Effects of 17beta-Estradiol and Estrogen Receptor Antagonists on the Proliferation of Gastric Cancer Cell Lines.
10.5230/jgc.2013.13.3.172
- Author:
Myung Jin KIM
1
;
Sung Il CHO
;
Kun Ok LEE
;
Hyung Joon HAN
;
Tae Jin SONG
;
Seong Heum PARK
Author Information
1. Department of Surgery, Korea University College of Medicine, Seoul, Korea. pshchw@korea.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Estrogens;
Receptors, estrogen;
Stomach neoplasms;
Cell line
- MeSH:
Cell Line;
Cell Proliferation;
Estrogens;
Humans;
Receptors, Estrogen;
RNA, Messenger;
Stomach Neoplasms
- From:Journal of Gastric Cancer
2013;13(3):172-178
- CountryRepublic of Korea
- Language:English
-
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 17beta-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 17beta-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 17beta-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, 17beta-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 17beta-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.
