Disassociation of MAPK activation and c-Fos expression in F9 embryonic carcinoma cells following retinoic acid-induced endoderm differentiation

J Biol Chem. 2001 Aug 24;276(34):32094-100. doi: 10.1074/jbc.M105009200. Epub 2001 Jun 11.

Abstract

Retinoic acid induces cell differentiation and suppresses cell growth in a wide spectrum of cell lines, and down-regulation of activator protein-1 activity by retinoic acid contributes to these effects. In embryonic stem cell-like F9 teratocarcinoma cells, which are widely used to study retinoic acid actions on gene regulation and early embryonic differentiation, retinoic acid treatment for 4 days resulted in suppression of cell growth and differentiation into primitive and then visceral endoderm-like cells, accompanied by a suppression of serum-induced c-Fos expression. The MAPK (ERK) pathway was involved in mitogenic signaling in F9 cells stimulated with serum. Surprisingly, although c-Fos expression was reduced, the MAPK activity was not decreased by retinoic acid treatment. We found that retinoic acid treatment inhibited the phosphorylation of Elk-1, a target of activated MAPK required for c-Fos transcription. In F9 cells, the MAPK/MEK inhibitor PD98059 suppressed Elk-1 phosphorylation and c-Fos expression, indicating that MAPK activity is required for Elk-1 phosphorylation/activation. Phosphoprotein phosphatase 2B (calcineurin), the major phosphatase for activated Elk-1, is not the target in the disassociation of MAPK activation and c-Fos expression since its inhibition by cyclosporin A or activation by ionomycin had no significant effects on serum-stimulated c-Fos expression and Elk-1 phosphorylation. Thus, we conclude that retinoic acid treatment to induce F9 cell differentiation uncouples Ras/MAPK activation from c-Fos expression by reduction of Elk-1 phosphorylation through a mechanism not involving the activation of phosphoprotein phosphatase 2B.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Calcineurin / metabolism
  • Carcinoma, Embryonal / enzymology
  • Carcinoma, Embryonal / metabolism*
  • Carcinoma, Embryonal / pathology
  • Cell Differentiation / drug effects*
  • DNA-Binding Proteins*
  • Enzyme Activation
  • Enzyme Inhibitors / pharmacology
  • Flavonoids / pharmacology
  • Mice
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinases / metabolism*
  • Phosphorylation
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-fos / metabolism*
  • Transcription Factors*
  • Tretinoin / pharmacology*
  • Tumor Cells, Cultured
  • ets-Domain Protein Elk-1

Substances

  • DNA-Binding Proteins
  • Elk1 protein, mouse
  • Enzyme Inhibitors
  • Flavonoids
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-fos
  • Transcription Factors
  • ets-Domain Protein Elk-1
  • Tretinoin
  • Mitogen-Activated Protein Kinases
  • Calcineurin
  • 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one