Abnormal Expression of has-miR-664b-5p in Allergic Rhinitis and Its Possible Impact on the Progression of the Disease

Background Prior microRNA expression profiling investigations have identified hsa-miR-664b-5p as one of the markedly upregulated microRNAs in patients with allergic rhinitis (AR), suggesting its potential important role in the pathogenesis of this condition. This study focused on hsa-miR-664b-5p, elucidate its fundamental mechanistic basis along with its influence on cellular proliferation and apoptotic processes. Methods Using reverse transcription-quantitative polymerase chain reaction, the expression profiles of hsa-miR-664b-5p and EGR2 were examined in nasal mucosal samples obtained from individuals with AR. The diagnostic usefulness of hsa-miR-664b-5p was evaluated through receiver operating characteristic (ROC) analysis. In human nasal epithelial cell lines (RPMI 2650 and primary HNEPCs), apoptotic rates were assessed by flow cytometry, and proliferative capacity was measured using the cell counting kit-8 assay. The targeting interaction between hsa-miR-664b-5p and EGR2 was verified by dual-luciferase reporter assay to investigate its regulatory mechanism. Results Results confirmed that hsa-miR-664b-5p was significantly upregulated in AR nasal mucosal tissues, while EGR2 was downregulated, showing a strong inverse correlation. ROC analysis demonstrated that hsa-miR-664b-5p holds considerable diagnostic value for AR ( area under the curve = 0.875). Overexpression of hsa-miR-664b-5p was found to promote proliferation and inhibit apoptosis in human nasal epithelial cells. Through dual-luciferase reporter assays, EGR2 was identified as a direct target of hsa-miR-664b-5p. Rescue experiments further supported that hsa-miR-664b-5p influences epithelial cell growth and death by specifically repressing EGR2. Conclusion The hsa-miR-664b-5p/EGR2 axis exerts a crucial role in the pathogenesis of AR and could serve as a novel molecular target for the diagnosis and treatment of AR.