Six1 Promotes Epithelial-Mesenchymal Transition in Bronchial Epithelial Cells via the TGF?1/Smad Signalling Pathway

<b><i>Introduction:</i></b> The homeodomain transcription factor sine oculis homeobox homolog 1 (Six1) plays a crucial role in embryogenesis and is not expressed normal adult tissue but many pathological processes, including airway remodelling asthma. current study aimed to reveal the effects of Six1 regulating its possible mechanism. <b><i>Methods:</i></b> A mouse model ovalbumin-induced asthma-associated wall bronchial epithelial cell (16HBE) transforming growth ?1 (TGF?1)-induced epithelial-mesenchymal transition (EMT) were used investigate Six1. Then, 16HBE cells transformed with expression vectors treated TGF?1 pathway inhibitor determine EMT. effect mechanism assessed by immunohistochemistry, RT-PCR, Western blot. <b><i>Results:</i></b> was elevated lungs an OVA allergic asthma TGF?1. overexpression promoted EMT-like phenotype decreased protein E-cadherin increased ?-smooth muscle actin (?-SMA) as well fibronectin cells; these appeared promote phospho-Smad2 (pSmad2) production, which are main products TGF?1/Smad signalling pathway, could be reduced inhibitor. <b><i>Conclusion:</i></b> These data that potentially part autocrine feedback loop induces EMT, factors can blocking pathway. As such, may represent promising novel therapeutic target for