ROS homeostasis and metabolism: a dangerous liason in cancer cells.
Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage and genomic instability, and ultimately, by reprogramming cancer cell metabolism. This review outlines the metabolic-dependent mechanisms that tumors engage in when faced with oxidative stress conditions that are critical for cancer progression by producing redox cofactors. In particular, we describe how the mitochondria has a key role in regulating the interplay between redox homeostasis and metabolism within tumor cells. Last, we will discuss the potential therapeutic use of agents that directly or indirectly block metabolism.
Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Turin, Turin, Italy.
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Panieri
Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Turin, Turin, Italy.|Laboratory of Endothelial Molecular Biology, Vesalius Research Center, VIB, Leuven B-3000, Belgium.|Laboratory of Endothelial Molecular Biology, Vesalius Research Center, Department of Oncology, University of Leuven, Leuven B-3000, Belgium.
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Santoro
D000818:Animals; D006706:Homeostasis; D006801:Humans; D053858:Metabolic Networks and Pathways; D008928:Mitochondria / Q000378:metabolism; D009369:Neoplasms / Q000378:metabolism*; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species / Q000378:metabolism*
D017382:Reactive Oxygen Species