| Literature DB >> 26277543 |
Annie L Hsieh1, Zandra E Walton2, Brian J Altman2, Zachary E Stine2, Chi V Dang3.
Abstract
The MYC proto-oncogene is frequently deregulated in human cancers, activating genetic programs that orchestrate biological processes to promote growth and proliferation. Altered metabolism characterized by heightened nutrients uptake, enhanced glycolysis and glutaminolysis and elevated fatty acid and nucleotide synthesis is the hallmark of MYC-driven cancer. Recent evidence strongly suggests that Myc-dependent metabolic reprogramming is critical for tumorigenesis, which could be attenuated by targeting specific metabolic pathways using small drug-like molecules. Understanding the complexity of MYC-mediated metabolic re-wiring in cancers as well as how MYC cooperates with other metabolic drivers such as mammalian target of rapamycin (mTOR) will provide translational opportunities for cancer therapy.Entities:
Keywords: Cancer; Metabolism; Myc; mTOR
Mesh:
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Year: 2015 PMID: 26277543 PMCID: PMC4818970 DOI: 10.1016/j.semcdb.2015.08.003
Source DB: PubMed Journal: Semin Cell Dev Biol ISSN: 1084-9521 Impact factor: 7.727