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Updated: May 23, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
HECTD1 promotes pulmonary fibrosis by targeting EMT and subsequent fibroblasts activation
Zewei Zhou1, Teng Geng2, Yiwei Hu3
1Department of Immunology, Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu 210000, China; Department of Physiology, School of Medicine, Southeast University, Nanjing, Jiangsu 210000, China.
Abstract:
Epithelial-mesenchymal transition (EMT) is characterized by enhanced fibroblast activation and excessive extracellular matrix deposition, ultimately leading to fibrosis. However, its specific role in silicosis and the underlying mechanisms remain poorly understood. In this study, we investigated the EMT process using a murine model of silicosis and epithelial cell lines (MLE12, A549, and BEAS-2B) exposed to SiO2. Notably, HECTD1 (HECT domain E3 ubiquitin protein ligase 1) was found to be significantly upregulated in epithelial cells during silicosis progression. HECTD1 induced EMT by upregulating mesenchymal markers (α-SMA, Vimentin, and Collagen I) and downregulating the epithelial marker E-cadherin, thereby promoting cell migration and proliferation and ultimately contributing to pulmonary fibrosis. Furthermore, HECTD1 facilitated fibroblast activation through promoting the release of inflammatory cytokines from epithelial cells, thereby exacerbating silicosis. Collectively, our findings establish a link between HECTD1-induced EMT and pulmonary fibrosis, providing new insights into HECTD1 as a potential target for the development of novel therapeutic strategies for silicosis.
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