Impact of MYC in regulation of tumor cell metabolism

Biochim Biophys Acta. 2015 May;1849(5):563-9. doi: 10.1016/j.bbagrm.2014.07.004. Epub 2014 Jul 17.

Abstract

The MYC proto-oncoproteins including c-MYC, MYCN and MYCL exert their functions as heterodimers with MAX, which in turn binds to E-box sequences at target promoters to regulate gene expression. It has been shown that MYC binds to 10-15% of all promoter regions and regulates genes involved in a wide variety of cellular functions. In normal cells the expression of MYC is tightly controlled whereas it is deregulated in the majority of human tumors. MYC contributes to malignant transformation by promoting multiple processes including uncontrolled cell proliferation, cell growth and genomic instability. Importantly, MYC promotes growth by activating genes involved in ribosomal and mitochondrial biogenesis, glucose and glutamine metabolism as well as lipid synthesis. Hence, MYC is contributing to the metabolic reprogramming essential for cancer cells to adapt to the tumor microenvironment. Here we give an overview of the role of MYC in regulation of metabolic pathways in tumor cells. This article is part of a Special Issue entitled: MYC proteins in cell biology and pathology.

Keywords: Cancer; MYC; Metabolic reprogramming; Metabolism; Mitochondria.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cell Proliferation / genetics
  • Genomic Instability
  • Glutamine / metabolism
  • Glycolysis
  • Humans
  • Lipid Metabolism*
  • Neoplasms / genetics
  • Neoplasms / metabolism*
  • Neoplasms / pathology
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism*
  • Tumor Microenvironment / genetics*

Substances

  • Proto-Oncogene Proteins c-myc
  • Glutamine