Abstract
MYC is a proto-oncogene regulating a large number of genes involved in a plethora of cellular functions. Its deregulation results in activation of MYC gene expression and/or an increase in MYC protein stability. MYC overexpression is a hallmark of malignant growth, inducing self-renewal of stem cells and blocking senescence and cell differentiation. This review summarizes the latest advances in our understanding of MYC-mediated molecular mechanisms responsible for its oncogenic activity. Several recent findings indicate that MYC is a regulator of cancer genome and epigenome: MYC modulates expression of target genes in a site-specific manner, by recruiting chromatin remodeling co-factors at promoter regions, and at genome-wide level, by regulating the expression of several epigenetic modifiers that alter the entire chromatin structure. We also discuss novel emerging therapeutic strategies based on both direct modulation of MYC and its epigenetic cofactors.
Highlights
The v-myc oncogene is a transforming factor of the avian virus MC29, observed for the first time in 1964 in chickens affected by spontaneous myelocytomatosis [1,2]
These findings suggest that each MYC transactivation homology boxes (MBs) region interacts with a specific protein group that has a role in opening chromatin across the transcription cycle [25]
Several studies showed that the majority of positive cell cycle regulators are MYC targets, including genes encoding for cyclins and cyclin-dependent kinases (CDKs), and for proteins involved in replication [26]
Summary
The v-myc oncogene is a transforming factor of the avian virus MC29, observed for the first time in 1964 in chickens affected by spontaneous myelocytomatosis [1,2]. A clear correlation exists between deregulated MYC function and cancer development and progression (Figure 1). MYC is overexpressed due to aberrations in MYC locus, including polymorphisms in MYC regulatory sequences, copy number variations, and chromosomal translocations, or by aberrant transduction pathways of MYC activation and repression [4]. All these events seem to link MYC expression to cancer-associated rearrangements. The MYC gene family encodes three well-characterized cellular oncogenes, MYC (previously known as c-MYC), MYCN, and MYCL, named “super-transcription factors”, which regulate atand leastFunction
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