FERMT1 contributes to the epithelial-mesenchymal transition of chronic rhinosinusitis with nasal polyps via PI3K/Akt signaling

• DOI: 10.1016/j.intimp.2024.113545
• Publication Date: 2024-11-02T22:03:47Z
• Authors: Zihui Dong; Yan Jiang; Jisheng Zhang; Chunge Zheng; Han Chen; Wenrui Tang; Xudong Yan; Longgang Yu; Lin Han; Lin Wang
• Keywords: Nasal Polyps; Chronic Rhinosinusitis

Epithelial-mesenchymal transition (EMT) is a key process of chronic rhinosinusitis with nasal polyps (CRSwNP). The molecular mechanism of EMT in CRSwNP remains unknown. In this study, we aimed to investigate the role of FERMT1 during the EMT process in CRSwNP.Western blotting, qRT-PCR, and immunohistochemistry (IHC) were performed to examine the expression of related proteins and mRNAs. The migration ability of human nasal epithelial cells (HNEpCs) was evaluated with wound scratch assay. RNA sequencing was performed to investigate the downstream genes of FERMT1. The CRSwNP mouse model was established to study the effect of FERMT1 in vivo.We found that FERMT1 was increased in nasal polyp tissues and correlated with the symptom scores of CRSwNP patients. Knockdown of FERMT1 inhibited the EMT process and cell migration induced by TGF-β1 through the PI3K/Akt pathway, and Akt inhibitor partially blocked the EMT induced by FERMT1 overexpression. In the CRSwNP mouse model, FERMT1 knockdown reduced nasal polyp formation and reversed the EMT process.Our data indicate that knockdown of FERMT1 inhibits migration and EMT process of HNEpCs via PI3K/Akt signaling pathway, suggesting that FERMT1 may be a novel and potential therapeutic target for CRSwNP treatment.