Genistein in the control of breast cancer cell growth: insights into the mechanism of action in vitro

Cancer Lett. 1998 Aug 14;130(1-2):143-52. doi: 10.1016/s0304-3835(98)00130-x.


Genistein significantly inhibited cell growth (IC50 around 10 microM) of MCF-7, MDAMB-231 and HBL-100 cell lines, but not of skin-derived fibroblasts and counteracted the growth-stimulatory effects exerted by estradiol and growth factors. It abolished the paracrine stimulation observed in MCF-7 cells in co-culture with MDAMB-231 or fibroblasts. Genistein-treated cells accumulated in the S and G2/M phases of the cell cycle and underwent apoptosis. Genistein decreased tyrosine phosphorylation induced upon treatment with transforming growth factor-alpha. Finally, genistein bound the estrogen receptor (ER) (relative affinity constant Kd = 4 nM), induced pS2 and cathepsin-D transcription and increased nuclear ER levels.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / metabolism
  • Antineoplastic Agents / pharmacology*
  • Apoptosis
  • Binding, Competitive
  • Breast Neoplasms* / metabolism
  • Breast Neoplasms* / pathology
  • Cell Cycle / drug effects
  • Cell Division / drug effects
  • Estradiol / metabolism
  • Estradiol / pharmacology
  • Female
  • Fibroblasts / cytology
  • Fibroblasts / drug effects
  • Genistein / metabolism
  • Genistein / pharmacology*
  • Growth Substances / pharmacology
  • Humans
  • Phosphorylation
  • Receptors, Estrogen / metabolism
  • Tumor Cells, Cultured / drug effects


  • Antineoplastic Agents
  • Growth Substances
  • Receptors, Estrogen
  • Estradiol
  • Genistein