Arecoline Promotes Migration of A549 Lung Cancer Cells through Activating the EGFR/Src/FAK Pathway.

摘要: Arecoline is the primary alkaloid in betel nuts, which are known as a risk factor for oral submucosal fibrosis and cancer. Lung cancer severe type of carcinoma with high cell motility that difficult to treat. However, detailed mechanisms correlation between lung not fully understood. Here, we investigated effect on migration lines its potential mechanism through muscarinic acetylcholine receptor 3 (mAChR3)-triggered EGFR/Src/FAK pathway. Our results indicate different concentrations treatment (10 µM, 20 40 µM) significantly increased ability A549 CL1-0 cells promoted formation filamentous actin (F-actin) cytoskeleton, crucial element migration. H460, CL1-5, H520 lines, have higher ability, was affected by treatment. The EGFR/c-Src/Fak pathway, responsible migration, activated treatment, decreased expression level E-cadherin, an epithelial marker, observed Arecoline-treated lines. Blockade pathway inhibitors EGFR (Gefitinib) or c-Src (Dasatinib) prevented Arecoline-promoted cells. Gefitinib Dasatinib disrupted Arecoline-induced localization phospho-Y576-Fak during focal adhesion Interestingly, blocked specific mAChR3 inhibitor (4-DAMP) neutralizing antibody matrix metalloproteinase (MMP7 Matrilysin). Taken together, our findings suggest might play essential role activation line.