The aim of the study was to determine the tumorigenic potential of two cell lines established from
N-nitrosodimethylamine induced rat hepatocarcinoma (HeDe) and mesenchymal renal
tumors (NeDe). The basis of the distinction is that human
cancers are known to overexpress facilitative GLUT transporters and
TGF-beta1 protein. These
proteins are linked to the increased metabolic energy consumption indicating uncontrolled growth and proliferation. We have assayed not only the expression of GLUT-1, GLUT-3 and
TGF-beta1 proteins, but also the uptake of 2-fluoro-[18F]-
2-deoxy-D-glucose (
18FDG), a tracer for
cancer diagnosis. Western blot analysis and whole body autoradiography were used to measure the
18FDG uptake of
tumor cells. Elevated
18FDG uptake was measured in both tumor cell lines. Whole body autoradiography provided evidence that the uptake of
18FDG was lower in the necrotic inner part than in the more vascularized outer parts of primary hepatocarcinoma and mesenchymal renal
tumors. GLUT-1 overexpression in hepatocarcinoma
tumor, and high levels of GLUT-3 were found in the NeDe cell line and in the mesenchymal renal
tumor.
TGF-beta-1 was overexpressed in hepatocarcinoma and mesenchymal renal
tumors. In vitro and in vivo parameters support the view that the tumorigenic potential of
cancer cells cannot be determined by the expression of a single parameter such as the expression of either GLUT-1, GLUT-3 or
18FDG uptake. Besides the tumorigenic potential of the hepatocarcinoma, the high metabolic activity of the renal
tumor indicated by its
18FDG uptake, GLUT-3 and
TGF-beta1 expression, the mesenchymal renal
tumor induced by N-nitroso-
dimethylamine is not a benign, but an an aggressive
renal carcinoma.