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学科主题基础医学
EGCG reverses human neutrophil elastase-induced migration in A549 cells by directly binding to HNE and by regulating alpha 1-AT
Xiaokaiti, Yilixiati1,2,3; Wu, Haoming4; Chen, Ya1,5; Yang, Haopeng1,2,3; Duan, Jianhui1,2,3; Li, Xin1,2,3; Pan, Yan1,2,3; Tie, Lu1,2,3; Zhang, Liangren1,5; Li, Xuejun1,2,3
刊名SCIENTIFIC REPORTS
2015-07-16
DOI10.1038/srep11494
5期:0
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]Respiratory Syndrome Coronavirus ; Lung-cancer ; 3c-like Proteinase ; In-vitro ; Alpha-1-antitrypsin ; Growth ; Tea ; Inhibition ; Carcinoma ; Deficiency
英文摘要

Lung carcinogenesis is a complex process that occurs in unregulated inflammatory environment. EGCG has been extensively investigated as a multi-targeting anti-tumor and anti-inflammatory compound. In this study, we demonstrated a novel mechanism by which EGCG reverses the neutrophil elastase-induced migration of A549 cells. We found that neutrophil elastase directly triggered human adenocarcinoma A549 cell migration and that EGCG suppressed the elevation of tumor cell migration induced by neutrophil elastase. We observed that EGCG directly binds to neutrophil elastase and inhibits its enzymatic activity based on the CDOCKER algorithm, MD stimulation by GROMACS, SPR assay and elastase enzymatic activity assay. As the natural inhibitor of neutrophil elastase, alpha 1-antitrypsin is synthesized in tumor cells. We further demonstrated that the expression of alpha 1-antitrypsin was up-regulated after EGCG treatment in neutrophil elastase-treated A549 cells. We preliminarily discovered that the EGCG-mediated induction of alpha 1-antitrypsin expression might be correlated with the regulatory effect of EGCG on the PI3K/Akt pathway. Overall, our results suggest that EGCG ameliorates the neutrophil elastase-induced migration of A549 cells. The mechanism underlying this effect may include two processes: EGCG directly binds to neutrophil elastase and inhibits its enzymatic activity; EGCG enhances the expression of alpha 1-antitrypsin by regulating the PI3K/AKT pathway.

语种英语
WOS记录号WOS:000357976500001
通讯作者邮箱xjli@bjmu.edu.cn
项目编号91129727 ; 81473235 ; 81020108031 ; 81270049 ; 81373405 ; B07001
资助机构National Natural Science Foundation of China ; Research Fund from the Ministry of Education of China
引用统计
被引频次:8[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/60835
专题北京大学基础医学院_药理学系
北京大学基础医学院
北京大学药学院_药物化学系
作者单位1.Peking Univ, Inst Syst Biomed, Beijing 100191, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Immunol, Beijing 100191, Peoples R China
3.Peking Univ, Sch Pharmaceut Sci, Beijing 100191, Peoples R China
4.Peking Univ, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China
5.Peking Univ, Sch Basic Med Sci, Dept Pharmacol, Beijing 100191, Peoples R China
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GB/T 7714
Xiaokaiti, Yilixiati,Wu, Haoming,Chen, Ya,et al. EGCG reverses human neutrophil elastase-induced migration in A549 cells by directly binding to HNE and by regulating alpha 1-AT[J]. SCIENTIFIC REPORTS,2015,5(0).
APA Xiaokaiti, Yilixiati.,Wu, Haoming.,Chen, Ya.,Yang, Haopeng.,Duan, Jianhui.,...&Li, Xuejun.(2015).EGCG reverses human neutrophil elastase-induced migration in A549 cells by directly binding to HNE and by regulating alpha 1-AT.SCIENTIFIC REPORTS,5(0).
MLA Xiaokaiti, Yilixiati,et al."EGCG reverses human neutrophil elastase-induced migration in A549 cells by directly binding to HNE and by regulating alpha 1-AT".SCIENTIFIC REPORTS 5.0(2015).
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