Genistein inhibits CCAAT/enhancer-binding protein beta (C/EBPbeta) activity and 3T3-L1 adipogenesis by increasing C/EBP homologous protein expression

Biochem J. 2002 Oct 1;367(Pt 1):203-8. doi: 10.1042/BJ20020300.

Abstract

The tyrosine kinase inhibitor genistein inhibits 3T3-L1 adipogenesis when present during the first 72 h of differentiation. In this report, we investigated the underlying mechanisms involved in the anti-adipogenic effects of genistein. We found that genistein blocked the DNA binding and transcriptional activity of CCAAT/enhancer-binding protein beta (C/EBPbeta) during differentiation by promoting the expression of C/EBP homologous protein, a dominant-negative member of the C/EBP family. Loss of C/EBPbeta activity was manifested as a loss of differentiation-induced C/EBPalpha and peroxisome-proliferator-activated receptor gamma protein expression and a dramatic reduction in lipid accumulation. Further, we documented for the first time that C/EBPbeta was tyrosine-phosphorylated in vivo during differentiation and in vitro by activated epidermal growth factor receptor. Genistein inhibited both of these events. Collectively, these results indicate that genistein blocks adipogenesis and C/EBPbeta activity by increasing the level of C/EBP homologous protein and possibly by inhibiting the tyrosine phosphorylation of C/EBPbeta.

Publication types

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

MeSH terms

  • 3T3 Cells
  • Adipocytes / cytology*
  • Adipocytes / metabolism
  • Animals
  • Anticarcinogenic Agents / pharmacology
  • Azo Compounds / pharmacology
  • CCAAT-Enhancer-Binding Protein-beta / antagonists & inhibitors*
  • Cell Differentiation
  • Cell Line
  • Cell Nucleus / metabolism
  • Coloring Agents / pharmacology
  • DNA / metabolism
  • Enzyme Inhibitors / pharmacology
  • Genistein / pharmacology*
  • Immunoblotting
  • Isoflavones / pharmacology
  • Lipid Metabolism
  • Mice
  • Phosphorylation
  • Precipitin Tests
  • Protein Binding
  • Receptors, Cytoplasmic and Nuclear / metabolism
  • Time Factors
  • Transcription Factors / metabolism
  • Transcription, Genetic
  • Transfection
  • Tyrosine / metabolism

Substances

  • Anticarcinogenic Agents
  • Azo Compounds
  • CCAAT-Enhancer-Binding Protein-beta
  • Coloring Agents
  • Enzyme Inhibitors
  • Isoflavones
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Tyrosine
  • daidzein
  • DNA
  • Genistein
  • oil red O