Abstract
Overexpression of MYC is a hallmark of many human cancers. The MYC 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.
Highlights
The importance of MYC in human development and disease has generated intense research interest over the past 30 years, resulting in numerous original articles and reviews
The fact that elevated levels of MYC proteins are found in 60–70% of all cancers and the discovery that tumors can be dependent on continuous MYC expression [9]
Their levels generally correlate with transcriptional activity, which is consistent with the recent finding that MYC enhances the expression of already active genes to boost the transcriptome of a given cell [40,41]
Summary
The importance of MYC in human development and disease has generated intense research interest over the past 30 years, resulting in numerous original articles and reviews (for example, see [1,2,3]). MYC–MAX complexes are known to recognize a consensus sequence known as Enhancer box (“E-box”), activating the transcription of genes [11,12,13] This finding sparked a comprehensive search for MYC target genes and their function and involvement in neoplastic transformation [14]. MYC acts rather weakly at many of its target of gene even genomic location profiles have profiles have often proven non-predictive of MYC-dependent transcriptional regulation [15]. MYC regulated in genomic locationand analyses, littlelocation overlap analyses, between MYC in different cell typesgenes has been different cell types has been [14,19] To these discrepancies, classic mechanistic found [14,19].
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