Next Article in Journal / Special Issue
A Systems Biology Approach to Investigating Apoptotic Stimuli as Effectors of Cell Metabolism: Practical Application of Top-Down Control Analysis to Attached Neurons
Previous Article in Journal
Quantum Dots — Characterization, Preparation and Usage in Biological Systems
Previous Article in Special Issue
Potential Mechanisms of Muscle Mitochondrial Dysfunction in Aging and Obesity and Cellular Consequences
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)
View Full-Text   |   Download PDF [179 KB, uploaded 19 June 2014]


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.
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) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Share & Cite This Article

Further Mendeley | CiteULike
Export to BibTeX |
EndNote |
MDPI and ACS Style

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

View more citation formats

Related Articles

Article Metrics

For more information on the journal, click here


[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert