Succinate dehydrogenase and fumarate hydratase: linking mitochondrial dysfunction and cancer

By A. King, M. A. Selak, Eyal Gottlieb. Oncogene, 2006

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Cancer as a metabolic disease (2010, background): “HIF-1α stabilization under aerobic conditions can be linked to mitochondrial dysfunction through abnormalities in calcium homeostasis, ROS generation, NFkB signaling, accumulation of TCA cycle metabolites (succinate and fumarate), and oncogenic viral infections [131-135].”
Revisiting the Warburg effect: historical dogma versus current understanding (2020, background): “by mutations (‘damage’) in the mitochondrial enzymes fumarate hydratase, succinate dehydrogenase and isocitrate dehydrogenase (King et al. 2006; Schmidt et al. 2020; Ratcliffe, 2007; Rasheed & Tarjan, 2018), and by overproduction of mitochondrial reactive oxygen species (ROS).”
Glucose-independent glutamine metabolism via TCA cycling for proliferation and survival in B-cells (2012, unknown): “, 1924) and numerous other alterations in the central metabolism of cancers (King et al., 2006; Samudio et al., 2009), these all point to the important role of metabolism in the development of many cancers and its therapeutic opportunities (Vander Heiden, 2011).”
With TOR less is more: a key role for the conserved nutrient sensing TOR pathway in aging (2010, unknown): “In addition to nitrogen starvation, carbon and phosphate starvation also lead to inhibition of TORC1 in S. cerevisiae (Kuruvilla et al., 2001; Shamji et al., 2000; Urban et al., 2007).”