The MYC network and cancer

Abstract

Deregulation of c-Myc (referred to as MYC] contributes to the development of the most human tumors [1-3]. In addition to MYC, the Myc gene family contains three related genes, N-Myc, L-Myc, and S-Myc, which are also implicated in the genesis of specific human tumors (for review, see ref [4]). MYC is a nuclear transcription factor, which is first identified as the cellular homologue of the cancer-causing gene in the avian myelocytomatosis retrovirus [5]. MYC functions in a heterodimeric complex with MAX to bind E-Box motifs in DNA, and transcriptionally regulates hundreds to thousands of target genes. The most recent estimates suggest that MYC could regulate as many as 15% of genes in genomes from flies to human [6]. A compilation of MYC-regulated genes and studies on MYC alterations in human cancers is available online at www.myccancergene.org [6]. This database emphasizes both the critical role of MYC in human cancers and the significance of MYC target genes in driving its oncogenic activity. The target genes are involved in diverse programs including cell cycle, cell growth, protein synthesis, cell adhesion and cytoskeleton, metabolism, apoptosis, angiogenesis, DNA repair, and microRNA [6-8]. The diversity of MYC target genes is illustrated in Fig. 24.1. Numerous excellent and comprehensive reviews have been written about MYC [9-12]. Therefore, in this chapter, we will focus mainly on the role of MYC in cancer with the emphasis on the most recent findings. © 2010 Springer-Verlag Berlin Heidelberg.