中文摘要：

目的探讨ECRG2影响人成纤维肉瘤HT1080细胞侵袭迁移的分子机制。方法利用ECRG2可诱导表达系统观察该基因对uPAR与β1整合素相互作用及下游Src/MAP信号通路的影响。结果ECRG2基因通过干扰uPAR与β1整合素的相互作用、阻断uPAR/β1/Src/MAP信号通路,从而抑制HT1080细胞的侵袭迁移;ECRG2基因缺失导致uPAR/β1整合素/Src/MAP信号通路活性增强,促进HT1080细胞的侵袭迁移。结论ECRG2基因通过干扰uPAR/β1整合素/Src/MAP信号通路参与肿瘤细胞侵袭迁移的调控。

英文摘要：

Objective To explore the molecular mechanisms of ECRG2 regulating HT1080 cell migration/invasion. Methods ECRG2 gene was overexpressed or depleted by using Tet-On inducible system. The interaction between uPAR and β1 integrin and Src/ MAP kinase activity were examined by using immunoprecipitation-Westem blotting. Results Overexpression of ECRG2 gene dismpted the interaction between uPAR and β1 integrin, blocked Src/MAP kinase pathway, thus inhibited HT1080 cell migration/invasion. Depletion of ECRG2 gene resulted in enhanced uPAR/β1 integrin/Src/MAP kinase signaling, and promoted HT1080 cell migration/invasion. Conclusion ECRG2 regulates tumor cell migration/invasion through uPAR/β1 integrin/Src/MAP kinase pathway, and may represent a novel therapeutic target for cancer.