Effect of genistein on p90RSK phosphorylation and cell proliferation in T47D breast cancer cells

Anticancer Res. 2011 Jan;31(1):209-14.

Abstract

Background: The molecular mechanisms of genistein's proliferative effects on breast cancer cells are largely unknown. This study aimed to examine estrogen-receptor (ER)-related signaling molecules involved in genistein-associated cell proliferation and survival (ERK1/2, p90RSK, JNK, Akt and NFκB) and to correlate these results to cell proliferation.

Materials and methods: The effect of genistein on cell-signaling molecules was determined in T47D breast cancer cells by a Bioplex phosphoprotein detection kit. These results were confirmed by Western blotting and were correlated to cell proliferation by MTT assay.

Results: Low and high concentrations of genistein induced an ERK1/2-independent decrease in phosphorylated p90RSK. This effect was accompanied by decreased cell proliferation at high concentrations and an increased response at low concentrations of genistein following a 48-hour exposure.

Conclusion: Concentration-dependent actions of genistein in T47D cells may be due to differential activation of signaling molecules.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anticarcinogenic Agents / pharmacology*
  • Blotting, Western
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Female
  • Genistein / pharmacology*
  • Humans
  • Phosphorylation / drug effects
  • Receptors, Estrogen / metabolism
  • Ribosomal Protein S6 Kinases, 90-kDa / metabolism*

Substances

  • Anticarcinogenic Agents
  • Receptors, Estrogen
  • Genistein
  • Ribosomal Protein S6 Kinases, 90-kDa