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Cell Growth & Differentiation Vol. 12, 297-306, June 2001
© 2001 American Association for Cancer Research

The Recruitment of Fas-associated Death Domain/Caspase-8 in Ras-induced Apoptosis1

Chang-Yan Chen2, Peter Juo, James S. Liou, Chong-Qing Li, Qiang Yu, John Blenis and Douglas V. Faller

Cancer Research Center, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118 [C-Y. C., P. J., J. S. L., C-Q. L., Q. Y., D. V. F.], and Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115 [J. B.]

Oncogenic Ras induces cells to undergo apoptosis after inhibition of protein kinase C (PKC) activity. The integration of differential signaling pathways is required for full execution of apoptosis. In this study, we used Jurkat as well as Fas/FADD-defective cell lines expressing v-ras to determine the upstream elements required for activation of the caspase cascade in PKC/Ras-mediated apoptosis. During this Ras-induced apoptotic process, caspase-8 was activated, possibly through its binding to Fas-associated death domain (FADD), in Jurkat/ras and Jurkat/Fasm/ras cells but not in Jurkat/FADDm/ras cells. c-Jun NH2-terminal kinase (JNK) was activated in all three cell lines expressing ras in response to apoptotic stimulation. Suppression of JNK by dn-JNK1 blocked the interaction of FADD and caspase-8 and partially protected Jurkat/ras and Jurkat/Fasm/ras cells from apoptosis. However, dn-JNK1 had no effect on PKC/Ras-induced apoptosis in Jurkat/FADDm/ras cells. The results indicate that FADD/caspase-8 signaling is involved in PKC/Ras-mediated apoptosis, and JNK may be an upstream effector of caspase activation.




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Molecular Cancer Research Cell Growth & Differentiation
Copyright © 2001 by the American Association of Cancer Research.