David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, UK.
Cell Cycle. 2010 Jul 15;9(14):2726-30. Epub 2010 Jul 27.
Over the past 8 years several lines of compelling evidence have indicated that microRNAs are critical downstream effectors of classic oncogene/tumour suppressor networks. The archetypal examples of oncogene and tumour suppressor microRNAs are the miR-17-92 (oncomir 1) polycistron and miR-34 respectively. Whilst the involvement of these two opposing families of microRNAs in oncogenesis has been known for some time, the mRNA targets through which they exert their phenotypes are only just beginning to be uncovered. Moreover, several recent reports have demonstrated that the relevant physiological targets of certain individual microRNAs are actually fairly limited, with repression of just one or two major targets sufficient to explain the observed phenotype. In this review we will discuss the emerging role of microRNAs in tumourigenesis with a specific focus on miR-34c-dependent regulation of Myc.
在过去的 8 年中，有几条令人信服的证据表明 microRNAs 是经典癌基因/肿瘤抑制因子网络的关键下游效应因子。癌基因和肿瘤抑制因子 microRNAs 的典型例子分别是 miR-17-92（oncomir 1）多顺反子和 miR-34。虽然这两种相反的 microRNA 家族在致癌作用中的参与已经有一段时间了，但它们发挥表型的 mRNA 靶标才刚刚开始被揭示。此外，最近的几项报告表明，某些特定 microRNA 的相关生理靶标实际上相当有限，仅抑制一两个主要靶标就足以解释观察到的表型。在这篇综述中，我们将讨论 microRNAs 在肿瘤发生中的新兴作用，特别关注 miR-34c 对 Myc 的依赖性调节。
