Evidence map›Paper›PMID 31426531›Full record

ArticleInternational journal of molecular sciences2019

Blockade of EGFR Activation Promotes TNF-Induced Lung Epithelial Cell Apoptosis and Pulmonary Injury.

Toshimitsu Yamaoka, Satoru Arata, Mayumi Homma, Tetsuya Homma, Sojiro Kusumoto, Koichi Ando, Ryou Manabe, Yasunari Kishino, Motoi Ohba, Junji Tsurutani and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
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

21 citing papers in PubMed, 35 citations in OpenAlex.

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  13. Targeting the EGFR-ERK axis using the compatible solute ectoine to stabilize CFTR mutant F508del.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Molecular and Clinical Features of EGFR-TKI-Associated Lung Injury.International journal of molecular sciences · 2021
    Review
  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

13 authors at 1 institution in 1 country.

Toshimitsu YamaokaAdvanced Cancer Translational Research Institute, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan. yamaoka.t@med.showa-u.ac.jp.ORCID 0000-0002-6182-6047
Satoru ArataDepartment of Biochemistry, Faculty of Arts and Sciences, Showa University, 4562 Kamiyoshida, Fujiyoshida, Yamanashi 403-0005, Japan.
Mayumi HommaDepartment of Pathology & Laboratory Medicine, Showa University School of Medicine, Tokyo 142-8555, Japan.
Tetsuya HommaDivision of Allergology and Respiratory Medicine, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Sojiro KusumotoDivision of Allergology and Respiratory Medicine, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Koichi AndoDivision of Allergology and Respiratory Medicine, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Ryou ManabeDivision of Allergology and Respiratory Medicine, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Yasunari KishinoDivision of Allergology and Respiratory Medicine, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Motoi OhbaAdvanced Cancer Translational Research Institute, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Junji TsurutaniAdvanced Cancer Translational Research Institute, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.ORCID 0000-0002-6260-6943
Masafumi TakimotoDepartment of Pathology & Laboratory Medicine, Showa University School of Medicine, Tokyo 142-8555, Japan.
Tohru OhmoriDivision of Allergology and Respiratory Medicine, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Hironori SagaraDivision of Allergology and Respiratory Medicine, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.
Showa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pneumonitis is the leading cause of death associated with the use of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) against non-small cell lung cancer (NSCLC). However, the risk factors and the mechanism underlying this toxicity have not been elucidated. Tumor necrosis factor (TNF) has been reported to transactivate EGFR in pulmonary epithelial cells. Hence, we aimed to test the hypothesis that EGFR tyrosine kinase activity regulates TNF-mediated bronchial epithelial cell survival, and that inhibition of EGFR activity increases TNF-induced lung epithelial cell apoptosis. We used surfactant protein C (SPC)-TNF transgenic (tg) mice which overexpress TNF in the lungs. In this model, gefitinib, an EGFR-TKI, enhanced lung epithelial cell apoptosis and lymphocytic inflammation, indicating that EGFR tyrosine kinase prevents TNF-induced lung injury. Furthermore, IL-17A was significantly upregulated by gefitinib in SPC-TNF tg mice and p38MAPK activation was observed, indicative of a pathway involved in lung epithelial cell apoptosis. Moreover, in lung epithelial cells, BEAS-2B, TNF stimulated EGFR transactivation via the TNF-α-converting enzyme in a manner that requires heparin binding (HB)-EGF and transforming growth factor (TGF)-α. These novel findings have significant implications in understanding the role of EGFR in maintaining human bronchial epithelial cell homeostasis and in NSCLC treatment.

Indexed as

ApoptosisADAM17 ProteinAnimalsCarcinoma, Non-Small-Cell LungCell LineEpithelial CellsErbB ReceptorsGefitinibHeparin-binding EGF-like Growth FactorHumansLungLung InjuryLung NeoplasmsMiceMice, TransgenicModels, AnimalADAM17 ProteinEGFR protein, humanErbB ReceptorsGefitinibHBEGF protein, humanHeparin-binding EGF-like Growth Factorp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsTGFA protein, humanTransforming Growth Factor alphaTumor Necrosis Factor-alphaapoptosisEGFRlung injuryTNFtransactivation

Identifiers

PMID31426531
PMCPMC6720446
OpenAlexW2968472012

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.