Objective To observe the effect of microRNA(miR)-155-5p on epithelial mesenchymal transition (EMT) of human nasal epithelial cells (HNEPC) and its targeting relationship with histone deacetylase 1 (SIRT1).
Methods A total of 50 patients who underwent endoscopic nasal surgery from May 2019 to December 2021 were selected as the research objects. According to whether nasal polyps were complicated or not, the patients were divided into chronic sinusitis with nasal polyps (CRSwNP) group (n=36) and chronic sinusitis without nasal polyps (CRSsNP) group (n=14). At the same time, 20 patients with nasal septum deviation who underwent nasal septum deviation surgery were selected as the control group. MiR-155-5p mimics, miR-155-5p inhibitor, miR-NC and vector plasmids were transfected into cells and divided into miR-155-5p group, miR-155-5p inhibitor group, miR-NC group and Vector group. Real time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression level of miR-155-5p in cells and tissues; western blot and immunofluorescence were used to detect tissue and cell SIRT1, E-cadherin, vimentin α smooth muscle actin (α-SMA), fibronectin expression; the bioinformatics tools and luciferase report experiment were used to analyze the targeting relationship between miR-155-5p and SIRT1.
Results The expression level of miR-155-5p in nasal mucosa of the CRSwNP group was significantly higher than that of the CRSsNP group and control group, and the expression level of miR-155-5p in nasal mucosa of the CRSsNP group was significantly higher than that of the control group (P < 0.01). The expression levels of E-cadherin and SIRT1 in nasal mucosa of the CRSwNP group were significantly lower than those of the CRSsNP group and control group, and the expression levels of E-cadherin and SIRT1 in nasal mucosa of the CRSsNP group were significantly lower than those of the control group (P < 0.05). The expression levels of Vimentin, α-SMA and Fibronectin innasal mucosa of the CRSwNP group were significantly higher than those in the CRSsNP group and control group, and the expression levels of Vimentin, α-SMA and Fibronectin in nasal mucosa of the CRSsNP group were significantly higher than those in the control group (P < 0.05). Up-regulation of miR-155-5p promoted the EMT process of HNEPC cells, while silencing miR-155-5p inhibited the EMT process of HNEPC cells. MiR-155-5p negatively targets SIRT1.
Conclusion The expressions of miR-155-5p and EMT related markers are increased in CRSwNP. Up-regulation of miR-155-5p can promote the EMT process of HNEPC by negatively targeting SIRT1.