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作 者:崔红霞[1] 孙超[1] 李刚[1] 王宏兰[1] 夏春辉[1] 王玉春[1]
机构地区:[1]齐齐哈尔医学院,161006
出 处:《齐齐哈尔医学院学报》2017年第20期2357-2359,共3页Journal of Qiqihar Medical University
基 金:黑龙江省自然科学基金项目(H201353)资助
摘 要:目的探讨ST3Gal Ⅲ沉默抑制乳腺癌MDA-MB-231细胞侵袭能力的分子机制。方法利用本室建立的稳定沉默ST3Gal Ⅲ基因的乳腺癌细胞(ST3Gal Ⅲ基因的2个靶向序列分别记作shRNA-2,shRNA-4)、人乳腺癌细胞MDA-MB-231细胞未转染组(M组),转染慢病毒对照组pGLV3-H1-GFP(P组),采用western blot检测侵袭相关分子整合素α3、基质金属蛋酶(matrix Mmetalloproteinase,MMP)-2、MMP-9黏着斑蛋白激酶(Focal Adhesion Kinase,FAK)蛋白的表达。结果与M组、P组相比,shRNA细胞侵袭相关分子整合素α3蛋白表达明显下调,MMP-2、MMP-9蛋白表达显著降低,p-FAK蛋白表达明显下调,差异有统计学意义(P<0.05)。结论 ST3Gal Ⅲ沉默可能通过FAK通路下调黏附侵袭相关分子整合素α3、基质金属蛋白MMP-2、-9表达从而抑制乳腺癌细胞侵袭。Objective To investigate the molecular mechanism of invasion silencing ST3Gal Ⅲ involved.Methods The 2 target sequences of breast cancer cells with stable ST3Gal gene( ST3Gal Ⅲ gene) were recorded as shRNA-2,shRNA-4 respectively,and the human breast cancer cell MDA-MB-231 cells were not transfected( group M),and then transfected into lentivirus control group p GLV3-H1-GFP( group P). Western blot was used to detect the expression of invasion related molecules,integrin alpha 3,matrix Mmetalloproteinase( MMP)-2 and MMP-9 plaque protein kinase( Focal Adhesion Kinase). Results The results showed that the expression of integrin α3,MMP-2/-9 were significantly decreased in shRNA cells compared with that in M and P( P〈0.05). The p-FAK expression was downregulated than those in the other 2 groups( P〈0.05). Conclusions The ST3Gal Ⅲ silencing could effectively inhibit invasion of breast cancer by reducing expression of integrin α3 and MMP-2,-9 through FAK pathway.
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