幽门螺杆菌CagA通过B-Raf和JNK2调节原癌蛋白CIP2A表达及其细胞生物学作用研究
发布时间：2018-08-17 08:33
【摘要】：目的了解幽门螺杆菌CagA上调CIP2A表达的分子机制。方法培养AGS细胞和GES-1细胞,一部分细胞分别转染CagA阳性质粒WT-cagA和阴性对照质粒pcDNA3.1;另一部分细胞用B-Raf和JNK2信号抑制剂作用,然后分别转染质粒WT-cagA和质粒pcDNA3.1,Western blot检测CIP2A表达,细胞克隆形成试验检测细胞增殖能力,细胞迁移试验检测细胞迁移能力结果 AGS细胞和GES-1细胞转染CagA阳性质粒WT-cagA后CIP2A表达量增多;细胞经B-Raf和JNK2的信号抑制剂作用后转染CagA阳性质粒WT-cagA,其CIP2A表达量比仅转染质粒WT-cagA的细胞表达量少,细胞的克隆数减少,细胞迁移能力降低。结论幽门螺杆菌CagA进入细胞通过B-Raf和JNK2及其参与的信号途径调节原癌蛋白CIP2A的表达,进而影响细胞的克隆形成能力和迁移能力。
[Abstract]:Objective to investigate the molecular mechanism of CagA upregulation of CIP2A expression in Helicobacter pylori. Methods AGS cells and GES-1 cells were cultured, some of them were transfected with CagA positive plasmid WT-cagA and the other were transfected with B-Raf and JNK2 signal inhibitors, and then transfected with WT-cagA and pcDNA3.1 Western blot to detect the expression of CIP2A. The ability of cell proliferation was detected by cell clone formation assay, and the expression of CIP2A was increased after transfection of CagA positive plasmid WT-cagA into AGS cells and GES-1 cells by cell migration assay. After transfection of WT-cagA into CagA positive plasmid WT-cagA by signal inhibitor of B-Raf and JNK2, the expression of CIP2A was less than that of only transfected plasmid WT-cagA, the number of cell clones was decreased, and the ability of cell migration was decreased. Conclusion Helicobacter pylori CagA enters the cells and regulates the expression of proto-oncoprotein CIP2A through B-Raf, JNK2 and its signal pathway, which affects the ability of cell clone formation and migration.
【作者单位】： 郑州大学第一附属医院麻醉科;泰山医学院病原生物学教研室;泰山医学院附属医院检验科;泰山医学院公共卫生学院;山东省泰山疗养院内科;泰山医学院第二临床医学院;
【基金】：国家自然科学基金项目(No.81602455) 山东省自然科学基金项目(No.ZR2013HM033,ZR2013HL057,ZR2013HL060) 泰山医学院重大科研专项(No.2014GCC10) 泰安市科研课题(No.2015NS2098,2016NS1074,2016NS1089)
【分类号】：R735.2
本文编号：2187060
[Abstract]:Objective to investigate the molecular mechanism of CagA upregulation of CIP2A expression in Helicobacter pylori. Methods AGS cells and GES-1 cells were cultured, some of them were transfected with CagA positive plasmid WT-cagA and the other were transfected with B-Raf and JNK2 signal inhibitors, and then transfected with WT-cagA and pcDNA3.1 Western blot to detect the expression of CIP2A. The ability of cell proliferation was detected by cell clone formation assay, and the expression of CIP2A was increased after transfection of CagA positive plasmid WT-cagA into AGS cells and GES-1 cells by cell migration assay. After transfection of WT-cagA into CagA positive plasmid WT-cagA by signal inhibitor of B-Raf and JNK2, the expression of CIP2A was less than that of only transfected plasmid WT-cagA, the number of cell clones was decreased, and the ability of cell migration was decreased. Conclusion Helicobacter pylori CagA enters the cells and regulates the expression of proto-oncoprotein CIP2A through B-Raf, JNK2 and its signal pathway, which affects the ability of cell clone formation and migration.
【作者单位】： 郑州大学第一附属医院麻醉科;泰山医学院病原生物学教研室;泰山医学院附属医院检验科;泰山医学院公共卫生学院;山东省泰山疗养院内科;泰山医学院第二临床医学院;
【基金】：国家自然科学基金项目(No.81602455) 山东省自然科学基金项目(No.ZR2013HM033,ZR2013HL057,ZR2013HL060) 泰山医学院重大科研专项(No.2014GCC10) 泰安市科研课题(No.2015NS2098,2016NS1074,2016NS1089)
【分类号】：R735.2
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