Biglycan及FAK信号通路对结肠癌细胞增殖能力的影响及分子机制

doi:10.11904/j.issn.1002-3070.2015.05.010

实用肿瘤学杂志 ›› 2015, Vol. 29 ›› Issue (5): 428-431.doi: 10.11904/j.issn.1002-3070.2015.05.010

• 辽宁省肿瘤医院院庆专题 • 上一篇下一篇

Biglycan及FAK信号通路对结肠癌细胞增殖能力的影响及分子机制

邢晓静¹, 谷小虎¹, 肖景东²

1.辽宁省肿瘤医院(沈阳 110042);
2.辽宁中医药大学

收稿日期:2015-06-23 出版日期:2015-10-28 发布日期:2015-10-30
通讯作者: 邢晓静,E-mail:13940066477@163.com
作者简介:邢晓静,女,(1974-),博士,副主任医师,从事消化肿瘤的研究
基金资助:
辽宁省自然科学基金(201102111);国家自然科学基金项目(81201968)

Effect of Biglycan and FAK signal pathway on the proliferation of colon cancer cells and its mechanisms

XING Xiaojing¹, GU Xiaohu¹, XIAO Jingdong²

1.Liaoning Cancer Hospital & Institute,Shenyang 110042,China;
2.Liaoning University of Traditional Chinese Medicine

Received:2015-06-23 Online:2015-10-28 Published:2015-10-30

摘要/Abstract

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。

关键词: Biglycan, 局部黏着斑激酶, 结肠癌, 细胞增殖

Abstract: 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),control 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 significantly 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.

Key words: Biglycan, Focal adhesion kinase(FAK), Colon cancer, Proliferation

中图分类号:

R735.3

邢晓静, 谷小虎, 肖景东. Biglycan及FAK信号通路对结肠癌细胞增殖能力的影响及分子机制[J]. 实用肿瘤学杂志, 2015, 29(5): 428-431.

XING Xiaojing, GU Xiaohu, XIAO Jingdong. Effect of Biglycan and FAK signal pathway on the proliferation of colon cancer cells and its mechanisms[J]. PRACTICAL ONCOLOGY JOURNAL, 2015, 29(5): 428-431.

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Biglycan及FAK信号通路对结肠癌细胞增殖能力的影响及分子机制

Effect of Biglycan and FAK signal pathway on the proliferation of colon cancer cells and its mechanisms

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