摘要
目的 研究Biglycan及FAK信号通路对结肠癌细胞增殖的调控作用及其分子机制. 方法 构建Biglycan过表达的人结肠癌HCT116细胞并采用FAK抑制剂处理. 分为5组：正常对照组、空载体对照组、空载体抑制剂处理组、Biglycan过表达组和Biglycan 过表达抑制剂处理组,处理时间为24h .通过Western blot 及MTT 检测的方法,观察各组HCT116 细胞的增殖能力以及FAK、p-FAK、PCNA、p53 的表达情况.结果 过表达Biglycan 能够显著促进HCT116 细胞的增殖以及FAK 的磷酸化（P ＜0.01）,并导致PCNA 表达水平的显著升高和p53 表达水平的显著抑制（P ＜0.01）;而FAK 抑制剂PF-562271 作用能够明显抑制细胞的增殖能力,Biglycan对p-FAK、PCNA、p53 蛋白表达水平的调控被抑制（P ＜0.01）.结论 Biglycan通过促进FAK 信号通路的活化调控结肠癌细胞的增殖.
Objective To investigate the effect of Biglycan and FAK signal pathway on the proliferation of colon cancer cells in vitro and its possible mechanisms.Methods Biglycan expression vector was constructed and transfected into the colon cancer cell line HCT116.FAK inhibitor was used for cell treatment as well.Cells were divided into 5 groups：control group（HCT116）,control group transfected with empty plasmid（Vector）,con-trol group with empty plasmid transfected and inhibitor treatment（Vector＋PF-562271）,group transfected with Biglycan expression vector（Biglycan）,group with Biglycan expression vector transfected and inhibitor treatment （ Biglycan＋PF-562271） .Treatment duration was 24 hours.The expressions of FAK,p-FAK,PCNA and p53 were detected by Western Blot.The proliferation of cells was detected by MTT.Results The overexpression of Biglycan significantly promoted the proliferation of HCT116 and the phosphorylation of FAK（P〈0.01）.It signif-icantly up-regulated PCNA and down-regulated p53（P〈0.01）.The FAK inhibitor PF-562271 treatment could obviously inhibit the proliferation of HCT116,and the regulation of Biglycan on the expression of p-FAK, PCNA.p53 proteins was reversed（P〈0.01）.Conclusion Biglycan regulates the proliferation of colon cancer cells by promoting the activation of FAK signal pathway.
出处
《实用肿瘤学杂志》
CAS
2015年第5期428-431,共4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）
