Ginsenoside Rc and Re Stimulate c-Fos Expression in MCF-7 Human Breast Carcinoma 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) ;
  • Ji, Sang-Mi (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) ;
  • Ban, Jae-Jun (College of Engineering, Institute of Biotechnology, Department of Bioscience and Biotechnology, Sejong University) ;
  • Lee, Seung-Ki (College of Pharmacy, Seoul National University)
  • Published : 2003.01.01

Abstract

We have found that ginsenoside Rc and Re induce c-fos in MCF-7 human breast carcinoma cells at both the mRNA and protein levels. However, neither ginsenoside activated the expression of reporter gene under the control of AP-1/TPA response elements. We have also examined the possibility that ginsenoside Rc and Re act by binding to intracellular steroid hormone receptors that act as transcriptional factors in the nucleus in inducing c-fos mRNA in MCF7 human breast carcinoma cells. However, ginsenoside Rc and Re did not bind to glucocorticoid, androgen, estrogen, or retinoic acid receptors as examined by the transcription activation of the luciferase reporter genes in CV-1 cells that were transiently transfected with the corresponding steroid hormone receptors and hormone responsive luciferase reporter plasmids. These data demonstrate that ginsenoside Rc and Re act via other transcription factors and not via estrogen receptor in c-Fos expression.

Keywords

References

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