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Originally published In Press as doi:10.1074/jbc.M111974200 on June 4, 2002

J. Biol. Chem., Vol. 277, Issue 34, 31099-31106, August 23, 2002
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Regulation of Raf-Akt Cross-talk

Karin MoellingDagger , Karen Schad§, Magnus Bosse, Sven Zimmermann, and Marc Schweneker

From the Institute of Medical Virology, University of Zurich, 8028 Zurich, Switzerland

We have recently shown that the Ras-Raf-MEK-ERK and phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathways can cross-talk in the human breast cancer cell line MCF-7. High Raf activity induces growth arrest and differentiation in these cells, whereas high PI3K/Akt activity correlates with cell survival and proliferation. Here we show that the Raf-Akt cross-talk is regulated in a concentration- and ligand-dependent manner. High doses of insulin-like growth factor I (IGF-I) activate Akt quickly and strongly enough to suppress Raf kinase activity via phosphorylation of Ser-259, whereas low doses of IGF-I do not trigger this cross-talk but are still mitogenic. Phorbol 12-myristate 13-acetate, a differentiation-inducing stimulus, potently activates the Ras-Raf-MEK-ERK pathway but only weakly activates PI3K/Akt and does not trigger the cross-talk. Thus, the herein analyzed parameters such as ligand type, concentration, and time course may contribute to the cellular response of either proliferation or differentiation. This is highly relevant to understanding cellular transformation and may be of use in areas like tissue engineering.

Dagger To whom correspondence should be addressed: Institute of Medical Virology, Gloriastrasse 30, 8028 Zurich, Switzerland. Tel.: 41-1-634-2652; Fax: 41-1-634-4967; E-mail: moelling@immv.unizh.ch.

§ Present address: Basilea Pharmaceutica Ltd., 4002 Basel, Switzerland.

Present address: UBS AG, 8001 Zurich, Switzerland.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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