miR‑155‑5p downregulation inhibits epithelial‑to‑mesenchymal transition by targeting SIRT1 in human nasal epithelial cells
- Niannian Yang
- Hao Cheng
- Qiao Mo
- Xiaobiao Zhou
- Minqiang Xie
Affiliations: Department of Otorhinolaryngology, Shaoyang Central Hospital, Shaoyang, Hunan 422000, P.R. China, Department of Nasopharyngeal Carcinoma, The First People's Hospital of Chenzhou, Southern Medical University, Chenzhou, Hunan 423000, P.R. China, Department of Pathology, Shaoyang Central Hospital, Shaoyang, Hunan 422000, P.R. China, Department of Otorhinolaryngology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, P.R. China
- Published online on: August 27, 2020 https://doi.org/10.3892/mmr.2020.11468
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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.