Dang C V, Resar L M, Emison E, Kim S, Li Q, Prescott J E, Wonsey D, Zeller K
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, 21205, USA.
Exp Cell Res. 1999 Nov 25;253(1):63-77. doi: 10.1006/excr.1999.4686.
The c-myc gene and the expression of the c-Myc protein are frequently altered in human cancers. The c-myc gene encodes the transcription factor c-Myc, which heterodimerizes with a partner protein, termed Max, to regulate gene expression. Max also heterodimerizes with the Mad family of proteins to repress transcription, antagonize c-Myc, and promote cellular differentiation. The constitutive activation of c-myc expression is key to the genesis of many cancers, and hence the understanding of c-Myc function depends on our understanding of its target genes. In this review, we attempt to place the putative target genes of c-Myc in the context of c-Myc-mediated phenotypes. From this perspective, c-Myc emerges as an oncogenic transcription factor that integrates the cell cycle machinery with cell adhesion, cellular metabolism, and the apoptotic pathways.
c-myc基因及c-Myc蛋白的表达在人类癌症中经常发生改变。c-myc基因编码转录因子c-Myc,它与一种称为Max的伙伴蛋白形成异源二聚体,以调节基因表达。Max还与Mad家族蛋白形成异源二聚体,以抑制转录、拮抗c-Myc并促进细胞分化。c-myc表达的组成性激活是许多癌症发生的关键,因此对c-Myc功能的理解取决于我们对其靶基因的理解。在本综述中,我们试图将c-Myc的假定靶基因置于c-Myc介导的表型背景中。从这个角度来看,c-Myc是一种致癌转录因子,它将细胞周期机制与细胞黏附、细胞代谢和凋亡途径整合在一起。