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目的 :通过观察干扰乳腺癌MDA-MB-231细胞内皮蛋白C受体(endothelial protein C receptor,EPCR)表达对内皮细胞的增殖、迁移、脉管形成能力的变化,分析EPCR在肿瘤血管形成中的作用。方法:采用si RNA方法降低人乳腺癌MDA-MB-231细胞EPCR的表达,通过RT-PCR及Western blot技术检测EPCR干扰效果,实验分为EPCR干扰组、无关序列组及未处理组。制备肿瘤条件培养基模拟肿瘤微环境培养HUVECs细胞,通过CCK-8法检测各组内皮细胞增殖能力,Transwell小室检测内皮细胞迁移能力,Matrigel检测内皮细胞脉管形成能力。结果:与未处理组及无关列序组相比,EPCR干扰组细胞的增殖、迁移及脉管形成能力均明显降低(P<0.05)。结论:干扰乳腺癌MDA-MB-231细胞EPCR的表达能够抑制内皮细胞增殖、迁移及脉管形成能力,提示EPCR可能在肿瘤血管形成中起重要作用。
OBJECTIVE: To investigate the effect of EPCR on the proliferation, migration and vascularization ability of endothelial cells in breast cancer MDA-MB-231 cells. effect. Methods: The si RNA method was used to reduce the expression of EPCR in human breast cancer cell line MDA-MB-231. The effect of EPCR was detected by RT-PCR and Western blot. The experiment was divided into EPCR interference group, unrelated sequence group and untreated group. The tumor-conditioned medium was prepared to simulate the tumor microenvironment culture HUVECs cells, the proliferation of endothelial cells was detected by CCK-8 method, the ability of endothelial cell migration was detected by Transwell chamber, and the vascularization ability of endothelial cells was detected by Matrigel. Results: The proliferation, migration and vascularization ability of EPCR interference group were significantly lower than those of untreated group and non-related sequence group (P <0.05). Conclusion: The expression of EPCR in breast cancer MDA-MB-231 cells can inhibit the proliferation, migration and vascularization of endothelial cells, suggesting that EPCR may play an important role in tumor angiogenesis.