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Papers In Press, published online ahead of print June 4, 2002
University Zurich, Institute of Medical Virology, Zurich 8028
Corresponding Author: moelling{at}immv.unizh.ch
We have recently shown that the Ras-Raf-MEK-ERK and PI3 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, while 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 Ser259, whereas low doses of IGF-I do not trigger this cross-talk while still mitogenic. Phorbol 12-myristate 13-acetate (PMA), 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 of high relevance for understanding cellular transformation and may be of use in areas like tissue engineering.
J. Biol. Chem, 10.1074/jbc.M111974200
Submitted on December 15, 2001
Revised on June 4, 2002
Accepted on June 3, 2002
Regulation of Raf-Akt cross-talk
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