TMEM106A inhibits cell proliferation, migration, and induces apoptosis of lung cancer cells

In this study, we evaluated the expression profile of TMEM106A in NSCLC tissues and cell line, and explored the roles of TMEM106A in NSCLC cell lines. Our results showed that TMEM106A expression was significantly decreased in human NSCLC tiss ues. In vitro assays showed that TMEM106A expression in NSCLC cell lines was much lower than that in the bronchial epithelial cell line. Besides, overexpression of TMEM106A reduced cell proliferation, migration, and invasion, while induced cell apoptosis in NSCLC cells. TMEM106A overexpression repre ssed epithelial‐mesenchymal transition (EMT), which was illustrated by increased E‐cadherin expression and decreased the expressions of N‐cadherin, and vimentin. In addition, TMEM106A overexpression suppressed the activation of phosphoinositide 3‐kinase/protein kinase B/nuclear factor‐κB (PI3K/Akt/NF‐κB) signaling pathway in NSCLC cells. Our results indicated that TMEM106A acted as a tumor suppressor in NSCLC, and could be a therapeutic target for the management of NSCLC.
Source: Journal of Cellular Biochemistry - Category: Biochemistry Authors: Tags: RESEARCH ARTICLE Source Type: research