$Ginsenoside-R_{b1}$ Acts as a Weak Phytoestrogen in MCF-7 Human Breast Cancer Cells

  • Lee, Young-Joo (College of Engineering, Institute of Biotechnology, Department of Bioscience and Biotechnology, Sejong University) ;
  • Jin, Young-Ran (College of Pharmacy, Seoul National University) ;
  • Lim, Won-Chung (College of Engineering, Institute of Biotechnology, Department of Bioscience and Biotechnology, Sejong University) ;
  • Park, Wan-Kyu (College of Engineering, Institute of Biotechnology, Department of Bioscience and Biotechnology, Sejong University) ;
  • Cho, Jung-Yoon (College of Engineering, Institute of Biotechnology, Department of Bioscience and Biotechnology, Sejong University) ;
  • Jang, Si-Youl (College of Engineering, Kookmin University) ;
  • Lee, Seung-Ki (College of Pharmacy, Seoul National University)
  • Published : 2003.01.01

Abstract

Ginseng has been recommended to alleviate the menopausal symptoms, which indicates that components of ginseng very likely contain estrogenic activity. We have examined the possibility that a component of Panax ginseng, $ginsenoside-R_{b1}$ acts by binding to estrogen receptor. We have investigated the estrogenic activity of $ginsenoside-R_{b1}$ in a transient transfection system using estrogen-responsive luciferase plasmids in MCF-7 cells. $ginsenoside-R_{b1}$ activated the transcription of the estrogen-responsive luciferase reporter gene in MCF-7 breast cancer cells at a concentration of 50 $\mu$M. Activation was inhibited by the specific estrogen receptor antagonist ICI 182,780, indicating that the estrogenic effect of $ginsenoside-R_{b1}$ is estrogen receptor dependent. Next, we evaluated the ability of $ginsenoside-R_{b1}$ to induce the estrogen-responsive gene c-fos by semi-quantitative RT-PCR assays and Western analyses. $ginsenoside-R_{b1}$ increased c-fos both at mRNA and protein levels. However, $ginsenoside-R_{b1}$ failed to activate the glucocorticoid receptor, the retinoic acid receptor, or the androgen receptor in CV-1 cells transiently transfected with the corresponding steroid hormone receptors and hormone responsive reporter plasmids. These data support our hypothesis that $ginsenoside-R_{b1}$ acts a weak phytoestrogen, presumably by binding and activating the estrogen receptor.

Keywords

References

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