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Originally published In Press as doi:10.1074/jbc.M107385200 on October 12, 2001

J. Biol. Chem., Vol. 276, Issue 50, 47100-47106, December 14, 2001
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Non-apoptotic Signaling Pathways Activated by Soluble Fas Ligand in Serum-starved Human Fibroblasts
MITOGEN-ACTIVATED PROTEIN KINASES AND NF-kappa B-DEPENDENT GENE EXPRESSION*

Jin-Hyung AhnDagger §, Sun-Mi ParkDagger §, Ho-Sung ChoDagger , Myung-Shik Lee||, Jong-Bok Yoon, Jan Vilcek**, and Tae H. LeeDagger Dagger Dagger

From the Dagger  Department of Biology and  Protein Network Research Center, Yonsei University, Seoul 120-749, Korea, || Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 135-710, Korea, and ** Department of Microbiology, New York University Medical Center, New York, New York 10016

Many Fas-expressing cells do not undergo cell death upon Fas stimulation. In the normal human diploid cell line GM6112, the addition of soluble Fas ligand (sFasL) leads to morphological signs of cell death in less than 1% of cells. Treatment of serum-starved GM6112 fibroblasts with sFasL resulted in a rapid and transient phosphorylation of ERK1/2 without a significant increase in JNK and p38 activities. Unless co-treated with the protein synthesis inhibitor anisomycin, sFasL did not show gene-inducing activity in cells maintained in complete medium. However, when cells were serum-starved for 4 days, treatment with sFasL alone induced interleukin-6 gene expression and, less strongly, interleukin-8 gene expression. Sensitization of the gene-inducing activity by serum starvation correlated with NF-kappa B activation by sFasL. Furthermore, we found that the expression of FADD and caspase-8 was significantly reduced in serum-starved cells, whereas the level of cFLIP remained unchanged. Transfection of GM6112 cells with the antisense caspase-8 expression construct sensitized cells toward sFasL-induced NF-kappa B-dependent reporter activation. Our results support the notion that a change in the ratio of cFLIP and caspase-8 may be responsible for turning on the Fas-activated NF-kappa B pathway, which otherwise is supplanted by the death-inducing pathway.

* This work was supported by Korea Research Foundation Grant KRF-2000-015-DP0407) and by a grant from Protein Network Research Center (Yonsei University), the Ministry of Science and Technology/Korea Science and Engineering Foundation, and by National Institutes of Health Grant CA75071 (United States Public Health Service).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.

§ These authors contributed equally to this work.

Dagger Dagger To whom correspondence should be addressed: Dept. of Biology, College of Science, Yonsei University, 134 Shinchon-Dong, Sudaemoon-Gu, Seoul 120-749, Korea. Tel.: 82-2-2123-4084; Fax: 82-2-312-2242; E-mail: thlee@yonsei.ac.kr.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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