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Int. J. Mol. Sci. 2009, 10(2), 674-701; doi:10.3390/ijms10020674

Mitochondrial DNA Instability and Metabolic Shift in Human Cancers

1
Institute of Pharmacology, National Yang-Ming University, Taipei, 112, Taiwan
2
Department of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, 112, Taiwan
*
Author to whom correspondence should be addressed.
Received: 4 February 2009 / Revised: 20 February 2009 / Accepted: 23 February 2009 / Published: 23 February 2009
(This article belongs to the Special Issue Molecular System Bioenergetics)
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Abstract

A shift in glucose metabolism from oxidative phosphorylation to glycolysis is one of the biochemical hallmarks of tumor cells. Mitochondrial defects have been proposed to play an important role in the initiation and/or progression of various types of cancer. In the past decade, a wide spectrum of mutations and depletion of mtDNA have been identified in human cancers. Moreover, it has been demonstrated that activation of oncogenes or mutation of tumor suppressor genes, such as p53, can lead to the upregulation of glycolytic enzymes or inhibition of the biogenesis or assembly of respiratory enzyme complexes such as cytochrome c oxidase. These findings may explain, at least in part, the well documented phenomena of elevated glucose uptake and mitochondrial defects in cancers. In this article, we review the somatic mtDNA alterations with clinicopathological correlations in human cancers, and their potential roles in tumorigenesis, cancer progression, and metastasis. The signaling pathways involved in the shift from aerobic metabolism to glycolysis in human cancers are also discussed. View Full-Text
Keywords: Cancer; Mitochondrial DNA; Somatic mutation; Metabolic shift; Genome instability Cancer; Mitochondrial DNA; Somatic mutation; Metabolic shift; Genome instability
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Lee, H.-C.; Wei, Y.-H. Mitochondrial DNA Instability and Metabolic Shift in Human Cancers. Int. J. Mol. Sci. 2009, 10, 674-701.

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