MYC, Metabolism and Malignancy: Opportunities for Therapeutic Intervention

Copyright: © 2013 Padmanabhan A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Metabolic regulation in cells is hugely dependent on the availability of nutrients. Proliferation of cells requires active nutrient uptake, synthesis of nucleic acids, proteins, and lipids and production of ATP. It is thus not surprising those oncogenes that drive cell proliferation also drives metabolic regulation either directly or indirectly. One of the hallmarks of rapidly growing tumor cells is their ability to sustain high rates of glycolysis for ATP generation, irrespective of oxygen availability a phenomenon known as the Warburg effect [1,2]. This shared property of tumor cells provides selective advantage to these cells but also opens up new opportunities for therapeutic intervention. Inhibitors of cellular proliferation that blocks or terminates DNA synthesis or that cross-links or fragments DNA have emerged as some of the classic anticancer agents. These drugs are directed toward normal cellular proliferation processes and therefore lack selectivity for neoplastic cells over proliferating normal cells. The same is true of classic inhibitors of intermediary metabolism, many of which are enzyme transition state analogues.