Lee L A, Dang C V
Department of Medicine, The Johns Hopkins University School of Medicine, Ross 1032, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Curr Top Microbiol Immunol. 2006;302:145-67. doi: 10.1007/3-540-32952-8_6.
The c-Myc oncogenic transcription factor plays a central role in many human cancers through the regulation of gene expression. Although the molecular mechanisms by which c-Myc and its obligate partner, Max, regulate gene expression are becoming better defined, genes or transcriptomes that c-Myc regulate are just emerging from a variety of different experimental approaches. Studies of individual c-Myc target genes and their functional implications are now complemented by large surveys of c-Myc target genes through the use of subtraction cloning, DNA microarray analysis, serial analysis of gene expression (SAGE), chromatin immunoprecipitation, and genome marking methods. To fully appreciate the differences between physiological c-Myc function in normal cells and deregulated c-Myc function in tumors, the challenge now is to determine how the authenticated transcriptomes effect the various phenotypes induced by c-Myc and to define how c-Myc transcriptomes are altered by the Mad family of proteins.
c-Myc致癌转录因子通过调控基因表达在多种人类癌症中发挥核心作用。尽管c-Myc及其紧密伙伴Max调控基因表达的分子机制正逐渐得到更清晰的界定，但通过各种不同实验方法才刚刚发现c-Myc所调控的基因或转录组。对单个c-Myc靶基因及其功能影响的研究，现在通过使用消减克隆、DNA微阵列分析、基因表达系列分析（SAGE）、染色质免疫沉淀和基因组标记方法对c-Myc靶基因进行大规模调查得到了补充。为了充分理解正常细胞中生理状态下的c-Myc功能与肿瘤中失调的c-Myc功能之间的差异，现在面临的挑战是确定经过验证的转录组如何影响由c-Myc诱导的各种表型，以及确定c-Myc转录组如何被Mad蛋白家族改变。
