TMC5 promotes lung adenocarcinoma cell proliferation, migration and invasion by regulating epithelial-mesenchymal transition

Abstract

Background/purposeIn recent years, evidence has indicated that transmembrane channel-like 5 (TMC5) plays an important role in various cancers. Previously, one study showed that TMC5 was highly expressed in lung adenocarcinoma (LUAD), but its mechanism in LUAD remained unclear. In this study, we aimed to investigate the effects of TMC5 and its underlying mechanisms in LUAD progression. MethodsThe expression level of TMC5 in LUAD tissues was detected by real-time quantitative PCR. TMC5 was knocked down in A549 and H1437 cell lines using lentiviral transfection. The oncogenic effect of TMC5 on LUAD cell proliferation was evaluated by CCK-8 assay and colony formation assay. Transwell assay was employed to assess migration and invasion. ResultsTMC5 was overexpressed in LUAD tissues compared with normal tissues. Suppression of TMC5 expression reduced proliferation, migration, and invasion, while also decreasing the expression of mesenchymal markers and increasing epithelial markers in A549 and H1437 cells. Conversely, higher TMC5 expression significantly increased the expression of mesenchymal markers and decreased epithelial markers. ConclusionTMC5 facilitates the malignant behaviors of LUAD cells by regulating epithelial-mesenchymal transition, suggesting its potential as a promising diagnostic and therapeutic target.