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Cancer as a “Mitochondriopathy”

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Author(s): Anna M Czarnecka | Antonella Marino Gammazza | Valentina Di Felice | Giovanni Zummo | Francesco Cappello

Journal: Journal of Cancer Molecules
ISSN 1816-0735

Volume: 3;
Issue: 3;
Start page: 71;
Date: 2007;
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Keywords: mtDNA | mitochondria | cancer | prohibitin | homoplasmy

ABSTRACT
Mitochondria are subcellular organelles, whose well-known function is to produce ATP through the oxidative phosphorylation system. Alterations in respiratory activity and mitochondrial DNA (mtDNA) appear to be a general feature of malignant cells. The presence of mtDNA mutations has been reported in various cancer cells, and the abundance of mtDNA damage is consistent with the intrinsic susceptibility to constitutive oxidative stress. Research about the functional aspects of mtDNA mutations in cancer development and therapeutic response is likely to be fruitful and to have significant clinical and prognostic impact. Although many studies to date have been focused on the identification and characterization of altered mtDNA, it is not clear if these accumulated mutations are the cause or the consequence of the carcinogenic process. This article provides a brief summary of our current understanding of mitochondrial pathobiology in cancer development.
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