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ARTICLE
Effect of Peroxiredoxin 1 on the biological function of airway epithelial cells and epithelial-mesenchymal transition
Department of Critical Care Medicine, Mindong Hospital Affiliated to Fujian Medical University, Ningde, 355000, China
* Corresponding Author: LING GU. Email:
(This article belongs to the Special Issue: Single Cell Technologies and Molecular Mechanisms of Diseases)
BIOCELL 2022, 46(12), 2671-2680. https://doi.org/10.32604/biocell.2022.018054
Received 25 June 2021; Accepted 15 April 2022; Issue published 10 August 2022
Abstract
Peroxiredoxin 1 (PRDX1) participates in tumor cell proliferation, apoptosis, migration, invasion, and the epithelial-to-mesenchymal transition (EMT). This study aimed to investigate the effect of PRDX1 on the EMT of airway epithelial cells stimulated with lipopolysaccharide (LPS) and transforming growth factor-beta 1 (TGF-β1). PRDX1 overexpression significantly increased the proliferation and migration of human bronchial epithelial (BEAS-2B) cells, reduced cell apoptosis (p < 0.01), and induced EMT and collagen deposition by upregulating the expression of the matrix metallopeptidase (MMP)2, MMP9, α-smooth muscle actin (α-SMA), N-cadherin, vimentin and twist proteins and inhibiting E-cadherin expression (p < 0.05). PRDX1 overexpression promoted TGF-β1-mediated inhibition of cell proliferation and migration and significantly enhanced the TGF-β1-induced EMT and collagen synthesis (p < 0.05). Knockdown of PRDX1 inhibited cell proliferation, migration, EMT, and collagen synthesis (p < 0.01), reversed LPS-mediated inhibition of cell proliferation and migration, and significantly suppressed LPS-induced EMT and collagen synthesis (p < 0.01). The result indicating that PRDX1 may be involved in LPS/TGF-1-induced EMT and collagen synthesis in human bronchial epithelial cells.Keywords
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