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微小RNA作为c-MYC功能的调节因子和介导因子

MicroRNAs as regulators and mediators of c-MYC function.

作者信息

Jackstadt Rene, Hermeking Heiko

机构信息

Experimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-Universität München, D-80337 Munich, Germany.

Experimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-Universität München, D-80337 Munich, Germany.

出版信息

Biochim Biophys Acta. 2015 May;1849(5):544-53. doi: 10.1016/j.bbagrm.2014.04.003. Epub 2014 Apr 13.

DOI:10.1016/j.bbagrm.2014.04.003
PMID:24727092
Abstract

In the past ten years microRNAs (miRNAs) have been widely implicated as components of tumor suppressive and oncogenic pathways. Also the proto-typic oncogene c-MYC has been connected to miRNAs. The c-MYC gene is activated in approximately half of all tumors, and its product, the c-MYC transcription factor, regulates numerous processes e.g. cell cycle progression, metabolism, epithelial-mesenchymal transition (EMT), metastasis, stemness, and angiogenesis, thereby facilitating tumor initiation and progression. c-MYC target-genes, which mediate these functions of c-MYC, represent a complex network of protein- and non-coding RNAs, including numerous miRNAs. For example, c-MYC directly regulates expression of the miR-17-92 cluster, miR-34a, miR-15a/16-1 and miR-9. Moreover, the expression and activity of c-MYC itself are under the control of miRNAs. Here, we survey how these networks mediate and regulate c-MYC functions. In the future, miRNAs connected to c-MYC may be used for diagnostic and therapeutic approaches. This article is part of a Special Issue entitled: Myc proteins in cell biology and pathology.

摘要

在过去十年中,微小RNA(miRNA)被广泛认为是肿瘤抑制和致癌途径的组成部分。此外,典型的原癌基因c-MYC也与miRNA有关。c-MYC基因在大约一半的肿瘤中被激活,其产物c-MYC转录因子调节众多过程,如细胞周期进程、代谢、上皮-间质转化(EMT)、转移、干性和血管生成,从而促进肿瘤的发生和发展。介导c-MYC这些功能的c-MYC靶基因代表了一个由蛋白质和非编码RNA组成的复杂网络,其中包括众多miRNA。例如,c-MYC直接调节miR-17-92簇、miR-34a、miR-15a/16-1和miR-9的表达。此外,c-MYC自身的表达和活性也受miRNA的控制。在此,我们综述这些网络如何介导和调节c-MYC的功能。未来,与c-MYC相关的miRNA可能用于诊断和治疗方法。本文是名为“细胞生物学和病理学中的Myc蛋白”的特刊的一部分。

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