Evidence map›Paper›PMID 30260967›Full record

ArticlePloS one2018

GPx3-mediated redox signaling arrests the cell cycle and acts as a tumor suppressor in lung cancer cell lines.

Byung Chull An, Yoo-Duk Choi, In-Jae Oh, Ju Han Kim, Jae-Il Park, Seung-Won Lee

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.4field-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

51 citing papers in PubMed, 83 citations in OpenAlex.

  1. The Journal of international medical research · 2020
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  20. Hydroxytyrosol produced by engineeredExperimental biology and medicine (Maywood, N.J.) · 2023
    Article
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

6 authors at 3 institutions in 1 country.

Byung Chull AnDepartment of Anatomy, Chonnam National University Medical School, Hwasun-eup, Hwasun-gun, Jeollanam-do, Korea.
Yoo-Duk ChoiDepartment of Pathology, Chonnam National University Hospital, Dong-gu, Gwangju, Korea.
In-Jae OhDepartment of Lung and Esophageal Cancer Clinic, Chonnam National University Hwasun Hospital, Hwasun-eup, Hwasun-gun, Jeollanam-do, Korea.ORCID 0000-0003-4837-1321
Ju Han KimDepartment of Internal Medicine, Chonnam National University Hospital, Dong-gu, Gwangju, Korea.
Jae-Il ParkAnimal Facility of Aging Science, Korea Basic Science Institute, Buk-gu, Gwangju, Korea.
Seung-Won LeeDepartment of Anatomy, Chonnam National University Medical School, Hwasun-eup, Hwasun-gun, Jeollanam-do, Korea.ORCID 0000-0002-4413-740X
Chonnam National University Hwasun Hospital · KRChonnam National University Hospital · KRKorea Basic Science Institute · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutathione peroxidase 3 (GPx3), a major scavenger of reactive oxygen species (ROS) in plasma, acts as a redox signal modulator. However, the mechanism underlying GPx3-mediated suppression of cancer cell growth is unclear. The aim of this study was to identify these mechanisms with respect to lung cancer. To enhance the redox modulating properties of GPx3, lung cancer cells were subjected to serum starvation for 12 h, resulting in ROS generation in the absence of oxidant treatment. We then investigated whether suppression of tumorigenesis under conditions of oxidative stress was dependent on GPx3. The results showed that GPx3 effectively suppressed proliferation, migration, and invasion of lung cancer cells under oxidative stress. In addition, GPx3 expression led to a significant reduction in ROS production by cancer cells and induced G2/M phase arrest. We also found that inactivation of cyclin B1 significantly suppressed by nuclear factor-κB(NF-κB) inactivation in lung cancer cells was dependent on GPx3 expression. To further elucidate the mechanism(s) underlying GPx3-medited suppression of tumor proliferation, we next examined the effect of GPx3-mediated redox signaling on the ROS-MKP3-extracellular signal-regulated kinase (Erk)-NF-κB-cyclin B1 pathway and found that GPx3 strongly suppressed activation of the Erk-NF-κB-cyclin B1 signaling cascade by protecting MKP3 (an Erk-specific phosphatase) from the effects of ROS. Thus, this study demonstrates for the first time that the GPx3 suppresses proliferation of lung cancer cells by modulating redox-mediated signals.

Indexed as

Cell CycleSignal TransductionCell Cycle CheckpointsCell Line, TumorCell ProliferationCyclin B1Down-RegulationDual Specificity Phosphatase 6Extracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingGlutathione PeroxidaseHumansLung NeoplasmsModels, BiologicalCyclin B1Dual Specificity Phosphatase 6Extracellular Signal-Regulated MAP KinasesGlutathione PeroxidaseGPX3 protein, humanNF-kappa BReactive Oxygen SpeciesTumor Suppressor Proteins

Identifiers

PMID30260967
PMCPMC6160013
OpenAlexW2894321487

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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.