Evidence map›Paper›PMID 32599262›Full record

ArticleToxicology in vitro : an international journal published in association with BIBRA2020

Chronic and acute arsenic exposure enhance EGFR expression via distinct molecular mechanisms.

Christine Kim, J Christopher States, Brian P Ceresa

Open access · greenAbstract read
In one paragraph

Article in Toxicology in vitro : an international journal published in association with BIBRA, 2020. 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
1.2field-weighted citation impact, top 24% 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. Review
  2. Article
  3. Article
  4. Epidermal growth factor receptor in placental health and disease: pathways, dysfunction, and chemical disruption.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023
    Article
  11. Article
  12. 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

3 authors at 1 institution in 1 country.

Christine KimDepartment of Pharmacology and Toxicology, University of Louisville, USA.
J Christopher StatesDepartment of Pharmacology and Toxicology, University of Louisville, USA.
Brian P CeresaDepartment of Pharmacology and Toxicology, University of Louisville, USA. Electronic address: brian.ceresa@louisville.edu.
University of Louisville · US

Funding

University of Louisville Center for Integrative Environmental Health SciencesP30ES030283 · NIEHS · UNIVERSITY OF LOUISVILLE · PI J CHRISTOPHER STATES · 2020 to 2026
$10.0M
UOFL ENVIRONMENTAL HEALTH SCIENCES TRAINING PROGRAMT32ES011564 · NIEHS · UNIVERSITY OF LOUISVILLE · PI David W Hein, John Pierce Wise · 2004 to 2026
$7.1M
Mechanism for arsenic induced carcinogenesisR01ES027778 · NIEHS · UNIVERSITY OF LOUISVILLE · PI J CHRISTOPHER STATES · 2017 to 2026
$4.3M
Chemical Optimization of c-Cbl Antagonists for Corneal Wound HealingR01EY028911 · NEI · UNIVERSITY OF LOUISVILLE · PI CERESA, BRIAN P. · 2019 to 2023
$1.9M
NEI NIH HHS R01 EY028911NIEHS NIH HHS P30 ES030283NIEHS NIH HHS R01 ES027778NIEHS NIH HHS T32 ES011564
6 · The paper itself

Abstract

The impacts of acute arsenic exposure (i.e. vomiting, diarrhea, and renal failure) are distinct from those brought about by sustained, low level exposure from environmental sources or drinking of contaminated well water. Chronic arsenic exposure is a risk factor for the development of pulmonary diseases, including lung cancer. How arsenic exposure leads to pulmonary disease is not fully understood. Both acute versus chronic arsenic exposure increase EGFR expression, but do so via distinct molecular mechanisms. BEAS-2B cells were exposed to either acute sodium arsenite (5 μM for 24 h) or chronic sodium arsenite (100 nM for 24 weeks). Cells treated with acute arsenic exhibited a decrease in viability, changes in morphology, and increased mRNA level of BTC. In contrast, during 24 weeks of arsenic exposure, the cells had increased EGFR expression and activity, and increased mRNA and protein levels of TGFα. Further, chronic arsenic treatment caused an increase in cell migration in the absence of exogenous ligand. Elevated TGFα and EGFR expression are features of many non-small cell lung cancers. We propose that lung epithelial cells chronically exposed to low level arsenic increases EGFR signaling via TGFα production to enhance ligand-independent cell migration.

Indexed as

ArsenitesBronchiCell LineCell MovementEpithelial CellsErbB ReceptorsHumansSodium CompoundsTransforming Growth Factor betaArsenitesEGFR protein, humanErbB Receptorssodium arseniteSodium CompoundsTransforming Growth Factor betaArsenicBEAS-2BEGFRTGFα

Identifiers

PMID32599262
PMCPMC7375208
OpenAlexW3037230909

What OpenQuestion holds

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LicenceTDM
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.