Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 May;1849(5):563-9.
doi: 10.1016/j.bbagrm.2014.07.004. Epub 2014 Jul 17.

Impact of MYC in regulation of tumor cell metabolism

Affiliations
Review

Impact of MYC in regulation of tumor cell metabolism

Therese Wahlström et al. Biochim Biophys Acta. 2015 May.

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.

PubMed Disclaimer

Publication types