Metformin regulates stromal-epithelial cells communication via Wnt2/β-catenin signaling in endometriosis

被引:24
作者
Zhang, Hui [1 ]
Xue, Jing [1 ]
Li, Mingjiang [1 ]
Zhao, Xingbo [1 ]
Wei, Deying [1 ]
Li, Changzhong [1 ]
机构
[1] Shandong Univ, Shandong Prov Hosp, Dept Obstet & Gynecol, Jinan 250021, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
Endometriosis; Metformin; Wnt2/beta-catenin; Stroma-epithelium communication; HEPATOCYTE GROWTH-FACTOR; IN-VITRO; EXPRESSION; CANCER; ACTIVATION; CARCINOMA;
D O I
10.1016/j.mce.2015.06.011
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
In previous studies, we found that endometriotic stromal cells lose the ability to regulate cell survival signaling in endometriotic epithelial cells. Here, we invested the effect of Metformin on the stromal-epithelial cells crosstalk in endometriosis and explored the pathway that might be involved. We found that ectopic endometriotic stromal cells (ESC) expressed and secreted higher Wnt2 protein compared with normal endometrial stromal cells (NSC). Conditioned medium (CM) from ESC supplemented with Wnt2 antibody significantly inhibited the growth of normal endometrial epithelial cells (NEC), while CM from ESC per se showed no significant effect on the growth of NEC. Metformin decreased the expression and secretion of Wnt2 in ESC. CM from Metformin-pretreated ESC significantly inhibited the growth of NEC. In conclusion, Wnt2/beta-catenin signaling was involved in stromal-epithelial cells interaction in endometriosis. Metformin might regulate the stroma-epithelium communication via Wnt2-mediated signaling in endometriosis. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:61 / 65
页数:5
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