趋化因子受体CXCR7与胰腺癌发生发展的关系研究  

Research on the relationship between the novel chemokine receptor CXCR7 and pancreatic carcinoma development and progression

作　　者：张鑫[1] 刘臻[1] 孙韶龙[1] 吴鑫[1] 孟祥鹏[1] 姚威[1] 王宝胜[1] 

机构地区：[1]中国医科大学附属盛京医院胰腺内分泌外科,沈阳110004

出　　处：《中国普外基础与临床杂志》2017年第8期940-945,共6页Chinese Journal of Bases and Clinics In General Surgery

基　　金：辽宁省科学技术计划项目(项目编号:2013225021)

摘　　要：目的探讨趋化因子受体CXCR7在胰腺癌发生发展中的作用。方法应用shRNA构建稳定敲除CXCR7的胰腺癌细胞,并采用MTT法、流式细胞术和侵袭实验分别检测胰腺癌细胞的增殖、细胞周期、凋亡和侵袭能力变化。结果与空白对照组相比,转染CXCR7-shRNA慢病毒表达载体AsPC-1细胞中CXCR7在mRNA及蛋白水平表达均显著降低(P<0.05),细胞增殖和侵袭能力显著降低(P<0.05),胰腺癌细胞休眠于G0/G1期,同时细胞凋亡率明显增加。结论CXCR7在调节胰腺癌细胞生长和侵袭能力中扮演重要角色,并且为胰腺癌的治疗提供了可能的潜在靶点。Objective To investigate the role of chemokine receptor CXCR7 in the development and progression of pancreatic carcinoma. Methods The short hairpin RNA （shRNA） targeting CXCR7 was designed and delivered into AsPC-1 pancreatic carcinoma cells to knock down CXCR7 expression. The cell proliferation, cell cycle, and apoptosis after CXCR7 knockdown was determined by MTT and flow cytometry, respectively. The invasive ability of pancreatic carcinoma cells was evaluated by using the Transwell system. Results Compared with the blank control group （BC group）, transfection of AsPC-1 cells with CXCR7-shRNA resulted in a significantly decreased expression of CXCR7 at both mRNA and protein levels （P〈0.05）, and the ability of proliferation and invasion significantly decreased （P〈0.05）. Knockdown of CXCR7 also significantly increase apoptosis （P〈0.05）, induce cell cycle arrest at G0/G1 phase （P〈0.05）. Condusions Taken together, the present study showes that the knockdown of CXCR7 expression may play an important role in pancreatic carcinoma development, invasion, and metastasis, CXCR7 may be a potential therapeutic target for the treatment of pancreatic carcinoma.

关 键 词：胰腺癌 趋化因子受体CXCR7 增殖 细胞周期 凋亡 侵袭 

分 类 号：R735.9[医药卫生—肿瘤]