Abstract

Objective: To investigate the inhibitory effect of Icotinib on proliferation and epithelial-mesenchymal transition of A549 cells. Methods: A549 cells were treated with Icotinib of different concentrations. The morphology of the cells was observed by inverted phase contrast microscope. The effect of different concentrations of Icotinib on the proliferation inhibition rate of A549 cells was detected by MTT assay. Flow cytometry was used to detect effect of Icotinib on the apoptosis rate of A549 cells. ELISA assay was used to detect the expression of EMT-related proteins, E-cadherin, N-cadherin, Vimentin and fibronectin, in A549 cells cultured supernatant. Transwell assay was used to examine the effects of different concentrations of Icotinib on the migration and invasion abilities of A549 cells. Results: Morphological changes were observed after A549 cells exposed to different concentrations of Icotinib for 48 hours. The inhibition rate of proliferation for each treatment group increased from MTT assay results. Flow cytometry results showed that cell apoptosis rate was significantly increased. Expression of E-cadherin was up-regulated and expression of N-cadherin, Vimentin and fibronectin were down-regulated from ELISA results. A549 cell migration and invasion abilities were significantly suppressed by Icotinib at different concentrations. Conclusion: Icotinib inhibits A549 cell proliferation, migration and invasion in both concentration and time-dependent manners, in turn it promotes A549 cell apoptosis in the same way. Icotinib also inhibits epithelial-mesenchymal transition by regulating EMT-related proteins expression in A549 cells.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.