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KMID : 0914820130130030172
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Journal of the Korean Gastric Cancer Association
2013 Volume.13 No. 3 p.172 ~ p.178
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Effects of 17?-Estradiol and Estrogen Receptor Antagonists on the Proliferation of Gastric Cancer Cell Lines
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Kim Myung-Jin
Cho Sung-Il
Lee Kun-Ok
Han Hyung-Joon
Song Tae-Jin
Park Seong-Heum
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Abstract
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Purpose: The aims of this study were as follow: 1) to de scribe the expression status of estrogen receptor-? and -? mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of 17?-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. Materials and Methods: Detection of estrogen receptor-? and estrogen receptor-? 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 ef-fect of 17?-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?-estradiol and estrogen receptor antagonists (methyl-piperidino-pyrazole and pyr-azolo [1,5-a] pyrimidine). Cell proliferation was assessed with the methylthiazol tetrazolium test. Results: Estrogen receptor-? and estrogen receptor-? mRNAs were expressed in three (KATO III, MKN28 and MKN45) and all of the five gastric cancer cell lines, respectively. At higher concentrations, 17?-estradiol inhibited cell growth of MKN28, MKN45 and KATO III cell lines. Neither estrogen receptor-? nor estrogen receptor-? antagonist blocked the anti-proliferative effect of 17?-estradiol. Conclusions: Our results indicate that estrogen receptor-? 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-? 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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KEYWORD
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Estrogens, Receptors, estrogen, Stomach neoplasms, Cell line
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