Skip Navigation



Carcinogenesis Advance Access published online on December 16, 2004
Carcinogenesis, doi:10.1093/carcin/bgi001
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
26/3/531    most recent
bgi001v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Hervouet, E.
Right arrow Articles by Godinot, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hervouet, E.
Right arrow Articles by Godinot, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Oxford University Press
Received July 8, 2004
Revised November 5, 2004
Accepted December 2, 2004

CANCER BIOLOGY

A new role for the von Hippel-Lindau tumor suppressor protein: stimulation of mitochondrial oxidative phosphorylation complex biogenesis

Eric Hervouet 1, Jocelyne Demont 1, Petr Pecina 2, Alena Vojtísková 2, Josef Houstek 2, Hélène Simonnet 1, and Catherine Godinot 1*

1 Centre de Génétique Moléculaire et Cellulaire, UMR 5534, Centre National de la Recherche Scientifique - Université Claude Bernard de Lyon 1 - 69622 Villeurbanne, France
2 Institute of Physiology and Centre for Integrated Genomics, Academy of Sciences of the Czech Republic, Vídenská 1083, 142 20 Prague, Czech Republic

* To whom correspondence should be addressed.
Catherine Godinot, E-mail: godinot{at}univ-lyon1.fr


  Abstract

Although mitochondrial deficiency in cancer has been described by Warburg, many years ago, the mechanisms underlying this impairment remain essentially unknown. Many types of cancer cells are concerned and, in particular, clear cell renal carcinoma (CCRC). In this cancer, the tumor suppressor gene, VHL (von Hippel-Lindau factor) is invalidated. Previous studies have shown that the transfection of the VHL gene in VHL-deficient cells originating from CCRCs could suppress their ability to form tumors when they were injected into nude mice. However, various additional genetic alterations are observed in such cancer cells. In order to investigate whether VHL invalidation was related to the mitochondrial impairment, we have studied the effects of wild type VHL transfection into VHL-deficient 786-0 or RCC10 cells on their oxidative phosphorylation subunit contents and functions. We show that the presence of wild type VHL protein (pVHL) increased mitochondrial DNA and respiratory chain protein contents and permitted the cells to rely on their mitochondrial ATP production to grow in the absence of glucose. In parallel to mtDNA increase, the presence of pVHL up regulated the mitochondrial transcription factor A, TFAM, as shown by western blot analysis. In conclusion, in CCRCs, pVHL deficiency is one of the factors responsible for down-regulation of the biogenesis of oxidative phosphorylation complexes.

Keywords: oxidative phosphorylation complex biogenesis; clear cell renal cancer; von Hippel-Lindau; Hypoxia Inducible Factor; mitochondrial transcription factor A, human.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 CarcinogenesisHome page
E. Hervouet, A. Cizkova, J. Demont, A. Vojtiskova, P. Pecina, N. L.W. Franssen-van Hal, J. Keijer, H. Simonnet, R. Ivanek, S. Kmoch, et al.
HIF and reactive oxygen species regulate oxidative phosphorylation in cancer
Carcinogenesis, August 1, 2008; 29(8): 1528 - 1537.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
A. M. Cervera, N. Apostolova, F. L. Crespo, M. Mata, and K. J. McCreath
Cells Silenced for SDHB Expression Display Characteristic Features of the Tumor Phenotype
Cancer Res., June 1, 2008; 68(11): 4058 - 4067.
[Abstract] [Full Text] [PDF]

Home page
 Hum Mol GenetHome page
G. Gasparre, E. Hervouet, E. de Laplanche, J. Demont, L. F. Pennisi, M. Colombel, F. Mege-Lechevallier, J.-Y. Scoazec, E. Bonora, R. Smeets, et al.
Clonal expansion of mutated mitochondrial DNA is associated with tumor formation and complex I deficiency in the benign renal oncocytoma
Hum. Mol. Genet., April 1, 2008; 17(7): 986 - 995.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
G. Melillo and G. L. Semenza
Meeting Report: Exploiting the Tumor Microenvironment for Therapeutics.
Cancer Res., May 1, 2006; 66(9): 4558 - 4560.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
C. van Waveren, Y. Sun, H. S. Cheung, and C. T. Moraes
Oxidative phosphorylation dysfunction modulates expression of extracellular matrix--remodeling genes and invasion
Carcinogenesis, March 1, 2006; 27(3): 409 - 418.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.