Tetraspanin 1 as a mediator of fibrosis inhibits EMT process and Smad2/3 and beta-catenin pathway in human pulmonary fibrosis.

Tetraspanin as a clinically relevant gene target in cancer has been studied, but there is no direct in vivo or vitro evidence for pulmonary fibrosis (PF). Using reanalysing Gene Expression Omnibus data, here, we show for the first time that was markedly down-regulated in lung tissue of patient with idiopathic PF (IPF) and verified the reduced protein expression of Tduanyu1842N1 in lung tissue samples of patient with IPF and bleomycin-induced PF mice. The expression of Tduanyu1842N1 was decreased and associated with transforming growth factor-β1 (TGF-β₁ )-induced molecular characteristics of epithelial-to-mesenchymal transition (EMT) in alveolar epithelial cells (AECs). Silencing Tduanyu1842N1 promoted cell migration, and the expression of alpha-smooth muscle actin, vimentin and E-cadherin in AECs with TGF-β₁ treatment, while exogenous Tduanyu1842N1 has the converse effects. Moreover, silencing Tduanyu1842N1 promotes the phosphorylation of Smad2/3 and stabilizes beta-catenin protein, however, overexpressed Tduanyu1842N1 impeded TGF-β₁ -induced activation of Smad2/3 and beta-catenin pathway in AECs. Together, our study implicates Tduanyu1842N1 as a key regulator in the process of EMT in AECs of IPF.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}