Biglycan enhances gastric cancer invasion by activating FAK signaling pathway
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Lei Hu1,*, Yan-tao Duan1,*, Jian-fang Li1, Li-ping Su1, Min Yan1, Zheng-gang Zhu1, Bing-ya Liu1, Qiu-meng Yang1
1 Shanghai Key Laboratory of Gastric Neoplasms, Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China.
* These authors contributed equally to this work
Bing-ya Liu, email:
Qiu-meng Yang, email:
Keywords: BGN, Gastric cancer, Metastasis, FAK
Received: January 1, 2014 Accepted: March 24, 2014 Published: March 26, 2014
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.
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