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- W83543572 abstract "We have recently proposed a new mechanism for explaining energy transfer in cancer metabolism. Cancer cells behave as metabolic parasites, by extracting nutrients from normal host cells, via the secretion of hydrogen peroxide. Oxidative stress in the tumor microenvironment then leads to autophagy-driven catabolism, mitochondrial dys-function, and aerobic glycolysis. This, in turn, produces high-energy nutrients drive the anabolic growth of tumor cells, via oxidative mitochondrial metabolism. A logical prediction of this new “parasitic” cancer model is that epithelial cancer cells should increase their oxidative mitochondrial capacity. Here, we subjected frozen sections from human breast tumors to a staining procedure that only detects functional mitochondria. This method detects the in situ enzymatic activity of cytochrome C oxidase (COX), also known as Complex IV. Remarkably, cancer cells show an over-abundance of COX activity, while adjacent stromal cells remain essentially negative. Thus, oxidative mitochondrial activity is selectively amplified in cancer cells." @default.
- W83543572 created "2016-06-24" @default.
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- W83543572 date "2012-04-01" @default.
- W83543572 modified "2023-10-01" @default.
- W83543572 title "Hyperactivation of Mitochondrial Metabolism in Cancer Cells In Situ" @default.
- W83543572 doi "https://doi.org/10.1096/fasebj.26.1_supplement.966.1" @default.
- W83543572 hasPublicationYear "2012" @default.
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