Biglycan enhances gastric cancer invasion by activating FAK signaling pathway.
Biglycan enhances gastric cancer invasion by activating FAK signaling pathway.
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Biglycan通过激活FAK信号通路增强胃癌侵袭能力
DOI：
10.18632/oncotarget.1871
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发表时间：
2014-04-15
期刊：
影响因子：
--
通讯作者：
Yang QM
中科院分区：
文献类型：
--
作者：
Hu L;Duan YT;Li JF;Su LP;Yan M;Zhu ZG;Liu BY;Yang QM
双糖蛋白聚糖（BGN）是富含亮氨酸的小分子蛋白聚糖家族的重要成员，与多种肿瘤的发生、发展密切相关。在此，我们报告BGN在体外和体内促进胃癌的侵袭和转移。BGN在胃癌组织中的表达显著增高，且与淋巴结转移、肿瘤浸润深度及TNM分期有关。BGN在体外可增强胃癌细胞的伤口愈合、迁移和侵袭能力以及内皮细胞的管形成能力。体内动物实验结果与体外结果一致。BGN诱导FAK（Tyr 576/577、Tyr 925和Tyr 397）和桩蛋白的磷酸化增加。这些结果表明，BGN上调，并发挥致癌作用，在胃癌转移中激活FAK信号通路。
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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