Evidence map›Paper›PMID 23625689›Full record

ArticleMolecular carcinogenesis2014

The Ah receptor regulates growth factor expression in head and neck squamous cell carcinoma cell lines.

Kaarthik John, Tejas S Lahoti, Kelly Wagner, Jarod M Hughes, Gary H Perdew

Abstract read
In one paragraph

Article in Molecular carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-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

32 citing papers in PubMed, 58 citations in OpenAlex.

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  20. AhR controls redox homeostasis and shapes the tumor microenvironment in BRCA1-associated breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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

5 authors at 1 institution in 1 country.

Kaarthik JohnCenter for Molecular Toxicology and Carcinogenesis and the Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania; DuPont Haskell Global Centers for Health and Environmental Sciences, Newark, Delaware.
Tejas S Lahoti
Kelly Wagner
Jarod M Hughes
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
Selective Ah Receptor Ligands Repress Acute-Phase ResponseR01ES019964 · NIEHS · PENNSYLVANIA STATE UNIVERSITY, THE · PI PERDEW, GARY H. · 2012 to 2016
$2.0M
BIOCHEMICAL CHARACTERIZATION OF THE AH RECEPTORR29ES004869 · NIEHS · PURDUE UNIVERSITY WEST LAFAYETTE · PI PERDEW, GARY H · 1989 to 1993
–
NIEHS NIH HHS ES004869NIEHS NIH HHS ES019964NIEHS NIH HHS R01 ES004869NIEHS NIH HHS R01 ES019964
6 · The paper itself

Abstract

Previous studies in head and neck squamous cell carcinoma (HNSCC) cell lines have revealed that the Ah receptor (AHR) plays a significant role in mediating the "aggressive" phenotype of these cells, which includes enhanced inflammatory signaling (e.g., IL6) and migratory potential. Here we sought to identify putative novel targets of the AHR associated with enhanced tumor invasiveness. Global gene expression analysis identified a number of genes that are repressed upon treatment of OSC-19 or HN30 cells with an AHR antagonist. Three growth factors were targets of AHR activity; amphiregulin (AREG), epiregulin (EREG), and platelet-derived growth factor A (PDGFA) were repressed by an AHR antagonist and further examined. Quantitative PCR analysis, ELISA, and siRNA-mediated knock down of AHR revealed an attenuation of basal and/or induced levels of expression of these growth factors in two HNSCC lines, following AHR antagonism. In silico analysis revealed that these growth factors possess dioxin-like response elements. Two other AHR ligands, 6-formylindolo[3,2-b]carbazole and benzo(a)pyrene (BP) also elicited similar responses. In conclusion, this study identified AREG, EREG, and PDGFA as growth factor targets of AHR activity associated with metastatic phenotype of HNSCC cells, suggesting that attenuation of AHR activity may be a therapeutic strategy.

Indexed as

Gene Expression Regulation, NeoplasticAzo CompoundsCarcinoma, Squamous CellCell Line, TumorCell SurvivalEpidermal Growth FactorEpiregulinFibroblast Growth Factor 2Gene ExpressionHead and Neck NeoplasmsHumansPlatelet-Derived Growth FactorPyrazolesReceptors, Aryl HydrocarbonSquamous Cell Carcinoma of Head and Neck2-methyl-2H-pyrazole-3-carboxylic acid (2-methyl-4-o-tolylazophenyl)amideAzo CompoundsEpidermal Growth FactorEpiregulinEREG protein, humanFibroblast Growth Factor 2Platelet-Derived Growth Factorplatelet-derived growth factor APyrazolesReceptors, Aryl HydrocarbonAHRantagonistaryl hydrocarbon receptordioxingrowth factorshead and neck cancer

Identifiers

PMID23625689
PMCPMC4388041
OpenAlexW1929633615

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.