Poole Candace J, van Riggelen Jan
Augusta University, Department of Biochemistry and Molecular Biology, 1410 Laney-Walker Blvd., Augusta, GA 30912, USA.
Genes (Basel). 2017 May 13;8(5):142. doi: 10.3390/genes8050142.
Overexpression of is a hallmark of many human cancers. The oncogene has long been thought to execute its neoplastic functions by acting as a classic transcription factor, deregulating the expression of a large number of specific target genes. However, MYC's influence on many of these target genes is rather modest and there is little overlap between MYC regulated genes in different cell types, leaving many mechanistic questions unanswered. Recent advances in the field challenge the dogma further, revealing a role for MYC that extends beyond the traditional concept of a sequence-specific transcription factor. In this article, we review MYC's function as a regulator of the cancer epigenome and transcriptome. We outline our current understanding of how MYC regulates chromatin structure in both a site-specific and genome-wide fashion, and highlight the implications for therapeutic strategies for cancers with high MYC expression.
[基因名称]的过表达是许多人类癌症的一个标志。长期以来，人们一直认为[基因名称]癌基因通过作为经典转录因子发挥作用，从而失调大量特定靶基因的表达来执行其肿瘤形成功能。然而，MYC对许多这些靶基因的影响相当有限，并且在不同细胞类型中MYC调控的基因之间几乎没有重叠，这使得许多机制问题仍未得到解答。该领域的最新进展进一步挑战了这一传统观念，揭示了MYC的作用超出了序列特异性转录因子的传统概念。在本文中，我们综述了MYC作为癌症表观基因组和转录组调节因子的功能。我们概述了目前对MYC如何以位点特异性和全基因组方式调节染色质结构的理解，并强调了对高MYC表达癌症治疗策略的影响。
