ECRG2基因通过干扰uPAR与β1整合素的相互作用抑制肿瘤细胞侵袭迁移  

ECRG2 gene regulates tumor cell migration/invasion through disrupting uPAR/β1 integrin interactions

作　　者：成晓龙[1] 宋肖静[2] 崔永萍[2] 

机构地区：[1]山西医科大学人体解剖教研室,太原030001 [2]山西医科大学细胞生物学与遗传学教研室

出　　处：《山西医科大学学报》2008年第12期1061-1063,共3页Journal of Shanxi Medical University

基　　金：国家自然科学基金资助项目(30500588);山西省自然科学基金资助项目(20051089)

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。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.

关 键 词：ECRG2 侵袭迁移 UPAR Β1整合素 

分 类 号：R730.2[医药卫生—肿瘤]