Role and mechanism of microRNA-423-5p targrted FOXP4 regulation in pulmonary fibrosis

Pulmonary fibrosis (PF) is a common disease that can severely affect patients’ prognosis. Epithelial-mesenchymal transition (EMT) plays a critical role in this process, and several studies have demonstrated that certain microRNAs contribute to the development of EMT. The aim of the present study was to investigate the function of miR-423-5p in PF processes and its underlying mechanism. A549 cells were used to construct an EMT model for PF. Fluorescence in situ hybridization analysis, RNA pull-down assay, and luciferase reporter assay were employed to identify the target gene of miR-423-5p. Additionally, wound healing assay, Transwell migration assay, enzyme-linked immunosorbent assay (ELISA), RT-qPCR, Western blot assay, and immunofluorescence staining were conducted to determine the function of miR-423-5p and its target gene in the EMT process in PF. Our study suggested that overexpression of miR-423-5p facilitates TGF-β1-induced EMT in A549 cells and vice versa. Furthermore, FOXP4 was identified as a potential target gene of miR-423-5p. In summary, overexpression of miR-423-5p could promote the EMT process in PF by downregulating FOXP4 expression. <fig><object-id>erj;64/suppl_68/PA3378/F1</object-id><object-id>F1</object-id><object-id>F1</object-id><graphic></graphic></fig> <fig><object-id>erj;64/suppl_68/PA3378/F2</object-id><object-id>F2</object-id><object-id>F2</object-id><graphic></graphic></fig>