S100A6上调人乳腺癌细胞系MCF-7中β-catenin及其机制  

S100A6 upregulates β-catenin and its mechanism in human breast cancer cell MCF-7

作　　者：武睿[1] 段亮[1] 叶立伟[1] 张昀源[1] 陈娴[1] 王海燕[1] 杨霞[1] 罗进勇[1] 周兰[1] 

机构地区：[1]重庆医科大学检验医学院临床检验诊断学教育部重点实验室,重庆400016

出　　处：《基础医学与临床》2013年第7期793-798,共6页Basic and Clinical Medicine

基　　金：国家自然科学基金(30772548)

摘　　要：目的探讨钙细胞周期蛋白S100A6对人乳腺癌细胞系MCF-7中β-catenin的影响及其机制。方法分别用表达S100A6及其siRNA的重组腺病毒AdS100A6与AdsiS100A6处理MCF-7细胞,RT-PCR、Western blot和免疫细胞化学检测β-catenin、E-钙黏蛋白(E-cadherin)和磷酸化糖原合酶激酶3β(p-GSK3β)表达或分布的变化。结果在MCF-7细胞中,S100A6可以上调β-catenin的蛋白表达水平(P<0.01),但对其mRNA表达无显著性影响;S100A6对E-cadherin的mRNA表达、蛋白质表达水平及分布均无显著性影响;S100A6可以提高β-catenin降解复合体的主要成员GSK3β磷酸化水平(P<0.01)。结论 S100A6上调β-catenin的可能机制是通过促进GSK3β磷酸化失活,而不是通过调节E-cadherin实现的。Objective To investigate the impact of S100A6 on β-catenin and its molecular mechanism in human breast cancer cell line MCF-7. Methods MCF-7 cells were infected by recombinant adenoviruses carrying human S100A6 and its siRNA gene, AdS100A6 and AdsiS100A6 respectively. RT-PCR,Western blot and immunocyto- chemistry were used to detect the expression and/or distribution of β-catenin, E-cadherin and p-GSK313. Results In MCF-7 cells, SIOOA6 increased the protein level of β-catenin（P 〈0. 01 ） ,but no significant difference in tran- scriptional level of β-catenin between S100A6 group and control group（ GFP group） （P 〉 0. 05 ） ; The mRNA, pro- tein level and distribution of E-cadherin had no significant difference between S100A6 group and control group（ P 〉 0.05 ） ; S100A6 increased phosphorylation of GSK3β （P 〈 0. 01 ）. Conclusions S100A6 may upregulate β-catenin by promoting phosphorylation of GSK3β, rather than via effect on E-cadherin.

关 键 词：S100A6 Β-CATENIN E-CADHERIN GSK3Β 

分 类 号：R737.9[医药卫生—肿瘤]