ArticleJournal of inflammation research2025
Role and Therapeutic Potential of miR-301b-3p in Regulating the PI3K-AKT Pathway via PIK3CB in Eosinophilic Chronic Rhinosinusitis.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Article
- Identification and dual-center histological validation of EMT core genes in chronic rhinosinusitis with nasal polyps: an integrated multi-cohort transcriptomic and single-cell analysis.Frontiers in immunology · 2026Article
- Integrated multi-omics, network pharmacology, and experimental validation reveal the protective mechanisms of curcumol against DSS-induced ulcerative colitis.Frontiers in immunology · 2026Article
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Authors and funding
10 authors.
Funding
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Abstract
Purpose: Type 2 inflammation and epithelial-mesenchymal transition (EMT) are critical components in the pathogenesis of eosinophilic chronic rhinosinusitis (ECRS), yet their upstream regulatory mechanisms remain poorly understood. This study aimed to explore the regulatory role of miR-301b-3p in these mechanisms and evaluate its therapeutic potential. Methods: High-throughput miRNA sequencing of human and mouse nasal mucosa tissues identified miR-301b-3p as a key candidate molecule. Mendelian randomization (MR) analysis confirmed its causal relationship with chronic rhinosinusitis (CRS). The role of miR-301b-3p and its target gene PIK3CB in ECRS was further investigated using bioinformatics analysis, dual-luciferase reporter assays, adeno-associated virus (AAV)-mediated modulation of miR-301b-3p expression, histological staining, and a range of molecular biology techniques to elucidate the underlying mechanisms. The role of PIK3CB was assessed using the PIK3CB inhibitor TGX-221. Results: hsa-miR-301b-3p was significantly downregulated in ECRS patient nasal mucosa (log2FC = -1.636, P = 0.010), and its expression level negatively correlated with disease severity; simultaneously, mmu-miR-301b-3p was significantly downregulated in the ECRS mouse model (log2FC = -2.256, P = 0.041). MR analysis demonstrated a causal relationship between reduced miR-301b levels and increased CRS risk (OR = 0.956; 95% CI, 0.918-0.996; P = 0.033). In vivo experiments revealed that miR-301b-3p knockdown led to PIK3CB upregulation and activation of the PI3K-AKT pathway, triggering type 2 inflammation and EMT. Conversely, overexpression of miR-301b-3p suppressed PIK3CB expression and mitigated these pathological changes. Notably, the PIK3CB inhibitor TGX-221 reversed PI3K-AKT hyperactivation induced by miR-301b-3p knockdown, alleviating type 2 inflammation and EMT. Conclusion: miR-301b-3p regulates type 2 inflammation and EMT in ECRS by targeting PIK3CB and modulating the PI3K-AKT pathway, suggesting both miR-301b-3p and PIK3CB as promising therapeutic targets. Given the limited sample size of this study, we plan to expand our cohort and implement a longitudinal follow-up design to monitor dynamic changes in miR-301b-3p expression and their relationship to disease progression.
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