Journal of Gastric Cancer

The Korean Gastric Cancer Association (대한위암학회)
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Effects of $17{\beta}$-Estradiol and Estrogen Receptor Antagonists on the Proliferation of Gastric Cancer Cell Lines

  • Kim, Myung-Jin (Department of Surgery, Korea University College of Medicine) ;
  • Cho, Sung-Il (Department of Surgery, Korea University College of Medicine) ;
  • Lee, Kun-Ok (HBP Research Laboratory, Department of Surgery, Korea University Ansan Hospital) ;
  • Han, Hyung-Joon (Department of Surgery, Korea University College of Medicine) ;
  • Song, Tae-Jin (Department of Surgery, Korea University College of Medicine) ;
  • Park, Seong-Heum (Department of Surgery, Korea University College of Medicine)
  • Received : 2013.06.01
  • Accepted : 2013.09.13
  • Published : 2013.09.30
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Abstract

Purpose: The aims of this study were as follow: 1) to de scribe the expression status of estrogen receptor-${\alpha}$ and -${\beta}$ mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. Materials and Methods: Detection of estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNA in five human gastric cancer cell lines (AGS, KATO III, MKN28, MKN45 and MKN74) was made by the reverse transcription-polymerase chain reaction system. To evaluate the effect of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of gastric cancer cell line, the cell lines which expressed both es trogen receptors were chosen and treated with $17{\beta}$-estradiol and estrogen receptor antagonists (methyl-piperidino-pyrazole and pyrazolo [1,5-a] pyrimidine). Cell proliferation was assessed with the methylthiazol tetrazolium test. Results: Estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNAs were expressed in three (KATO III, MKN28 and MKN45) and all of the five gastric cancer cell lines, respectively. At higher concentrations, $17{\beta}$-estradiol inhibited cell growth of MKN28, MKN45 and KATO III cell lines. Neither estrogen receptor-${\alpha}$ nor estrogen receptor-${\beta}$ antagonist blocked the anti-proliferative effect of $17{\beta}$-estradiol. Conclusions: Our results indicate that estrogen receptor-${\beta}$ mRNAs are preferentially expressed in gastric cancers and also imply that hormone therapy rather than estrogen receptor blockers may be a useful strategy for the treatment of estrogen receptor-${\beta}$ positive gastric cancer. Its therapeutic significance in gastric cancer are, however, limited until more evidence of the roles of estrogen receptors in the gastric cancer are accumulated.

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References

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