睾酮通过PI3K/mTOR信号通路促进子宫内膜癌细胞增殖的机制研究  

Mechanism of Testosterone Promoting Endometrial Carcinoma Cell Proliferation Through PI3K/mTOR Signaling Pathway

作　　者：汤艳红[1] 魏江[2] 刘霞[1] 仲艳 于洋[2] TANG Yanhong;WEI Jiang;LIU Xia;ZHONG Yan;YU Yang(Department of Gynecology, Changzhou First People's Hospital, Changzhou 213000, China;Comprehensive Laboratory, Changzhou First People's Hospital, Changzhou 213000, China)

机构地区：[1]常州市第一人民医院妇科,江苏常州213000 [2]常州市第一人民医院综合实验室,江苏常州213000

出　　处：《肿瘤基础与临床》2018年第5期372-375,共4页journal of basic and clinical oncology

摘　　要：目的证实睾酮促进子宫内膜癌Ishikawa细胞增殖的效应并探讨其具体的分子机制。方法常规培养子宫内膜癌Ishikawa细胞后,CCK-8法检测不同浓度睾酮对子宫内膜癌Ishikawa细胞生长的影响,Western blot和qPCR法检测凋亡相关基因B细胞淋巴瘤/白血病-2(Bcl-2)、B细胞淋巴瘤/白血病-2相关X蛋白(Bax)的表达水平,同时检测PI3K/mTOR信号通路相关蛋白PI3K和mTOR的活化水平。结果 10、20、40、80 ng·mL^(-1)睾酮作用于子宫内膜癌Ishikawa细胞48 h后,睾酮以剂量依赖性的方式促进细胞增殖。使用20 ng·mL^(-1)睾酮作用于细胞不同时间后,细胞倍增时间显著缩短(P<0.05)。Western blot和qPCR法结果表明,20 ng·mL^(-1)睾酮作用于细胞后显著上调了Bcl-2的表达水平(P<0.05),同时显著降低了Bax的表达水平(P<0.05)。Western blot发现20 ng·mL^(-1)睾酮作用于细胞后,PI3K和mTOR的活化水平显著上调(P<0.05)。结论睾酮能够促进子宫内膜癌Ishikawa细胞增殖,该效应可能与激活PI3K/mTOR信号通路而调节其下游基因Bcl-2、Bax的表达有关。Objective To confirm the effect of testosterone on the proliferation of endometrial carcinoma Ishikawa cells and to explore its molecular mechanism.Methods The effects of testosterone at different concentrations on the growth of Ishikawa cells were detected by CCK-8method after the normal culture of Ishikawa cells.The expressions of apoptosis-related gene Bcl-2and Bax were detected by Western blot and qPCR,and the activation levels of PI3K/mTOR signal transduction related proteins activated PI3K and mTOR were also detected.Results The concentration was10,20,40,8.0ng·mL^-1testosterone stimulated the proliferation of Ishikawa cells in a dose-dependent manner after48h.The cell doubling time was significantly shortened after the treatment of20ng·mL^-1testosterone for different time(P<0.05).The results of Western blot and qPCR showed that the expression level of Bcl-2gene were up-regulated by testosterone for20ng·mL^-1(P<0.05),and the expression level of Bax gene were significantly decreased(P<0.05).The activation levels of PI3K and mTOR were significantly up-regulated by testosterone(P<0.05).Conclusion Testosterone can promote the proliferation of endometrial carcinoma Ishikawa cells,and this effect may be produced by activating the PI3K/mTOR signaling pathway and regulating the expressions of Bcl-2and Bax.

关 键 词：睾酮 PI3K/mTOR信号通路 子宫内膜癌 细胞增殖 

分 类 号：R737.33[医药卫生—肿瘤] R730.23[医药卫生—临床医学]