Overexpression of ERα inhibits proliferation and invasion of MKN28 gastric cancer cells by suppressing β-catenin.
Overexpression of ERα inhibits proliferation and invasion of MKN28 gastric cancer cells by suppressing β-catenin.
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DOI：
10.3892/or.2013.2610
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发表时间：
2013-10
期刊：
影响因子：
4.2
通讯作者：
Jichun Zhou;Rong-yue Teng;Chaoyang Xu;Qinchuan Wang;Jufeng Guo;Chenpu Xu;Zi-Duo li;S. Xie;Jian-guo Shen;Linbo Wang
中科院分区：
文献类型：
--
作者：
Jichun Zhou;Rong-yue Teng;Chaoyang Xu;Qinchuan Wang;Jufeng Guo;Chenpu Xu;Zi-Duo li;S. Xie;Jian-guo Shen;Linbo Wang
雌激素受体（ER）α与胃癌患者预后的关系已被证实，但ER α在胃癌中的确切作用仍有待充分阐明。本研究旨在探讨ER α对胃癌细胞增殖、迁移和侵袭的影响。本研究探讨ER α过表达对胃癌细胞的生物学效应。建立了稳定高表达ER α的MKN 28胃癌细胞株。通过检测细胞存活率、集落形成、细胞周期进程和细胞凋亡来评估ER α过表达对细胞生长的影响。通过Transwell迁移/侵袭实验检测细胞迁移和侵袭。蛋白质水平的几个潜在的参与基因，通过蛋白质印迹法来阐明潜在的分子机制。学生t检验用于确定各个实验组和对照组之间的统计学差异，单向ANOVA检验用于确定三个或更多个组之间的差异。结果显示，ER α过表达可明显抑制细胞生长和增殖，阻滞细胞进入G1/G0期，促进细胞凋亡。此外，ER α还能抑制胃癌细胞的运动和侵袭能力。这些表型可能部分由ER α过表达引起的β-catenin表达减少来解释。ER α过表达可通过抑制β-catenin抑制胃癌细胞的生长和肿瘤的进展，是一个具有潜在治疗潜力的靶点。
The relationship between estrogen receptor (ER)α and patient prognosis has been identified in gastric cancer; however, the definite role of ERα in gastric cancer remains to be fully elucidated. The aim of the present in vitro study was to investigate the impact of ERα on cell proliferation, migration and invasion in gastric cancer cell lines. We investigated the biological effect of ERα overexpression on gastric carcinoma cells. An MKN28 gastric cancer cell line stably overexpressing ERα was established. The effect of ERα overexpression on cell growth was assessed by evaluating cell survival, colony formation, cell cycle progression and apoptosis. Cell migration and invasion were detected by Transwell migration/invasion assays. The protein levels of several potentially involved genes were determined by western blotting to elucidate the underlying molecular mechanisms. The Student's t-test was used to determine the statistical differences between various experimental and control groups, and one-way ANOVA test was used to determine the difference between three or more groups. The results showed that ERα overexpression significantly inhibited cell growth and proliferation, blocked cell entry into the G1/G0 phase and promoted cell apoptosis. In addition, ERα reduced the motility and invasion of gastric cancer cells. These phenotypes may partly be explained by a decrease in β-catenin expression caused by ERα overexpression. ERα overexpression effectively inhibited cell growth and cancer progression by suppressing β-catenin in gastric cancer, identifying ERα as a promising target with therapeutic potential for development of new approaches to treat gastric cancer.