EPCR通过活化PAR-1促进人乳腺癌MCF-7细胞增殖及迁移  

Endothelial cell protein C receptor promotes human breast cancer cell MCF-7 proliferation and migration by activating PAR-1

作　　者：汤洋洋 徐炎炎 杨红丽 卓倩 王庆苓 TANG Yang-yang, XU Yan-yan, YANG Hong-li, ZHUO Qian, WANG Qing-ling(Department of Pathology, Xuzhou Medical University, Xuzhou 221004, Chin)

机构地区：[1]徐州医科大学病理学教研室,徐州221004

出　　处：《临床与实验病理学杂志》2018年第3期244-247,共4页Chinese Journal of Clinical and Experimental Pathology

基　　金：国家自然科学青年基金(81101493)

摘　　要：目的探讨内皮细胞蛋白C受体(endothelial protein C receptor,EPCR)对乳腺癌增殖、迁移的影响及机制研究。方法采用siRNA技术降低人乳腺癌MCF-7细胞中EPCR的表达;添加抗PAR-1抗体阻断PAR-1作用,然后采用CCK-8检测细胞的增殖能力、Transwell检测迁移能力、Cell-ELISA检测EPCR对PAR-1活性的影响。结果 EPCR干扰后,与空白对照组及无关序列组相比,EPCR干扰组MCF-7细胞的增殖及迁移能力均明显降低(P<0.05)。抗PAR-1抗体处理后,与空白对照组相比,PAR-1抗体处理组细胞的增殖迁移能力均明显降低(P<0.05)。并且Cell-ELISA结果显示EPCR干扰组未裂解活化的PAR-1抗体结合率明显升高(P<0.05)。结论 EPCR可以通过活化PAR-1促进人乳腺癌MCF-7细胞增殖迁移。Endothelial cell protein C receptor promotes human breast cancer cell MCF-7 proliferation and migration by activating PAR-1 TANG Yang-yang, XU Yan-yan, YANG Hong-li, ZHUO Qian, WANG Qing-ling （Department of Pathology, Xuzhou Medical University, Xuzhou 221004, China）ABSTRACT Purpose To investigate the effect of EPCR on the proliferation and migration, and to explore the molecular mechanism of EPCR affecting the tumor growth and metastasis in human breast cancer cell line MCF-7. Methods MCF-7 cell was transfected with EPCR siRNA and treated with anti-PAR-1 antibody. Then CCK-8 assay was performed to determine the proliferation of MCF-7 cell. Transwell migration assay was em- ployed to determine the cell＇ s migration. Cell-ELISA was used to detect the activation of PAR-1 on the membranes of MCF-7. Result After EPCR siRNA transfection, the proliferation and mi- gration ability of the MCF-7 in the interference of EPCR gene group was significantly decreased compared with the negativecontrol and untreated control group. After treated with anti-PAR- 1 antibody, the proliferation and migration of ability of MCF-7 were decreased significantly compared with the negative control group and the untreated control group. Cell-ELISA assay indica- ted that the activation of PAR-1 in the cells surface of MCF-7 cell in the EPCR gene interference group was mitigated versus the negative control and untreated control group. Conclusion EPCR may promote the proliferation and migration of MCF-7 cell by activating PAR-1.

关 键 词：乳腺肿瘤 EPCR PAR-1 增殖 迁移 

分 类 号：R73-3[医药卫生—肿瘤] R737.9[医药卫生—临床医学]