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[Cancer Research 59, 5017-5022, October 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 5017-5022, October 1, 1999]
© 1999 American Association for Cancer Research

Tumor Biology

Paradoxical Inhibition of c-myc-induced Carcinogenesis by Bcl-2 in Transgenic Mice1

Alix de La Coste, Alexandre Mignon2, Monique Fabre2, Emmanuelle Gilbert, Arlette Porteu, Terry Van Dyke, Axel Kahn and Christine Perret3

Institut National de la Santé et de la Recherche, U129, ICGM, Université Paris V René Descartes, 75014 Paris, France [A. d. L. C., A. M., E. G., A. P., A. K., C. P.]; Hôpital du Kremlin Bicêtre, Service d’Anatomopathologie du Pr. Bedossa, 94275 Le Kremlin-Bicecirc;tre, France [M. F.]; and Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27299 [T. V. D.]

Here, we investigated changes in apoptosis during tumor progression by analyzing the effect of coexpressing various antiapoptotic genes on the multistage process of c-myc-induced hepatocarcinogenesis in transgenic mice. Whereas continuous c-myc gene overexpression in the liver led to cellular hepatocarcinoma, the coexpression of the bcl-2 gene inhibited the emergence of liver tumors, by inhibiting a pretumoral phase characterized by increased proliferation and apoptosis. This antioncogenic effect was specific to Bcl-2 and was not shared by other antiapoptotic genes such as bcl-xL and a dominant negative form of p53. Thus, we have shown that Bcl-2 can have a tumor suppressor effect in vivo on c-myc-induced hepatocarcinogenesis during the emergence of neoplastic foci.




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Cancer Research Clinical Cancer Research
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Molecular Cancer Research Cancer Prevention Research
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Copyright © 1999 by the American Association for Cancer Research.