Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation

Prostate. 1993;22(4):335-45. doi: 10.1002/pros.2990220408.


The effect of the isoflavones, genistein, daidzein, and biochanin A on the growth of the LNCaP and DU-145 human prostate cancer cell lines has been examined. Genistein and biochanin A, but not daidzein, inhibit both serum and EGF-stimulated growth of LNCaP and DU-145 cells (IC50 values from 8.0 to 27 micrograms/ml for serum and 4.3 to 15 micrograms/ml for EGF), but have no significant effect of the EGF receptor tyrosine autophosphorylation. In contrast, tyrphostin 25, a specific EGF receptor tyrosine kinase inhibitor, inhibits EGF-stimulated growth and EGF receptor tyrosine autophosphorylation in these whole cells, but does not inhibit serum-stimulated growth. These data suggest that the mechanism of action of genistein and biochanin A does not depend on inhibition of EGF receptor tyrosine autophosphorylation, but on a more distal event in the EGF receptor-mediated signal transduction cascade.

MeSH terms

  • Anticarcinogenic Agents / pharmacology*
  • Catechols / pharmacology
  • Cell Division / drug effects
  • Epidermal Growth Factor / pharmacology
  • ErbB Receptors / metabolism
  • Estrogens, Non-Steroidal / pharmacology
  • Genistein
  • Humans
  • Isoflavones / pharmacology*
  • Male
  • Nitriles / pharmacology
  • Phosphorylation
  • Prostatic Neoplasms / prevention & control*
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Tumor Cells, Cultured
  • Tyrosine / metabolism
  • Tyrphostins*


  • Anticarcinogenic Agents
  • Catechols
  • Estrogens, Non-Steroidal
  • Isoflavones
  • Nitriles
  • Tyrphostins
  • tyrphostin 47
  • Tyrosine
  • Epidermal Growth Factor
  • daidzein
  • Genistein
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • biochanin A