Sarto C, Marocchi A, Sanchez JC, Giannone D, Frutiger S, Golaz O,
Wilkins MR, Doro G, Cappellano F, Hughes G, Hochstrasser DF, Mocarelli P.
Renal cell carcinoma and normal kidney protein expression.
Electrophoresis. 1997 Mar-Apr;18(3-4):599-604. doi: 10.1002/elps.1150180343.
Renal cell carcinoma (RCC), a human kidney cancer from the proximal tubular
epithelium, accounts for about 3% of adult malignancies. Molecular and
cytogenetic analysis have highlighted deletions, translocations, or loss of
heterozygosity in the 3p21-p26, a putative RCC locus, as well as in 6q, 8p, 9pq,
and 14pq. Studies on phenotypic expression of human kidney tissue and on
post-translational modifications in RCC have not yet provided a marker for early
renal cell carcinoma diagnosis. Current diagnostic methods do not help to detect
the tumor before advanced stages. We therefore used two-dimensional
polyacrylamide gel electrophoresis (2-D PAGE) to study normal and tumor kidney
tissues in ten patients suffering from RCC. A human kidney protein map in the
SWISS-2DPAGE database accessible through the ExPASy WWW Molecular Biology Server
was established. Of 2789 separated polypeptides, 43 were identified by gel
comparison, amino acid analysis, N-terminal sequencing, and/or immunodetection.
The comparison between normal and tumor kidney tissues showed four polypeptides
to be absent in RCC. One of them was identified as ubiquinol cytochrome c
reductase (UQCR), whose locus has elsewhere been tentatively assigned to
chromosome 19p12 or chromosome 22. A second polypeptide was identified as
mitochondrial NADH-ubiquinone oxido-reductase complex I whose locus is located on
chromosome 18p11.2 and chromosome 19q13.3. These result suggest that the lack of
UQCR and of mitochondrial NADH-ubiquinone oxidoreductase complex I expression in
RCC may be caused by unknown deletions, or by changes in gene transcription or
translation. It might indicate that mitochondrial disfunction plays a major role
in RCC genesis or evolution.
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