MCP-1诱导人胃癌细胞NF-κB-p65的表达和核移位  

MCP-1 induces expression of NF-κB-p65 and nuclear translocation in human gastric cancer

作　　者：宋军民[1] 刘明华[1] 李岩[1] 

机构地区：[1]中国医科大学附属盛京医院消化内科,辽宁沈阳110004

出　　处：《胃肠病学和肝病学杂志》2013年第9期841-843,共3页Chinese Journal of Gastroenterology and Hepatology

摘　　要：目的研究MCP-1对人胃癌细胞NF-κB-p65的表达和核移位的影响。方法人胃癌细胞系SGC7901中加入MCP-1及其受体(CCR2)拮抗剂RS102895,应用Western blotting方法分别检测NF-κB-p65和p65-NLS(活性p65)蛋白的表达,同时应用免疫组化方法分别检测42例人胃癌石蜡包埋组织中MCP-1、NF-κB-p65和p65-NLS蛋白的表达。结果 MCP-1能显著上调人胃癌SGC7901细胞NF-κB-p65和p65-NLS蛋白的表达(P<0.01),而RS102895预先处理能显著抑制MCP-1的上调效应(P<0.01);人胃癌组织中MCP-1蛋白与NF-κB-p65和p65-NLS蛋白的表达显著相关(P均<0.05)。结论 MCP-1能显著诱导人胃癌细胞NF-κB-p65的表达和核移位,从而在NF-κB通路的活化过程中发挥作用。Objective To investigate the effect of MCP-1 on expression of NF-κB-p65 and nuclear translocation in human gastric cancer. Methods Human gastric cancer cell line, SGC7901, was treated with MCP-1 with or without pretreatment of MCP-1 receptor （CCR2） antagonist, RS102895, then NF-κB-p65 and p65-NLS （active p65） were examined by Western blotting analysis; MCP-1, NF-κB-p65 and p65-NLS were also examined by immunohistochemical analysis in 42 paraffin-imbedded human gastric cancer tissues. Results MCP-1 upregulated expression of NF-κB-p65 and p65-NLS significantly （P〈0.01）in SGC7901 cells, which was suppressed by pretreatment of RS102895 （ P 〈 0.01 ）. In human gastric cancer tissue, MCP-1 correlated with expression of NF-κB-p65 and p65-NLS significantly （P 〈 0.05）. Conclusion MCP-1 induces expression of NF-κB-p65 and nuclear translocation, and thus plays a role in the activation of NF-κB pathway in human gastric cancer.

关 键 词：胃癌 单核细胞趋化蛋白-1 核因子-ΚB P65 

分 类 号：R735.2[医药卫生—肿瘤]