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J Biol Chem, Vol. 274, Issue 25, 17612-17618, June 18, 1999
From the Chemotherapeutic drugs that damage DNA kill tumor
cells, in part, by inducing the expression of a death receptor such as
Fas or its ligand, FasL. Here, we demonstrate that epidermal growth factor (EGF) stimulation of T47D breast adenocarcinoma and embryonic kidney epithelial (HEK293) cells protects these cells from Fas-induced apoptosis. EGF stimulation of epithelial cells also inhibited Fas-induced caspase activation and the proteolysis of signaling proteins downstream of the EGF receptor, Cbl and Akt/protein kinase B
(Akt). EGF stimulation of Akt kinase activity blocked Fas-induced apoptosis. Expression of activated Akt in MCF-7 breast adenocarcinoma cells was sufficient to block Fas-mediated apoptosis. Inhibition of
EGF-stimulated extracellular signal-regulated kinase (ERK) activity did
not affect EGF protection from Fas-mediated apoptosis. The findings
indicate that EGF receptor stimulation of epithelial cells has a
significant survival function against death receptor-induced apoptosis
mediated by Akt.
Epidermal Growth Factor Protects Epithelial Cells against
Fas-induced Apoptosis
REQUIREMENT FOR Akt ACTIVATION
,,,
Program in Molecular Signal Transduction, Pharmacology,
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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