中文摘要：

目的 ：探讨前列腺素E2（PGE2）上调人卵巢癌SKOV3细胞CXC趋化因子受体4（CXC chemokine receptor 4,CXCR4）的表达从而促进细胞侵袭能力的机制。方法：用PGE2、EP1受体激动剂或抑制剂、CXCR4抑制剂、蛋白激酶C（PKC）抑制剂和钙离子螯合剂处理SKOV3细胞,通过real-time PCR、Western blot、Transwell实验检测CXCR4 m RNA水平、蛋白水平以及细胞的侵袭能力。结果：5μmol/L PGE2处理SKOV3细胞后,CXCR4 m RNA及蛋白水平与对照组相比分别上升了60.33%、122.88%（P均〈0.01）,细胞的侵袭能力较对照组增强了112.24%（P〈0.01）;而经10μmol/L CXCR4抑制剂AMD3465处理后,细胞的侵袭水平较PGE2处理组下降了54.00%（P〈0.05）;5μmol/L EP1受体激动剂17-PT-PGE2处理SKOV3细胞后,CXCR4 m RNA及蛋白水平与对照组相比分别上升了47.90%（P〈0.01）、85.56%（P〈0.05）,细胞的侵袭能力较对照组增强了108.79%（P〈0.01）;而10μmol/L EP1受体抑制剂sc-51322处理后,CXCR4蛋白表达水平较PGE2处理组下降了54.86%（P〈0.05）,细胞的侵袭水平较PGE2处理组下降了65.37%（P〈0.05）;5μmol/L PKC抑制剂BIS-1、10μmol/L钙离子螯合剂BAPTA-AM处理后,CXCR4蛋白表达水平较17-PT-PGE2处理组分别下降了57.38%、56.14%（P均〈0.05）,细胞的侵袭水平较17-PT-PGE2处理组下降了52.63%、55.26%（P〈均0.05）。结论：PGE2可通过激活EP1受体经Gαq/Ca2＋/PKC信号转导通路上调卵巢癌SKOV3细胞CXCR4的表达,从而增强肿瘤细胞的侵袭能力。

英文摘要：

Objective：To investigate the effect of prostaglandin E2 （PGE2） on the invasion ability of ovarian cancer SKOV3 cell via upregulating the receptor of stromal cell-derived factor-I （chemokine receptor 4,CXCR4）. Methods：SKOV3 cells were treated with PGE2,EP1 receptor agonist,CXCR4 antagonist,EP1 receptor antagonist,protein kinase C （PKC） inhibitor and Ca2＋ chelating agent. Real-time PCR, Western Blot and Transwell were performed to detect the levels of CXCR4 mRNA and CXCR4 protein as well as the invasion ability in SKOV3 cells. Results：The mRNA level of CXCR4 increased by 60.33%（P 〈0.01）,while the level of CXCR4 protein increased by 122.88%（P 〈 0.01 ）,and the invasion ability of SKOV3 ceils increased by 112.24%（P 〈 0.01） after treated with 5 μmol/L PGE2. The invasion ability of SKOV3 cells decreased by 54.00% （P 〈 0.05） after treated with 10 μmol/L CXCR4 antagonist AMD3465 compared with the cells treated with PGE2. When treated with 5 μmol/L EP1 receptor agonist 17-FF-PGE2, the mRNA level of CXCR4 increased by 47.90 % （P 〈0.01）,the level of CXCR4 protein increased 85.56%（P 〈 0.05）,and the invasion ability of SKOV3 cells increased by 108.79%（P 〈 0.01 ）. The protein level decreased by 54.86%（P 〈 0.05） and the invasion ability of SKOV3 cells decreased by 65.37% （P 〈 0.05） after treated with 10 μmol/L EP1 receptor antagonist sc-51322 compared with the cells treated with PGE2. When treated with 5μmol/L PKC inhibitor BIS-1 and 10 μmol/L Ca2＋ chelating agent BAPTA-AM,the protein levels of CXCR4 were decreased by 57.38% （P 〈 0.05） and 56.14%（P 〈 0.05） respectively,and the invasion ability of SKOV3 cells decreased by 52.63%（P 〈 0.05） and 55.26% （P 〈 0.05） respectively compared with the cells treated with 17-PT-PGE2. Conclusion： PGE2 might up-regulate the expression level of CXCR4 through EP1 receptor which could be partly related to the Gαq/ Cαq/PKC signaling pathway in ovarian cancer SKOV3 cells,and promote the tumo