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Cell Growth & Differentiation Vol. 11, 185-190, April 2000
© 2000 American Association for Cancer Research


Articles

Lung-targeted Expression of the c-Raf-1 Kinase in Transgenic Mice Exposes a Novel Oncogenic Character of the Wild-Type Protein1

Eugen Kerkhoff, Lev M. Fedorov, Renate Siefken, Annette O. Walter, Thomas Papadopoulos and Ulf R. Rapp2

Institut für medizinische Strahlenkunde und Zellforschung, Universität Würzburg, D-97078 Würzburg, Germany [E. K., L. M. F., R. S., A. O. W., U. R. R.], and Pathologisches Institut, Histologisches Labor, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054 Erlangen, Germany [T. P.]

Abstract

The c-Raf-1 kinase is a downstream effector of Ras signaling. Both proteins are highly oncogenic when they are mutationally activated, but only the Ras GTPase is frequently mutated in naturally occurring tumors. Although the c-Raf-1 protein was found to be amplified in different lung cancer cell lines, overexpression of the wild-type c-Raf-1 protein was shown to be insufficient to transform cultured cells. Here we have addressed the question of whether overexpression of the wild-type c-Raf-1 kinase can induce lung cancer in mice. We show that lung-targeted expression of oncogenically activated or wild-type c-Raf-1 proteins induces morphologically indistinguishable lung adenomas in transgenic mice. Compared with mice transgenic for the activated c-Raf-1-BxB, tumor development is delayed and occurs at a lower incidence in wild-type c-Raf-1 transgenic mice. Our studies show that the c-Raf-1 expression level is a critical parameter in tumor development and should be analyzed in more detail to evaluate its potential in the induction of cancer.




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