMID:35388487
Abstract

N6-methyladenosine (m6A) is an extremely common and conservative posttranscriptional modification, that can specifically target and regulate the expression or stability of a series of tumor-related genes, thus playing critical roles in the occurrence and development of tumors. c-Myc is an important tumorigenic transcription factor that promotes tumorigenesis and development by mainly regulating the expression of downstream target genes. Increasing evidence shows that m6A modification, as well as abnormal expression and regulation of c-Myc, is critical molecular mechanisms driving tumorigenesis and development. Although more evidence has been uncovered about the individual roles of m6A modification or c-Myc in tumors, the interaction between m6A modification and c-Myc in tumorigenesis and development has not been systematically summarized. Therefore, this review is focused on the mutual regulation between m6A modification and c-Myc expression and stability as well as its roles in tumorigenesis and development. We also summarized the potential value of the interaction between m6A modification and m6A expression and stability in tumor diagnosis and treatment, which provides a specific reference for revealing the mechanism of tumor occurrence and development as well as clinical diagnosis and treatment.

摘要

N6-甲基腺苷(m6A)是一种极其普遍且保守的转录后修饰,它能够特异性地靶向和调节一系列与肿瘤相关的基因的表达或稳定性,从而在肿瘤的发生和发展中发挥关键作用。c-Myc 是一种重要的致癌转录因子,主要通过调节下游靶基因的表达来促进肿瘤的发生和发展。越来越多的证据表明,m6A 修饰以及 c-Myc 的异常表达和调控是驱动肿瘤发生和发展的关键分子机制。尽管已经有更多的证据揭示了 m6A 修饰或 c-Myc 在肿瘤中的单独作用,但 m6A 修饰与 c-Myc 在肿瘤发生和发展中的相互作用尚未得到系统总结。因此,本综述重点关注 m6A 修饰与 c-Myc 表达和稳定性之间的相互调节及其在肿瘤发生和发展中的作用。我们还总结了 m6A 修饰与 m6A 表达和稳定性之间相互作用在肿瘤诊断和治疗中的潜在价值,为揭示肿瘤发生发展的机制以及临床诊断和治疗提供了具体参考。

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