Estrogen Inhibits Bcl-2 Expression and Stimulates Apoptosis Mediated by 2,3,7,8-Tetrachlrodibenzo-p-dioxirn

  • Hwang, Sohyun (Department of Biological Science, Korea Advanced Institute of Science and Technology) ;
  • Such, Jaehong (Department of Biological Science, Korea Advanced Institute of Science and Technology) ;
  • Byun, Boo-Hyeong (Department of Biological Science, Korea Advanced Institute of Science and Technology) ;
  • Joe, Cheol O. (Department of Biological Science, Korea Advanced Institute of Science and Technology)
  • Published : 2003.12.01

Abstract

The effects of estrogen on apoptosis induced by 2,3,7,8-tetrachlorodibenzo-p-doxin (TCDD) were examined in cultured MCF-7 cells. TCDD stimulated apoptosis and inhibited the expression of bcl-2 gene in MCF-7 cells grown in the media supplemented with 10% fetal bovine serum. However, TCDD failed to induce apoptosis if cells were grown in the media deprived of all estrogen-like compounds. Removal of estrogen-like compounds from the growth media also led to the activation of bcl-2 gene expression in cells treated with TCDD. Combined treatment of estrogen with TCDD abrogated the binding of Aryl hydrocarbon Receptor (AhR)-TCDD complex to Dioxin response element (DRE) of bcl-2 gene leading to the inhibition of bcl-2 gene expression as well as stimulation of apoptosis. The present study suggests that the binding of estrogen receptor (ER)-estrogen complex to the estrogen responsive element (E) interferes with the binding of AhR- TCDD complex to the DRE and inhibits the bcl-2 expression.

Keywords

References

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