Evidence map›Paper›PMID 26177797›Full record

ArticleScientific reports2015

EGCG reverses human neutrophil elastase-induced migration in A549 cells by directly binding to HNE and by regulating α1-AT.

Yilixiati Xiaokaiti, Haoming Wu, Ya Chen, Haopeng Yang, Jianhui Duan, Xin Li, Yan Pan, Lu Tie, Liangren Zhang, Xuejun Li

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Neutrophil elastase: From mechanisms to therapeutic potential.Journal of pharmaceutical analysis · 2023
    Review
  5. Review
  6. Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  7. Review
  8. Matcha Green Tea Exhibits Bactericidal Activity againstAntibiotics (Basel, Switzerland) · 2021
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Yilixiati Xiaokaiti1] State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China [2] Department of Pharmacology, School of Basic Medical Science, Peking University and Institute of System Biomedicine, Peking University, Beijing 100191, China.
Haoming WuDepartment of Immunology, Peking University Health Science Center, Beijing 100191, China.
Ya Chen1] State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China [2] School of Pharmaceutical Sciences, Peking University, Beijing 100191, China.
Haopeng Yang1] State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China [2] Department of Pharmacology, School of Basic Medical Science, Peking University and Institute of System Biomedicine, Peking University, Beijing 100191, China.
Jianhui Duan1] State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China [2] Department of Pharmacology, School of Basic Medical Science, Peking University and Institute of System Biomedicine, Peking University, Beijing 100191, China.
Xin Li1] State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China [2] Department of Pharmacology, School of Basic Medical Science, Peking University and Institute of System Biomedicine, Peking University, Beijing 100191, China.
Yan Pan1] State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China [2] Department of Pharmacology, School of Basic Medical Science, Peking University and Institute of System Biomedicine, Peking University, Beijing 100191, China.
Lu Tie1] State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China [2] Department of Pharmacology, School of Basic Medical Science, Peking University and Institute of System Biomedicine, Peking University, Beijing 100191, China.
Liangren Zhang1] State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China [2] School of Pharmaceutical Sciences, Peking University, Beijing 100191, China.
Xuejun Li1] State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China [2] Department of Pharmacology, School of Basic Medical Science, Peking University and Institute of System Biomedicine, Peking University, Beijing 100191, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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, α1-antitrypsin is synthesized in tumor cells. We further demonstrated that the expression of α1-antitrypsin was up-regulated after EGCG treatment in neutrophil elastase-treated A549 cells. We preliminarily discovered that the EGCG-mediated induction of α1-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 α1-antitrypsin by regulating the PI3K/AKT pathway.

Indexed as

alpha 1-AntitrypsinBiosensing TechniquesCatechinCell Line, TumorCell MovementCell ProliferationHumansLeukocyte ElastasePhosphatidylinositol 3-KinasesProtein BindingProto-Oncogene Proteins c-aktSignal TransductionSurface Plasmon Resonancealpha 1-AntitrypsinCatechinepigallocatechin gallateLeukocyte ElastasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID26177797
PMCPMC4503950

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.