Evidence map›Paper›PMID 21104991›Full record

ArticleMolecular carcinogenesis2011

Ah receptor antagonism inhibits constitutive and cytokine inducible IL6 production in head and neck tumor cell lines.

Brett C DiNatale, Jennifer C Schroeder, Gary H Perdew

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.8field-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

47 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  12. The aryl hydrocarbon receptor suppresses immunity to oral squamous cell carcinoma through immune checkpoint regulation.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  13. Article
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  15. Article
  16. Article
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  18. Review
  19. Epigenetic Regulations of AhR in the Aspect of Immunomodulation.International journal of molecular sciences · 2020
    Review
  20. Aryl Hydrocarbon Receptor Connects Inflammation to Breast Cancer.International journal of molecular sciences · 2020
    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

3 authors at 1 institution in 1 country.

Brett C DiNataleDepartment of Veterinary and Biomedical Sciences, Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802, USA.
Jennifer C Schroeder
Gary H Perdew
Pennsylvania State University · US

Funding

REGULATION OF THE AH RECEPTORR01ES004869 · NIEHS · PURDUE UNIVERSITY WEST LAFAYETTE · PI PERDEW, GARY H. · 1994 to 2017
$5.3M
BIOCHEMICAL CHARACTERIZATION OF THE AH RECEPTORR29ES004869 · NIEHS · PURDUE UNIVERSITY WEST LAFAYETTE · PI PERDEW, GARY H · 1989 to 1993
–
NIEHS NIH HHS ES04869NIEHS NIH HHS R01 ES004869
6 · The paper itself

Abstract

There is increasing evidence that the aryl hydrocarbon receptor (AHR) plays a role in tumor progression through numerous mechanisms. We have previously shown that, in certain cancer cell lines that are typically nonresponsive to cytokine-mediated IL6 induction, activation of the AHR with the agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin derepresses the IL6 promoter and allows for synergistic induction following IL1β treatment. The mechanism by which this occurs involves liganded AHR binding upstream from the transcription start site and dismissing HDAC-containing corepressor complexes, giving rise to a promoter structure that is more amenable to NF-κB activation. This fact, combined with observations of multiple endogenously produced chemicals activating the AHR, led us to study its role in basal expression among high cytokine-producing cancer cell lines. The current study provides evidence that several head and neck squamous cell carcinoma cell lines have a level of constitutively bound AHR at the IL6 promoter, allowing for higher basal and readily inducible IL6 transcription. Treatment of these cell lines with an AHR antagonist led to dismissal of the AHR from the IL6 promoter and recruitment of corepressor complexes, thus diminishing cytokine expression. Head and neck squamous cell carcinoma is typically a high cytokine-producing tumor type, with IL6 expression levels correlating with disease aggressiveness. For this reason, AHR antagonist treatment could represent a novel adjuvant therapy for patients, lowering pro-growth and antiapoptotic signaling with minimal systemic side effects.

Indexed as

Blotting, WesternCarcinoma, Squamous CellChromatin ImmunoprecipitationEnzyme-Linked Immunosorbent AssayHead and Neck NeoplasmsHumansInterleukin-1betaInterleukin-6NF-kappa BPolychlorinated DibenzodioxinsPromoter Regions, GeneticReceptors, Aryl HydrocarbonReverse Transcriptase Polymerase Chain ReactionRNA, MessengerRNA, Small InterferingSignal TransductionInterleukin-1betaInterleukin-6NF-kappa BPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonRNA, MessengerRNA, Small Interfering

Identifiers

PMID21104991
PMCPMC3044777
OpenAlexW1986090515

What OpenQuestion holds

Textmetadata
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.