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Cadherin-26 Promotes Airway Remodeling via Stabilizing Epithelial Expression of the Epidermal Growth Factor Receptor in Asthma

Year: 2026

Type: article

Abstract: PURPOSE: Activation of epidermal growth factor receptor (EGFR) signaling in airway epithelial cells leads to epithelial-mesenchymal transformation (EMT) and airway remodeling in asthma. However, the mechanism regulating EGFR expression is not fully understood. We hypothesized that cadherin-26 (CDH26), a highly expressed cadherin in airway epithelium, promotes airway remodeling via regulating EGFR signaling in asthma. METHODS: -deficient mice. The role and mechanism of CDH26 in epidermal growth factor (EGF)-induced EMT were measured in cultured human bronchial epithelial BEAS-2B cells. RESULTS: deficiency significantly reduced airway hyperresponsiveness and remodeling in HDM-sensitized and -challenged mouse model. In cultured human bronchial epithelial BEAS-2B cells, CDH26 knockdown inhibited EGF-induced EMT, whereas overexpression of CDH26 promoted EGF-induced EMT. Furthermore, CDH26 knockdown suppressed EGF-induced activation of EGFR signaling including phosphatidylinositol 3-kinase and AKT phosphorylation. By contrast, CDH26 overexpression intensified EGF-induced activation of EGFR signaling. Mechanistically, CDH26 knockdown promoted the proteasomal degradation of the EGFR. CONCLUSIONS: CDH26 promoted airway remodeling via stabilizing the epithelial expression of EGFR and sustaining the activation of EGFR signaling in asthma. Thus, CDH26 can be a potential therapeutic target for airway remodeling in asthma.

Source: Allergy Asthma and Immunology Research

DOI: 10.4168/aair.2026.18.5.702