JBC Invitrogen Ultrasensitive Cytokine Assays

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J Biol Chem, Vol. 273, Issue 27, 16700-16709, July 3, 1998

Differential Regulation of Discrete Apoptotic Pathways by Ras

Chang-Yan ChenDagger , James LiouDagger , Lora W. FormanDagger , and Douglas V. FallerDagger

From the Dagger  Cancer Research Center and the  Departments of Medicine, Biochemistry, Pediatrics, Microbiology, Pathology, and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118

The products of the ras genes are known to regulate cell proliferation and differentiation; recently, they have been found to play a role in apoptosis. The expression of oncogenic p21ras in a number of cell types, including Jurkat (a human T lymphoblastoid cell line) and murine fibroblasts, makes the cells susceptible to apoptosis following suppression of protein kinase C (PKC) activity (PKC/Ras-mediated apoptosis). Engagement of Fas antigen, a potent effector of apoptosis, activates cellular p21ras, which may be required for completion of the cell death program. To further investigate the role of p21ras in the regulation of apoptosis, the cellular mechanisms employed in these two apoptotic processes in which Ras activity is involved (PKC/Ras-related and Fas-triggered apoptosis), was explored. Increasing p21ras activity by expressing v-ras or by treatment with an antisense oligonucleotide to the GTPase-activating protein was found to accelerate the Fas-mediated apoptotic process in Jurkat and mouse LF cells. PKC/Ras-related apoptosis was associated with, and required, cell cycle progression, accompanied by the expression of the G1/S cyclins. In contrast, Fas engagement, although inducing a vigorous and PKC-independent activation of endogenous p21ras, did not alter cell cycle progression, nor did it require such progression for apoptosis. Both the protein synthesis inhibitor cycloheximide and cyclin E antisense oligonucleotides partially abolished PKC/Ras-mediated apoptosis but had only a moderate effect on Fas-induced apoptosis. In contrast, the CED-3/interleukin-1beta -converting enzyme (ICE) protease inhibitor Z-VADfmk efficiently suppressed Fas-induced apoptosis and only marginally inhibited PKC/Ras-mediated apoptosis. Induction of both pathways resulted in activation of the Jun NH2-terminal kinase/JUN signaling system. These results suggest that different cell death programs, such as PKC/Ras-mediated and Fas-mediated apoptosis, may be interconnected via p21ras and perhaps Jun NH2-terminal kinase/JUN. In response to various death stimuli, p21ras may act as a common intermediate regulator in the transduction of apoptotic signals.

Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.


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