Abstract
We have previously shown that integrin β1 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 β1 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 β1 reverses EMT, meanwhile overexpression and activation of integrin β1 aggravates EMT. Lastly, we further identified that integrin β1 enhanced EMT via FAK-AKT signaling pathway. These findings highlight a novel relation of integrin β1 and EMT in EGFR TKI resistant NSCLC.
Keywords: Integrin beta 1, epidermal-mesenchymal transition, EGFR TKI, resistance, non-small cell lung cancer
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