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J. Biol. Chem., Vol. 277, Issue 5, 3776-3783, February 1, 2002
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From the Regulation of death receptor-mediated apoptosis
is incompletely understood. Previous studies have demonstrated that
phorbol 12-myristate 13-acetate (PMA), a protein kinase C activator,
inhibits Fas (CD95)-mediated apoptosis in Jurkat (type II) cells but
not SKW6.4 (type I) cells. In this study, we demonstrated that PMA also
protects Jurkat cells from apoptosis induced by tumor necrosis factor-
Phorbol 12-myristate 13-Acetate Inhibits Death Receptor-mediated
Apoptosis in Jurkat Cells by Disrupting Recruitment of
Fas-associated Polypeptide with Death Domain*
,§¶
Division of Oncology Research, Mayo Clinic,
and § Department of Molecular Pharmacology, Mayo Graduate
School, Rochester, Minnesota 55905
and the tumor necrosis factor--related apoptosis-inducing ligand (TRAIL). Interestingly, PMA failed to protect Jurkat cells from
apoptosis induced by other agents, including etoposide,
camptothecin, and 
-irradiation. Analysis of the initial events
induced by agonistic anti-Fas antibodies revealed that PMA inhibited
Fas binding to Fas-associated polypeptide with death domain (FADD) in
Jurkat cells but not in SKW6.4 cells. Although the protein kinase
inhibitor bisindoylmaleimide VIII increased apoptosis induced by
agonistic anti-Fas antibody, tumor necrosis factor-, and TRAIL,
these effects were not observed with the protein kinase C inhibitor H7
and were not associated with increased FADD recruitment to Fas. These
results indicate that PMA inhibits death signaling induced by a number of discrete receptors and suggest that the effects are mediated at the
level of receptor-mediated adaptor molecule recruitment.
*
This work was supported in part by National Institutes of
Health Grant R01 CA69008.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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