Abstract
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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.