Evidence map›Paper›PMID 29906488›Full record

ArticleCancer letters2018

Nrf2-activated expression of sulfiredoxin contributes to urethane-induced lung tumorigenesis.

Murli Mishra, Hong Jiang, Hedy A Chawsheen, Matthieu Gerard, Michel B Toledano, Qiou Wei

Abstract read
In one paragraph

Article in Cancer letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. CRL3Nature communications · 2024
    Article
  4. Review
  5. Article
  6. Review
  7. Hyperoxidation of Peroxiredoxins and Effects on Physiology ofAntioxidants (Basel, Switzerland) · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. 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

6 authors at 2 institutions in 2 countries.

Murli MishraDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.
Hong JiangDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA; Markey Cancer Center, University of Kentucky, Lexington, KY, 40536, USA.
Hedy A ChawsheenDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA.
Matthieu GerardEpigenetic Regulation and Cancer Group, Institut de Biologie et de Technologies de Saclay (iBiTecS), CEA-Saclay, 91191, Gif-sur-Yvette, France.
Michel B ToledanoOxidative Stress and Cancer Group (LSOC), Institut de Biologie et de Technologies de Saclay (iBiTecS), CEA-Saclay, 91191, Gif-sur-Yvette, France.
Qiou WeiDepartment of Toxicology and Cancer Biology, University of Kentucky, Lexington, KY, 40536, USA; Markey Cancer Center, University of Kentucky, Lexington, KY, 40536, USA. Electronic address: qiou.wei@uky.edu.
University of Kentucky · USCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FR

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
Role of Sulfiredoxin in Colorectal Cancer DevelopmentR01CA222596 · NCI · UNIVERSITY OF KENTUCKY · PI WEI, QIOU · 2018 to 2022
$1.7M
NCI NIH HHS P30 CA177558NCI NIH HHS R01 CA222596
6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer death worldwide. Cigarette smoking and exposure to chemical carcinogens are among the risk factors of lung tumorigenesis. In this study, we found that cigarette smoke condensate and urethane significantly stimulated the expression of sulfiredoxin (Srx) at the transcript and protein levels in cultured normal lung epithelial cells, and such stimulation was mediated through the activation of nuclear related factor 2 (Nrf2). To study the role of Srx in lung cancer development in vivo, mice with Srx wildtype, heterozygous or knockout genotype were subjected to the same protocol of urethane treatment to induce lung tumors. By comparing tumor multiplicity and volume between groups of mice with different genotype, we found that Srx knockout mice had a significantly lower number and smaller size of lung tumors. Mechanistically, we demonstrated that loss of Srx led to a decrease of tumor cell proliferation as well as an increase of tumor cell apoptosis. These data suggest that Srx may have an oncogenic role that contributes to the development of lung cancer in smokers or urethane-exposed human subjects.

Indexed as

AnimalsApoptosisCarcinogenesisCarcinogensCell ProliferationCells, CulturedFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceMice, KnockoutNF-E2-Related Factor 2Oxidative StressOxidoreductases Acting on Sulfur Group DonorsReactive Oxygen SpeciesCarcinogensNfe2l2 protein, mouseNF-E2-Related Factor 2Oxidoreductases Acting on Sulfur Group DonorsReactive Oxygen Speciessulfiredoxin protein, mouseUrethaneAntioxidantCell growth and proliferationOxidative stressPeroxiredoxinsSignal transduction

Identifiers

PMID29906488
PMCPMC6886468
OpenAlexW2807750737

What OpenQuestion holds

Textmetadata
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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.