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Carcinogenesis Advance Access published online on October 12, 2005
Carcinogenesis, doi:10.1093/carcin/bgi242
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received March 31, 2004
Revised May 13, 2005
Accepted October 4, 2005

CANCER BIOLOGY

Oxidative phosphorylation dysfunction modulates expression of extracellular matrix-remodeling genes and invasion

Corina van Waveren 1, Yubo Sun 2, Herman S. Cheung 2, and Carlos T. Moraes 3*

1 Department of Cell Biology & Anatomy, University of Miami School of Medicine
2 Department of Medicine, University of Miami School of Medicine
3 Department of Cell Biology & Anatomy, University of Miami School of Medicine; Department of Neurology, University of Miami School of Medicine

* To whom correspondence should be addressed.
Carlos T. Moraes, E-mail: cmoraes{at}med.miami.edu


  Abstract

A number of recent studies suggest that mitochondrial function is a player in tumor development and progression. In this study, we have used gene expression arrays to examine transcriptional differences between Oxidative Phosphorylation (OXPHOS) competent and OXPHOS impaired human osteosarcoma cells. Genes associated with extracellular matrix remodeling, including members of the metalloproteinases and inhibitors of metalloproteinases (MMP/TIMP) family, urokinase plasminogen activator and its inhibitor Plasminogen-activator inhibitor-1 (PAI1), and CTGF and CYR61 (members of the Cysteine-rich 61, Connective Tissue Growth Factor and Nephroblastoma-overexpressed (CCN) gene family of growth regulators) were among the ones significantly altered in the OXPHOS deficient cells. These changes were confirmed by RT-PCR and promoter reporter assays. Alterations at the protein level for some of these factors were also observed, though at a lower magnitude, with the exception of TIMP1, where a marked change in steady-state levels of the protein was observed after induction of OXPHOS dysfunction. Repopulation of mtDNA-less cells with wild-type mtDNA reduced matrigel invasion, whereas repopulation with a mutated mtDNA did not. Taken together our data suggests that OXPHOS dysfunction modulates the invasive phenotype by transcriptional regulation of genes coding for members of the MMP/TIMP system, uPA/PAI1, and CCN proteins.


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