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Effects of 17β-Estradiol and Estrogen Receptor Antagonists on the Proliferation of Gastric Cancer Cell Lines

PURPOSE: The aims of this study were as follow: 1) to de scribe the expression status of estrogen receptor-α and -β mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of 17β-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. MATERIALS AND...

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Detalles Bibliográficos
Autores principales: Kim, Myung-Jin, Cho, Sung-Il, Lee, Kun-Ok, Han, Hyung-Joon, Song, Tae-Jin, Park, Seong-Heum
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Gastric Cancer Association 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3804676/
https://www.ncbi.nlm.nih.gov/pubmed/24156037
http://dx.doi.org/10.5230/jgc.2013.13.3.172
Descripción
Sumario:PURPOSE: The aims of this study were as follow: 1) to de scribe the expression status of estrogen receptor-α and -β mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of 17β-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. MATERIALS AND METHODS: Detection of estrogen receptor-α and estrogen receptor-β 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 17β-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 17β-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-α and estrogen receptor-β mRNAs were expressed in three (KATO III, MKN28 and MKN45) and all of the five gastric cancer cell lines, respectively. At higher concentrations, 17β-estradiol inhibited cell growth of MKN28, MKN45 and KATO III cell lines. Neither estrogen receptor-α nor estrogen receptor-β antagonist blocked the anti-proliferative effect of 17β-estradiol. CONCLUSIONS: Our results indicate that estrogen receptor-β 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-β 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.