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