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目的：探讨前列腺素E2（ProstaglandinE2,PGE2）上调人子宫内膜癌Ishikawa细胞CXCR4（chemokine receptor 4）的表达机制。方法用PGE2、EP1受体激动剂或抑制剂、蛋白激酶C（PKC）抑制剂和钙离子螯合剂处理Ishikawa细胞，通过Real-time PCR、Western Blot实验检测CXCR4 mRNA水平以及蛋白水平。结果5μmol/L PGE2处理Ishikawa细胞后，CXCR4 mRNA水平及蛋白水平与对照组相比分别上升了75.7%（<0.05），70.93%（<0.01）；5μmol/L EP1受体激动剂17-PT-PGE2处理Ishikawa细胞后，CXCR4蛋白水平与对照组相比上升了84.82%%（<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54.62%（<0.05）；5？mol/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50.17%，56.33%(均<0.05)。结论 PGE2可通过激活EP1受体经Ca2+/PKC信号转导通路上调人子宫内膜癌Ishikawa细胞CXCR4的表达。“,”Objective To investigate the ef ect of prostaglandin E2 (PGE2) on the receptor of stromal cel -derived factor-1 (chemokine receptor 4, CXCR4)in Endometrial Cancer Ishikawa cel s. Methods Ishikawa cel s were treated with PGE2, EP1 receptor agonist, EP1 receptor antagonist, protein kinase C (PKC)inhibitor and Ca2+chelating agent, Real-time PCR,Western Blot were employed to detect the level of CXCR4 mRNA and CXCR4 protein in Ishikawa cel s. Results The mRNA level of CXCR4 increased 75.7% ( <0.05),while the level of CXCR4 protein increased 70.93% ( <0.01) after treated with 5μmol/L PGE2. When treated with 5μmol/L EP1 receptor agonist 17-PT-PGE2, the level of CXCR4 protein increased 84.82% ( <0.01).The protein level decreased%54.62%( <0.05) after treated with 10μmol/L EP1 receptor antagonist sc-51322 compared with the cel s treated with PGE2.When treated with 5μmol/L PKC inhibitor BIS-1, 10μmol/L Ca2+chelating agent BAPTA-AM, the protein levels of CXCR4 were decreased 50.17%( <0.05),56.33%( <0.05)compared with the cel s 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 Ca2+/PKC signaling pathway in Endometrial Cancer Ishikawa cel s.