Evidence map›Paper›PMID 31035533›Full record

ArticleCancers2019

A Protective Role of Aryl Hydrocarbon Receptor Repressor in Inflammation and Tumor Growth.

Christoph F A Vogel, Yasuhiro Ishihara, Claire E Campbell, Sarah Y Kado, Aimy Nguyen-Chi, Colleen Sweeney, Marius Pollet, Thomas Haarmann-Stemmann, Joseph M Tuscano

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. The aryl hydrocarbon receptor: a new frontier in male reproductive system.Reproductive biology and endocrinology : RB&E · 2025
    Review
  3. Article
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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 4 institutions in 3 countries.

Christoph F A VogelDepartment of Environmental Toxicology, University of California, One Shields Avenue, Davis, CA 95616, USA. cfvogel@ucdavis.edu.
Yasuhiro IshiharaCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA. yaishihara@ucdavis.edu.ORCID 0000-0001-9751-7660
Claire E CampbellCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA. cecampbell@ucdavis.edu.
Sarah Y KadoCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA. sykado@ucdavis.edu.
Aimy Nguyen-ChiCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA. aimy.nguyenchi@gmail.com.
Colleen SweeneyDepartment of Biochemistry & Molecular Medicine, School of Medicine, University of California, Davis, CA 95817, USA. casweeney@ucdavis.edu.
Marius PolletCenter for Health and the Environment, University of California, One Shields Avenue, Davis, CA 95616, USA. mpollet@ucdavis.edu.
Thomas Haarmann-StemmannLeibniz Research Institute for Environmental Medicine, 40225 Düsseldorf, Germany. haarmann@uni-duesseldorf.de.
Joseph M TuscanoDivision of Hematology & Oncology, Department of Internal Medicine, University of California Davis Comprehensive Cancer Center, Sacramento, CA 95817, USA. jtuscano@UCDAVIS.EDU.
University of California, Davis · USLeibniz Institute of Environmental Medicine · DEHiroshima University · JPUniversity of California Davis Medical Center · US

Funding

UC Davis Environmental Health Sciences Core CenterP30ES023513 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Nicholas J. KENYON · 2015 to 2026
$26.0M
Importance of AhR for the cellular function and communication of dendritic cellsR01ES019898 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2012 to 2016
$1.7M
The protective role of the AhR Repressor in breast cancer developmentR21ES030419 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2019 to 2020
$432k
NIEHS NIH HHS P30 ES023513NIEHS NIH HHS P30-ES023513NIEHS NIH HHS R01 ES019898NIEHS NIH HHS R21 ES030419University of California Cancer Center Cancer Immunology 48649
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is known for mediating the toxicity of environmental pollutants such as dioxins and numerous dioxin-like compounds, and is associated with the promotion of various malignancies, including lymphoma. The aryl hydrocarbon receptor repressor (AhRR), a ligand-independent, transcriptionally inactive AhR-like protein is known to repress AhR signaling through its ability to compete with the AhR for dimerization with the AhR nuclear translocator (ARNT). While AhRR effectively blocks AhR signaling, several aspects of the mechanism of AhRR's functions are poorly understood, including suppression of inflammatory responses and its putative role as a tumor suppressor. In a transgenic mouse that overexpresses AhRR (AhRR Tg) we discovered that these mice suppress 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)- and inflammation-induced tumor growth after subcutaneous challenge of EL4 lymphoma cells. Using mouse embryonic fibroblasts (MEF) we found that AhRR overexpression suppresses the AhR-mediated anti-apoptotic response. The AhRR-mediated inhibition of apoptotic resistance was associated with a suppressed expression of interleukin (IL)-1β and cyclooxygenase (COX)-2, which was dependent on activation of protein kinase A (PKA) and the CAAT-enhancer-binding protein beta (C/EBPβ). These results provide mechanistic insights into the role of the AhRR to suppress inflammation and highlight the AhRR as a potential therapeutic target to suppress tumor growth.

Indexed as

AhRAhRRcarcinogenicityC/EBPβcyclooxygenase 2inflammationinterleukin 1lymphomaTCDD

Identifiers

PMID31035533
PMCPMC6563059
OpenAlexW2941252175

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.