The role of mitogen-activated protein kinases and their relationship with NF-kappaB and PPARgamma in indomethacin-Induced apoptosis of colon cancer cells

Ann N Y Acad Sci. 2002 Nov:973:241-5. doi: 10.1111/j.1749-6632.2002.tb04641.x.

Abstract

We have evaluated the role of mitogen-activated protein kinases (MAPKs) and their relationship with nuclear factor kappaB (NF-kappaB) and peroxisome proliferator-activated receptor gamma (PPARgamma) in indomethacin-induced apoptosis of colon cancer cells. We demonstrated that indomethacin can induce the prolonged activation of MAPKs in colon cancer cells; and that of these MAPKs, p38 MAPK may play a partial but significant role in indomethacin-induced apoptosis. Furthermore, indomethacin-induced p38 MAPK-mediated apoptosis of colon cancer cell lines is independent of caspase activation and not associated with indomethacin-induced NF-kappaB suppression and PPARgamma activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Colonic Neoplasms / pathology*
  • Humans
  • Indomethacin / pharmacology*
  • MAP Kinase Signaling System / drug effects
  • MAP Kinase Signaling System / physiology*
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / metabolism*
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Transcription Factors / metabolism*
  • Tumor Cells, Cultured

Substances

  • NF-kappa B
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Mitogen-Activated Protein Kinases
  • Indomethacin