Effects Of Epidermal Growth Factor Receptor Signal Pathway On Proliferation, Invasion And E-Cadherin/Vimentin Protein Expression In Laryngeal Carcinoma Hep-2 Cells

Epidermal growth factor receptor (EGFR) is one transmembrane receptor with a high expression in more than 90% of head-neck squamous carcinoma cells. This study investigated the role of EGFR signal pathway on proliferation, invasion and expression of related proteins E-cadherin/Vimentin expression in laryngeal carcinoma cells. Laryngeal carcinoma Hep-2 cells were treated with EGFR agonist EGF or inhibitor Gefitinib followed by measuring cell cycle, proliferation index (PI) and apoptosis by flow cytometry. Transwell assay was employed for cell invasion and migration. Western blotting was further employed to test E-cadherin and Vimentin level. Compared to blank control group, EGF-treated cells had significantly lower S percentage of cell cycle at 6 h, 12 h and 24 h, plus higher PI. With prolonged incubation time, S ratio and PI were further significantly elevated, with more potent cell invasion and migration abilities, lower E-cadherin and Vimentin protein levels (p < 0.05). Gefitnib significantly elevated S ratio at 6 h, 12 h and 24 h cell cycle, reduced PI, invasion or migration ability, as upregulated E-cadherin and downregulated Vimentin protein (p < 0.05). Suppressing EGFR signal pathway could inhibit proliferation of laryngeal carcinoma cells, decrease cell invasion or migration, upregulate E-cadherin and downregulate Vimentin.