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 ep...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.展开更多
基金The study was supported by the Fujian Provincial Science and Technology Department of the Project Fund under Grant(Grant No.2015J01573)the Medical Innovation Projects of Fujian Province’s Health and Scientific Research Talent Training Project under Grant(Grant No.2019-CXB-25).
文摘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.
