J Cancer 2019; 10(24):6014-6024. doi:10.7150/jca.35017 This issue
1. Department of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou 215006, China
2. Suzhou Key Laboratory for Respiratory Diseases, Suzhou 215006, China
3. Institute of Respiratory Diseases, Soochow University, Suzhou 215006, China
*These authors contributed equally to this work
Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide. SMAD family member 2 (SMAD2) is a key element downstream of the transforming growth factor beta (TGF-β) signaling pathway that regulates cancer metastasis by promoting the epithelial-mesenchyme transition (EMT). MicroRNA miR-486-5p is a tumor suppressor in NSCLC progression. However, it remains unclear whether miR-486-5p is implicated in TGF-β signaling and EMT in NSCLC. In the present study, high expression of SMAD2 mRNA was detected in NSCLC tissues and cell lines, and was associated with poor survival of patients with NSCLC. By contrast, miR-486-5p was downregulated in NSCLC tissues and cell lines. In silico prediction showed that SMAD2 was a potential target of miR-486-5p. The prediction was verified using a dual-luciferase reporter assay. Transwell assays showed that knockdown of SMAD2 inhibited TGF-β-induced EMT and migration and invasion in NSCLC cells. Similarly, miR-486-5p overexpression suppressed TGF-β-induced EMT and migration and invasion of NSCLC cells. The present study provides a new insight into the role of miR-486-5p in regulating TGF-β-mediated EMT and invasion in NSCLC.