Mitochondria and Cancer

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Science  28 Jan 2005:
Vol. 307, Issue 5709, pp. 485
DOI: 10.1126/science.307.5709.485b

Human tumors often contain mutations in mitochondrial DNA (mtDNA). Whether these mutations are causally involved in tumorigenesis and the mechanisms by which they might contribute are pressing questions that remain unanswered. One hypothesis suggests that tumor-associated mtDNA mutations lead to increased production of reactive oxygen species (ROS), a by-product of mitochondrial oxidative phosphorylation, which can stimulate cell proliferation. Data from a new study of mtDNA in human prostate tumors are consistent with this hypothesis. Petros et al. identified mutations in two mitochondrial genes encoding proteins involved in oxidative phosphorylation: cytochrome oxidase subunit I and ATP6. Notably, when mtDNA containing an ATP6 mutation close to the site of the tumor-associated mutation was introduced into prostate cancer cells, the cells generated significantly more ROS in comparison with wild-type controls and grew at a much faster rate in mice, supporting the notion that such mutations play a causal role in tumorigenesis. — PAK

Proc. Natl. Acad. Sci. U.S.A. 102, 719 (2005).

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