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作 者:左建宏[1,2] 李新辉[1] 李茂玉[1] 万恂恂[1] 曾谷清[1] 贺秋艳[1] 李建璜[1] 肖志强[1]
机构地区:[1]中南大学湘雅医院卫生部肿瘤蛋白质组学重点实验室,长沙410008 [2]南华大学公共卫生学院,衡阳421001
出 处:《生物化学与生物物理进展》2011年第9期850-858,共9页Progress In Biochemistry and Biophysics
基 金:国家自然科学基金资助项目(30973290);芙蓉学者特聘教授科学研究基金资助项目(湘教通[2007]362号);湖南省高校科技创新团队支持计划资助项目~~
摘 要:为探讨细胞基质Ⅰ型胶原(Col-Ⅰ)对头颈鳞癌细胞转移和增殖能力的影响,以头颈鳞癌细胞株为对象,运用transwell小室检查细胞的体外迁移能力,用倒置显微镜成像系统检测细胞的运动速度和扩散能力,Western blotting或/和免疫细胞荧光染色检测细胞表面黏附分子E-cadherin的表达和β-catenin的细胞定位,采用MTT以及PCNA的表达水平评价细胞增殖.结果显示,Col-Ⅰ能够促进头颈鳞癌细胞迁移、提高细胞运动速度、加快细胞扩散,其可能机制是通过上调β-连环蛋白磷酸化,从而下调黏附蛋白E-cadherin的表达.Col-Ⅰ还能促进头颈鳞癌细胞的增殖,其可能机制是增加β-catenin的核移位,提高细胞周期蛋白D1(cyclin D1)表达.研究结果表明,Col-Ⅰ通过上调β-catenin磷酸化水平,以及促进β-catenin核移位,从而增强头颈鳞癌细胞的转移和增殖能力.To detect whether Col- I has some contribution to migration and proliferation of head and neck squamous carcinoma cell (HNSCC) in tumor microenvironment, transwells were applied to measure cell migration, cell velocity and cell scattering were analyzed by Zeiss Axiovert inverted microscope. The expression of E-cadherin as one of cell surface adhesion molecules and cell location of β-catenin were detected by Western blotting and/or immunofluorescence, then proliferation was analyzed by MTT and the PCNA expression. Results showed that Col- I promoted cell metastasis, cell velocity and cell scattering, which E-cadherin was repressed possibly by the increased phosphorylation of [3-catenin. The nuclear translocation of β-catenin led to an increasing expression of cyclin D1 and proliferation. Together, a conclusion is made that Col-I promotes HNSCC metastasis via upregulation of phosphorylation of β-catenin and proliferation by the nuclear translocation of β-catenin.
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