Evidence map›Paper›PMID 29463039›Full record

ArticleInternational journal of molecular sciences2018

The Significance of MMP-1 in EGFR-TKI-Resistant Lung Adenocarcinoma: Potential for Therapeutic Targeting.

Ryoko Saito, Yasuhiro Miki, Naoya Ishida, Chihiro Inoue, Masayuki Kobayashi, Shuko Hata, Hisafumi Yamada-Okabe, Yoshinori Okada, Hironobu Sasano

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. The Role of MMP8 in Cancer: A Systematic Review.International journal of molecular sciences · 2019
    Pooled it
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  9. Lipofection of Single Guide RNA TargetingMedicina (Kaunas, Lithuania) · 2021
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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

9 authors at 3 institutions in 1 country.

Ryoko SaitoDepartment of Pathology, Tohoku University Graduate School of Medicine, 980-8575, Sendai, Japan. saitoarlu@patholo2.med.tohoku.ac.jp.ORCID 0000-0003-3627-1788
Yasuhiro MikiDepartment of Pathology, Tohoku University Graduate School of Medicine, 980-8575, Sendai, Japan. miki@patholo2.med.tohoku.ac.jp.ORCID 0000-0003-3618-5652
Naoya IshidaDepartment of Pathology, Tohoku University Graduate School of Medicine, 980-8575, Sendai, Japan. naoya0618utss@gmail.com.
Chihiro InoueDepartment of Pathology, Tohoku University Graduate School of Medicine, 980-8575, Sendai, Japan. chihiro_inoue@med.tohoku.ac.jp.ORCID 0000-0002-3514-8166
Masayuki KobayashiDepartment of Pathology, Tohoku University Graduate School of Medicine, 980-8575, Sendai, Japan. masayuki.kobayashi.p1@dc.tohoku.ac.jp.
Shuko HataDepartment of Pathology, Tohoku Medical and Pharmaceutical University School of Medicine, 981-8558 Sendai, Japan. hatashu@med.tohoku.ac.jp.
Hisafumi Yamada-OkabeCHUGAI Pharmaceutical Co., Ltd., 412-8513, Gotemba, Japan. okabehsf@chugai-pharm.co.jp.
Yoshinori OkadaDepartment of Thoracic Surgery, Tohoku University Hospital, 980-8574, Sendai, Japan. yoshinori.okada.a1@tohoku.ac.jp.
Hironobu SasanoDepartment of Pathology, Tohoku University Graduate School of Medicine, 980-8575, Sendai, Japan. hsasano@patholo2.med.tohoku.ac.jp.ORCID 0000-0002-6600-8641
Tohoku University · JPTohoku Medical and Pharmaceutical University · JPTohoku University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance is one of the most important problems in lung cancer therapy. Lung adenocarcinoma with EGFR-TKI resistance was reported to have higher abilities of invasion and migration than cancers sensitive to EGFR-TKI, but the function of matrix metalloproteinases (MMPs) has not been explored in EGFR-TKI-resistant lung adenocarcinoma. This study aims to clarify the significance of MMP-1 in EGFR-TKI-resistant lung adenocarcinoma. From the results of in vitro studies of migration and invasion assays using EGFR-TKI-sensitive and -resistant cell lines and phosphorylation antibody arrays using EGF and rapamycin, we first demonstrate that overexpression of MMP-1, which might follow activation of a mammalian target of rapamycin (mTOR) pathway, plays an important role in the migration and invasion abilities of EGFR-TKI-resistant lung adenocarcinoma. Additionally, immunohistochemical studies using 89 cases of lung adenocarcinoma demonstrate that high expression of MMP-1 is significantly correlated with poor prognosis and factors such as smoking history and the subtype of invasive mucinous adenocarcinoma. These are consistent with the results of this in vitro study. To conclude, this study provides insights into the development of a possible alternative therapy manipulating MMP-1 and the mTOR signaling pathway in EGFR-TKI-resistant lung adenocarcinoma.

Indexed as

Drug Resistance, NeoplasmMolecular Targeted TherapyAdenocarcinomaAdenocarcinoma of LungAgedCell Line, TumorCell MovementErbB ReceptorsFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMatrix Metalloproteinase 1Multivariate AnalysisNeoplasm InvasivenessErbB ReceptorsMatrix Metalloproteinase 1MMP1 protein, humanProtein Kinase InhibitorsRNA, MessengerTOR Serine-Threonine KinasesEGFR-TKI resistancelung adenocarcinomaMMP-1mTOR

Identifiers

PMID29463039
PMCPMC5855831
OpenAlexW2783371025

What OpenQuestion holds

Textmetadata
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.