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机构地区:[1]辽宁省肿瘤医院,沈阳110042 [2]辽宁中医药大学
出 处:《实用肿瘤学杂志》2015年第5期444-449,共6页Practical Oncology Journal
基 金:辽宁省自然科学基金(201102111);国家自然科学基金项目(81201968)
摘 要:目的 观察Biglycan对局部黏着斑激酶( Focal adhesion kinase,FAK)活化的影响,探索其是否通过调控FAK信号通路影响结肠癌细胞的侵袭和迁移. 方法 构建过表达Biglycan的人结肠癌细胞系HCT116并施加FAK抑制剂处理. 实验设置空白对照组(HCT116)、空载体对照组(Vector),空载体抑制剂处理组(Vector+PF-562271)、Biglycan过表达组(Biglycan)和Biglycan过表达抑制剂处理组(Bigly-can+PF-562271). 抑制剂处理24 h后,采用Western blot技术检测FAK、p-FAK在各组结肠癌细胞中的表达;采用Transwell实验分析各组结肠癌细胞的侵袭和迁移能力. 结果 Biglycan过表达后会显著提高FAK的磷酸化水平,促进HCT116细胞的侵袭和迁移(P〈0.01);FAK抑制剂PF-562271能够明显降低p-FAK的表达,逆转Biglycan对结肠癌细胞侵袭和迁移能力有影响( P〈0.01). 结论 Biglycan通过激活FAK信号通路影响结肠癌细胞系HCT116的侵袭和转移.Objective To observe the influence of Biglycan on the focal adhesion kinase( FAK) activa-tion and to explore whether it regulates the invasion and metastasis of colon cancer through FAK signaling path-way.Methods The overexpressive plasmid of Biglycan was constructed and then transfected into the colon canc-er cell line HCT116.Meanwhile,FAK inhibitor was used to treat cells.Control group(HCT116),empty plasmid group(Vector),empty plasmid and inhibitor treatment group(Vector +PF -562271),Biglycan overexpression group( Biglycan) ,Biglycan overexpression and inhibitor treatment group( Biglycan+PF-562271) were set.Twen-ty four hours after exposure to inhibitor,the expression of FAK and p-FAK in each group was detected by West-ern Blot.The invasion and metastasis of colon cancer cells was detected by transwell assay.Results Overexpres-sion of Biglycan significantly enhanced the phosphorylation level of FAK and promoted the invasion and metastasis of HCT116(P〈0.01).The inhibitor of FAK PF-562271 could significantly reduce the expression of p-FAK and reverse the effect of Biglycan on the invasion and metastasis of colon cancer cells.Conclusion Biglycan reg-ulates the invasion and metastasis of colon cancer cells through activation FAK signaling pathway.
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