Integrin beta 1 enhances the epithelial-mesenchymal transition in association with gefitinib resistance of non-small cell lung cancer

被引:30
作者
Ju, Lixia [1 ]
Zhou, Caicun [2 ,3 ]
机构
[1] Tongji Univ, Sch Med, Shanghai Pulm Hosp, Dept Tradit Chinese Med, Shanghai 200433, Peoples R China
[2] Tongji Univ, Sch Med, Shanghai Pulm Hosp, Dept Oncol, Shanghai 200433, Peoples R China
[3] Tongji Univ, Sch Med, Shanghai Pulm Hosp, Inst Canc, Shanghai 200433, Peoples R China
关键词
Integrin beta 1; epidermal-mesenchymal transition; EGFR TKI; resistance; non-small cell lung cancer; UP-REGULATION; SENSITIVITY; GROWTH; LINES; EGFR; DETERMINES; INHIBITORS; CARCINOMA; APOPTOSIS; KINASE;
D O I
10.3233/CBM-130362
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
We have previously shown that integrin beta 1 associates with gefitinib resistance. As epithelial-mesenchymal transition (EMT) also induces gefitinib resistance in vitro, we wished to determine the relation of them in gefitinib resistance. In this study, we show that integrin beta 1 induced epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) resistance in xenograft tumors and gefitinib-resistant NSCLC tumors acquired EMT phenotype. Furthermore, inhibition of integrin beta 1 reverses EMT, meanwhile overexpression and activation of integrin beta 1 aggravates EMT. Lastly, we further identified that integrin beta 1 enhanced EMT via FAK-AKT signaling pathway. These findings highlight a novel relation of integrin beta 1 and EMT in EGFR TKI resistant NSCLC.
引用
收藏
页码:329 / 336
页数:8
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