Abstract
Dysregulated expression of the cell surface protein, CD146, has been implicated in various types of cancer in humans, including in lung cancer. The present study aimed to clarify the mechanism underlying abnormal CD146 expression in human pulmonary large cell neuroendocrine carcinoma (LCNEC) cell lines (NCI-H460 and NCI-H810). The functions of CD146 were investigated by measuring cell migration and viability following CD146 knockdown or overexpression via small interference RNA and plasmid transfection. The findings demonstrated that decreased protein expression of CD146 could inhibit migration and viability in LCNEC cells. Furthermore, CD146 was determined to influence the expression of epithelial-mesenchymal transition markers (epithelial cadherin, vimentin and Snail) and promoted AKT phosphorylation. The present results imply CD146 may function in the migration and proliferation of pulmonary LCNEC cells.