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学科主题: 基础医学
题名:
EGCG reverses human neutrophil elastase-induced migration in A549 cells by directly binding to HNE and by regulating alpha 1-AT
作者: 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
发表日期: 2015-07-16
DOI: 10.1038/srep11494
卷: 5
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
所属项目编号: 91129727 ; 81473235 ; 81020108031 ; 81270049 ; 81373405 ; B07001
项目资助者: National Natural Science Foundation of China ; Research Fund from the Ministry of Education of China
WOS记录号: WOS:000357976500001
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/60835
Appears in Collections:基础医学院_药理学系_期刊论文

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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

Recommended Citation:
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.
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