Dysregulation of SMURF1 by miR-1292-5p involves in lung adenocarcinoma EMT via BMPR2/p-Smad5 signal pathway

Abstract

Abstract MicroRNAs have been shown to play a vital role in lung adenocarcinoma (LUAD) progression. In this study, we examined the underlying mechanism and biological functions of miR-1292-5p in LUAD. In LUAD tissues and cell lines, the expression of miR-1292-5p was detected using quantitative real-time polymerase chain reaction. The impact of miR-1292-5p in LUAD cells was assessed both in vitro and in vivo, while the formation of filopodia was analyzed through immunofluorescence staining. Analysis of clinical features revealed the correlation of miR-1292-5p expression and LUAD prognosis. The regulatory relationship of miR-1292-5p and SMURF1 was investigated by dual-luciferase assay and rescue experiment. The signal pathway of epithelial-to-mesenchymal transition was analyzed by western blot. The expression of miR-1292-5p, an upregulated miRNA, was detected in LUAD tissues and cell lines. Its expression showed correlation with the prognosis of LUAD. In vitro and in vivo experiments demonstrated that the overexpression of miR-1292-5p led to the promotion of migration and invasion in LUAD cells. Additionally, it induced the formation of filopodia. Mechanistically, miR-1292-5p targeted SMURF1 to regulate epithelial-to-mesenchymal transition via the BMPR2/p-Smad5 signal pathway in LUAD cells. Our study reveals that dysregulation of SMURF1 targeted by miR-1292-5p influences migration and invasion, and induces epithelial-to-mesenchymal transition by activating the BMPR2/p-Smad5 signal pathway in LUAD.