miR-155-5p downregulation inhibits epithelial-to-mesenchymal transition by targeting SIRT1 in human nasal epithelial cells

Abstract

Epithelial-to-mesenchymal transition (EMT) in nasal epithelial cells is involved with tissue remodeling of nasal polyps. The present study investigated the molecular mechanisms through which miR-155-5p regulated EMT in chronic rhinosinusitis (CRS). Patients were divided into the following groups: CRSsNP, CRS without nasal polyposis group, CRSwNP, CRS with nasal polyposis and controls. The expression of transforming growth factor (TGF)-β1, EMT markers, sirtuin 1 (SIRT1) and miR-155-5p were determined by western blotting and reverse transcription-quantitative PCR. Cell morphology following TGF-β1 treatment in the presence of miR-155-5p inhibitors or controls was observed under a microscope. Target genes and potential binding sites between miR-155-5p and SIRT1 were predicted by TargetScan and confirmed using dual-luciferase reporter assay. In patients with CRS, the expression levels of E-cadherin were downregulated and the expression levels of TGF-β1, mesenchymal markers and miR-155-5p were upregulated. Additionally, these changes in expression levels were reduced or increased to a greater extent in the CRSwNP group compared with the CRSsNP group. Furthermore, TGF-β1 expression promoted EMT in human nasal epithelial cells (HNEpCs) and upregulated miR-155-5p expression. These effects were reversed by miR-155-5p inhibitors. Additionally, SIRT1 was predicted as a target gene of miR-155-5p. Downregulation of miR-155-5p upregulated epithelial marker expression and downregulated mesenchymal marker expression by regulating SIRT1. Therefore, the downregulation of miR-155-5p inhibited EMT in HNEpCs by targeting SIRT1.