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Carcinogenesis, Vol. 21, No. 2, 161-166, February 2000
© 2000 Oxford University Press

Cancer Biology

Suppression of apoptosis in C3H mouse liver tumors by activated Ha-ras oncogene

Steffen Frey, Albrecht Buchmann, Wilfried Bursch1, Rolf Schulte-Hermann1 and Michael Schwarz2

Institut für Toxikologie, Universität Tübingen, Wilhelmstraße 56, 72074 Tübingen, Germany and
1 Institut für Tumorbiologie-Krebsforschung, Universität Wien, Austria

Liver tumors were induced in male C3H mice by a single injection of N-nitrosodiethylamine and characterized with respect to the presence of base substitutions in the hot-spot position at codon 61 of the Ha-ras proto-oncogene. An increase in Ha-ras mutation prevalence was found with time after induction of tumors, suggesting that the activated ras gene provides a selective growth advantage. However, no significant differences in 5-bromodeoxyuridine labeling indices were evident between ras mutated and ras wild-type tumors, demonstrating that cell division rates in the two tumor populations were very similar. Apoptotic indices were determined by counting eosinophilic apoptotic bodies. The frequency of occurrence of apoptotic bodies was found to be approximately five times lower in tumors with Ha-ras mutations when compared with tumors not showing the mutation. This demonstrates that the activated p21Ras protein has anti-apoptotic activity in transformed mouse hepatocytes in vivo and suggests that the preferential outgrowth of Ha-ras-mutated hepatoma cells is mediated by suppression of apoptosis rather than by stimulation of cell division.

Abbreviations: BrdUrd, 5-bromodeoxyuridine; DEN, N-nitrosodiethylamine; H&E, hematoxylin and eosin; NF{kappa}B, nuclear factor {kappa}B; PI3 kinase, phosphatidylinositide 3'-OH kinase.


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