Fas-associated death domain protein (FADD) and caspase-8 mediate up-regulation of c-Fos by Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) via a FLICE inhibitory protein (FLIP)-regulated pathway

J Biol Chem. 2001 Aug 31;276(35):32585-90. doi: 10.1074/jbc.M100444200. Epub 2001 May 30.

Abstract

Fas, a death domain-containing member of the tumor necrosis factor receptor family and its ligand FasL have been predominantly studied with respect to their capability to induce cell death. However, a few studies indicate a proliferation-inducing signaling activity of these molecules too. We describe here a novel signaling pathway of FasL and the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) that triggers transcriptional activation of the proto-oncogene c-fos, a typical target gene of mitogenic pathways. FasL- and TRAIL-mediated up-regulation of c-Fos was completely dependent on the presence of Fas-associated death domain protein (FADD) and caspase-8, but caspase activity seemed to be dispensable as a pan inhibitor of caspases had no inhibitory effect. Upon overexpression of the long splice form of cellular FADD-like interleukin-1-converting enzyme (FLICE) inhibitory protein (cFLIP) in Jurkat cells, FasL- and TRAIL-induced up-regulation of c-Fos was almost completely blocked. The short splice form of FLIP, however, showed a rather stimulatory effect on c-Fos induction. Together these data demonstrate the existence of a death receptor-induced, FADD- and caspase-8-dependent pathway leading to c-Fos induction that is inhibited by the long splice form FLIP-L.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Alternative Splicing
  • Antibodies, Monoclonal / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Apoptosis Regulatory Proteins
  • CASP8 and FADD-Like Apoptosis Regulating Protein
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • Caspase 8
  • Caspase 9
  • Caspases / metabolism*
  • Fas Ligand Protein
  • Fas-Associated Death Domain Protein
  • Gene Expression Regulation*
  • Genes, fos*
  • Humans
  • Intracellular Signaling Peptides and Proteins*
  • Jurkat Cells
  • Membrane Glycoproteins / physiology*
  • Models, Biological
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins c-fos / genetics
  • Recombinant Proteins / metabolism
  • TNF-Related Apoptosis-Inducing Ligand
  • Transfection
  • Tumor Necrosis Factor-alpha / physiology*
  • fas Receptor / physiology*

Substances

  • Adaptor Proteins, Signal Transducing
  • Antibodies, Monoclonal
  • Apoptosis Regulatory Proteins
  • CASP8 and FADD-Like Apoptosis Regulating Protein
  • CFLAR protein, human
  • Carrier Proteins
  • FADD protein, human
  • FASLG protein, human
  • Fas Ligand Protein
  • Fas-Associated Death Domain Protein
  • Intracellular Signaling Peptides and Proteins
  • MAS1 protein, human
  • Membrane Glycoproteins
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins c-fos
  • Recombinant Proteins
  • TNF-Related Apoptosis-Inducing Ligand
  • TNFSF10 protein, human
  • Tumor Necrosis Factor-alpha
  • fas Receptor
  • CASP8 protein, human
  • CASP9 protein, human
  • Caspase 8
  • Caspase 9
  • Caspases