Biglycan enhances gastric cancer invasion by activating FAK signaling pathway

被引：107

作者：

Hu, Lei ^{[1
]}

Duan, Yan-tao ^{[1
]}

Li, Jian-fang ^{[1
]}

Su, Li-ping ^{[1
]}

Yan, Min ^{[1
]}

Zhu, Zheng-gang ^{[1
]}

Liu, Bing-ya ^{[1
]}

Yang, Qiu-meng ^{[1
]}

机构：

[1] Shanghai Jiao Tong Univ, Sch Med, Shanghai Key Lab Gastr Neoplasms, Shanghai Inst Digest Surg,Ruijin Hosp, Shanghai 200030, Peoples R China

来源：

ONCOTARGET | 2014年 / 5卷 / 07期

基金：

中国国家自然科学基金; 高等学校博士学科点专项科研基金;

关键词：

BGN; Gastric cancer; Metastasis; FAK; FOCAL ADHESION KINASE; SQUAMOUS-CELL CARCINOMA; EXTRACELLULAR-MATRIX; PANCREATIC-CANCER; POOR-PROGNOSIS; COLON-CANCER; EXPRESSION; METASTASIS; LOCALIZATION; MALIGNANCY;

D O I：

10.18632/oncotarget.1871

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Biglycan (BGN) is an important member of small leucine-rich proteoglycans family, and has been implicated in oncogenesis and development of various human cancer types. Here we report that BGN promotes tumor invasion and metastasis of gastric cancer both in vitro and in vivo. BGN expression is significantly higher in gastric cancer tissues and associated with lymph node metastasis, depth of tumor invasion and TNM stage. BGN enhances gastric cancer cell wound healing, migration and invasion ability as well as the tube formation ability of endothelial cells in vitro. Animal experiments results in vivo are consistent with outcomes in vitro. BGN induces increased phosphorylation of FAK (Tyr576/577, Tyr925 and Tyr397) and Paxillin. These results indicate that BGN is upregulated, and plays an oncogenic role, in gastric cancer metastasis by activating the FAK signaling pathway.

引用

页码：1885 / 1896

页数：12

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