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Carcinogenesis Advance Access originally published online on February 4, 2004
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Carcinogenesis, Vol. 25, No. 6, 1005-1010, June 2004
Carcinogenesis vol.25 no.6 © Oxford University Press 2004; all rights reserved.

ARTICLE

Decrease of mitochondrial DNA content and energy metabolism in renal cell carcinoma

David Meierhofer1, Johannes A. Mayr1, Ulrike Foetschl1, Alexandra Berger1, Klaus Fink2, Nikolaus Schmeller2, Gerhard W. Hacker3, Cornelia Hauser-Kronberger4, Barbara Kofler1,5 and Wolfgang Sperl1

1 Department of Pediatrics, 2 Department of Urology, 3 Research Institute for Frontier Questions of Medicine and Biotechnology and 4 Institute of Pathology, Paracelsus Private Medical University Salzburg, Muellner Hauptstr. 48, A-5020 Salzburg, Austria

5 To whom correspondence should be addressed Email: b.kofler{at}lks.at

To elucidate the relationship between tumorgenesis and the mitochondrial energy metabolism in renal neoplasms, we studied three individual enzyme activities of the oxidative phosphorylation, two components of the Krebs cycle and the mitochondrial DNA content of renal carcinomas including 29 conventional, five papillary, two unclassified carcinomas with sarcomatoid features and one collecting duct carcinoma. A significant reduction of all mitochondrial enzyme activities including complex V, as well as of the mitochondrial DNA content was detected in 34 of 37 renal carcinoma tissues as compared with control kidney. Mitochondrial enzyme activities and mitochondrial DNA levels were not statistically different between the conventional, papillary and unclassified sarcomatoid type of renal carcinoma and did not correlate with tumour grade, metastasis, ploidy and proliferative activity as determined by Ki-67 staining. Taken together, our data indicate that a co-ordinated down-regulation of all components necessary for mitochondrial energy metabolism occurs in most renal carcinomas as an early event in carcinoma formation, which does not change with progression of the disease.


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