中文摘要：

目的：探讨G蛋白偶联受体（GPR 30）下调对子宫内膜癌细胞及裸鼠移植瘤组织PI3K／Akt信号通路的影响。方法：采用免疫细胞化学SP法观察子宫内膜癌细胞系HEC-1A和Ishikawa细胞中GPR30、Akt和磷酸化Akt （p-Akt）蛋白的定位。以pGFP-V-RS（对照）和pGFP-V-RS-GPR30（干扰）分别转染两种细胞，用蛋白印迹法检测两种细胞中GPR30、Akt及p-Akt蛋白的表达水平。构建裸鼠移植瘤模型（分别接种上述4种转染细胞，共4组），用免疫组化SP法检测4组裸鼠移植瘤组织中p-Akt蛋白的表达。结果：①HEC-1A和Ishikawa细胞中，GPR30、Akt和p-Akt蛋白阳性表达均呈棕黄色，定位于细胞质。②稳定转染pGFP-VR-S -GPR30的两种细胞株中GPR30和p -Akt的表达均下调（ P＜0．05）。③与接种转染pGFP-V-RS细胞的2组裸鼠相比，接种转染pGFP-V-RS-GPR30细胞的2组裸鼠移植瘤组织中p-Akt表达降低。结论：在子宫内膜癌细胞及裸鼠移植瘤组织中， GPR30下调可能抑制了PI3K／Akt通路的活化。

英文摘要：

Aim：To investigate the influence of down-regulation of G protein-coupled estrogen receptor 30 （ GPR30 ） on activation of PI3K/Akt signaling pathway in endometrial carcinoma cells and tumor tissue of nude mice .Methods：The location of GPR30, Akt and p-Akt protein in HEC-1A and Ishikawa cells was detected by immunocytochemical SP method . The expression of GPR30 in HEC-1A and Ishikawa cells was down-regulated by transfection with pGFP-V-RS-GPR30, a GPR30 antisense expression vector , and the cells transfected with pGFP-V-RS were the control; the levels of GPR30,Akt and p-Akt were detected by Western blot .The nude mice were allocated into 4 groups and inoculated the above transfected cells, and immunohistochemistry was performed to observe the changes of the expression level of p -Akt in the xenograft tis-sue.Results：Immunocytochemical SP method showed that GPR 30, Akt and p-Akt was stained as brown and yellow in cell cytoplasm of HEC-1A and Ishikawa cells.Western blot analysis showed that the expressions of GPR 30 and p-Akt were de-creased in tumor cells transfected by pGFP-V-RS-GPR30 compared with the control （P〈0.05）.The expression of p-Akt was decreased in the mice inoculated the tumor cells transfected by pGFP-V-RS-GPR30 .Conclusion： Down-regulation of GPR30 inhibit the activation of PI3K/Akt signaling pathway in Ishikawa and HEC-1A cells and tumor tissue of nude mice .