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Assessment of Tumor Necrosis Factor Receptor and Fas Signaling Pathways by Transcriptional Profiling¹

Division of Molecular Pharmacology, Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112

Apoptosis, or programmed cell death, is an important mechanism by which cells are eliminated during immune regulation and embryonic development. Aberrations in the signaling pathways leading to apoptosis may result in cancer, autoimmune diseases, or inflammatory disorders. In view of this, an understanding of the signaling capabilities of apoptosis-inducing or death receptors is essential to understanding their roles in biology and disease. We used cDNA microarrays to examine the downstream transcriptional effects of two members of the tumor necrosis factor (TNF) family of death receptor ligands. We compared the transcriptional responses of a model colon cancer cell line, HT29, to TNF- and anti-Fas activating antibody. Both ligands induced a subset of genes characteristic of activation of the transcription factor nuclear factor-B (NF-B). Follow-up analyses demonstrated that, although TNF- activated NF-B through IB- degradation, -Fas treatment led to NF-B activation through a mechanism distinct from IB- degradation.

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