miR-1287-5p upregulation inhibits the EMT and pro-inflammatory cytokines in LPS-induced human nasal epithelial cells (HNECs)

BackgroundChronic rhinosinusitis is an intractable symptom that influences daily lives of patients. miR-1287-5p was discovered to play a suppressive role in cervical cancer and HBV-related infection.PurposeThis study investigated the potential role of miR-1287-5p in the in-vitro model of chronic rhinosinusitis.MethodsGSE169376 dataset was analyzed and differential miRNAs in nasal mucosa tissues in the chronic rhinosinusitis group were screened out. LPS was used to treat HNECs for 12h, 24h and 48h. Cells underwent LPS treatment after SNAI1 downregulation, miR-1287-5p upregulation or pretreatment of the HMGB1 inhibitor, Glycyrrhizin. RT-PCR was used to measure the RNA expression of miR-1287-5p, SNAI1 and HMGB1. ELISA was used for the detection of IL-6, IL-8, TNF-α changes. Targetscan and starBase were used to predict the targets (SNAI1 and HMGB1) of miR-1287-5p. Dual-luciferase reporter assays were applied to validate this. Western blot was used to analyze the protein changes of Snai1, Vimentin, E-cadherin and HMGB1.ResultsmiR-1287-5p was downregulated in the chronic rhinosinusitis group and decreased after LPS treatment in HNECs. The upregulation of miR-1287-5p inhibited IL-6, IL-8, TNF-α and EMT. miR-1287-5p targeted and inhibited SNAI1 and HMGB1. SNAI1 downregulation led to inhibition in EMT while loss of HMGB1 contributed to the decrease in pro-inflammatory cytokines. Knockdown of SNAI1 decreased HMGB1, resulting in the reduction of pro-inflammatory cytokines while HMGB1 inhibitor reduced SNAI1 and thus suppressed the EMT process.ConclusionmiR-1287-5p downregulation was associated with chronic rhinosinusitis and its upregulation inhibited the EMT and inflammation in LPS-induced HNECs through Snai1/HMGB1 pathway.