@Article{biocell.2022.018054,
AUTHOR = {HUOGEN LIU, YUNDI SHI, XIN WAN, YING LIU, HAILIN SHU, FENGMING HUANG, ZHENBIN GONG, LING GU},
TITLE = {Effect of Peroxiredoxin 1 on the biological function of airway epithelial cells and epithelial-mesenchymal transition},
JOURNAL = {BIOCELL},
VOLUME = {46},
YEAR = {2022},
NUMBER = {12},
PAGES = {2671--2680},
URL = {http://www.techscience.com/biocell/v46n12/49259},
ISSN = {1667-5746},
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 (<i>p</i> < 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 (<i>p</i> < 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 (<i>p</i> < 0.05). Knockdown of PRDX1 inhibited cell proliferation, migration, EMT, and collagen synthesis (<i>p</i> < 0.01), reversed LPS-mediated inhibition of cell proliferation and migration, and significantly suppressed LPS-induced EMT and collagen synthesis (<i>p</i> < 0.01). The result indicating that PRDX1 may be involved in LPS/TGF-1-induced EMT and collagen synthesis in human bronchial epithelial cells.},
DOI = {10.32604/biocell.2022.018054}
}