Alternative splicing variants of c-FLIP transduce the differential signal through the Raf or TRAF2 in TNF-induced cell proliferation

Biochem Biophys Res Commun. 2001 Dec 21;289(5):1205-10. doi: 10.1006/bbrc.2001.6086.

Abstract

In human cancer, despite apoptotic activity, death-ligand promotes the cell cycle progression under certain conditions. In this study, we demonstrated that TNF-alpha-induced cell proliferation is achieved through the c-FLIP. In addition, alternative splicing variants (c-FLIP(L) and c-FLIP(S)) contribute the TNF-alpha-induced cell cycle promotion through distinct pathways. The long form of c-FLIP (c-FLIP(L)) activates the Raf, which enhance the activity of Erk and PI3K, whereas short form (c-FLIPS) are activated by c-jun-N-terminal Kinase (JNK) through the TNF receptor-associated factor (TRAF) 2. Since, however, recruitment of c-FLIP(L) into FADD is later than that of c-FLIP(S), the activation of PI3K and Erk show the late response to activation of JNK. We also show that each c-FLIP variant is regulated by a distinct molecular mechanism at the transcriptional level; c-FLIP(L) is induced by Erk, whereas c-FLIP(S), through the JNK activation, is like an autocrine regulatory loop. Therefore, the induction of c-FLIP(L) in response to TNF-alpha is achieved in a more delayed manner than that of c-FLIP(S). Our present study also implies that other alternative splicing variants perform differential roles in spite of the same pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alternative Splicing
  • CASP8 and FADD-Like Apoptosis Regulating Protein
  • Carrier Proteins / genetics*
  • Carrier Proteins / metabolism*
  • Cell Division / drug effects
  • Cell Division / physiology
  • Cell Line
  • Enzyme Activation / drug effects
  • Genetic Variation
  • Humans
  • Intracellular Signaling Peptides and Proteins*
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Protein Serine-Threonine Kinases*
  • Proteins / metabolism*
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-akt
  • Proto-Oncogene Proteins c-raf / metabolism*
  • Signal Transduction
  • TNF Receptor-Associated Factor 2
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • CASP8 and FADD-Like Apoptosis Regulating Protein
  • CFLAR protein, human
  • Carrier Proteins
  • Intracellular Signaling Peptides and Proteins
  • Proteins
  • Proto-Oncogene Proteins
  • TNF Receptor-Associated Factor 2
  • Tumor Necrosis Factor-alpha
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Proto-Oncogene Proteins c-raf
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases