Evidence map›Paper›PMID 16091746›Full record

ArticleOncogene2005

The aryl hydrocarbon receptor constitutively represses c-myc transcription in human mammary tumor cells.

Xinhai Yang, Donghui Liu, Tessa J Murray, Geoffrey C Mitchell, Eli V Hesterman, Sibel I Karchner, Rebeka R Merson, Mark E Hahn, David H Sherr

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Aryl Hydrocarbon Receptor: From Homeostasis to Tumor Progression.Frontiers in cell and developmental biology · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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  17. Review
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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 3 institutions in 1 country.

Xinhai YangDepartment of Environmental Health, Boston University School of Public Health, Boston, MA 02118, USA.
Donghui Liu
Tessa J Murray
Geoffrey C Mitchell
Eli V Hesterman
Sibel I Karchner
Rebeka R Merson
Mark E Hahn
David H Sherr
Boston University · USWoods Hole Oceanographic Institution · USFurman University · US

Funding

Training CoreP42ES007381 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MONTI, STEFANO · 1995 to 2019
$46.1M
Signaling Pathways in Stages of TumorigenesisP01ES011624 · NIEHS · TUFTS UNIVERSITY BOSTON · PI SONENSHEIN, GAIL E. · 2001 to 2012
$11.4M
HOW ENVIRONMENTAL CHEMICALS IMPAIR IMMUNITYR01ES006086 · NIEHS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SHERR, DAVID H · 1993 to 2009
$2.4M
NIEHS NIH HHS P01-ES11624NIEHS NIH HHS P42-ES07381NIEHS NIH HHS R01-ES06086
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is an environmental carcinogen-activated transcription factor associated with tumorigenesis. High levels of apparently active AhR characterize a variety of tumors, even in the absence of environmental ligands. Despite this association between transformation and AhR upregulation, little is known of the transcriptional consequences of constitutive AhR activation. Here, the effects of constitutively active and environmental ligand-induced AhR on c-myc, an oncogene whose promoter contains six AhR-binding sites (AhREs (aryl hydrocarbon response elements)), were investigated. A reporter containing the human c-myc promoter, with its six AhREs and two NF-kappaB-binding sites, was constructed. This vector, and variants with deletions in the NF-kappaB and/or AhR-binding sites, was transfected into a human breast cancer cell line, Hs578T, which expresses high levels of apparently active, nuclear AhR. Results indicate that: (1) the AhR constitutively binds the c-myc promoter; (2) there is a low but significant baseline level of c-myc promoter activity, which is not regulated by NF-kappaB and is not affected by an environmental AhR ligand; (3) deletion of any one of the AhREs has no effect on constitutive reporter activity, while deletion of all six increases reporter activity approximately fivefold; (4) a similar increase in reporter activity occurs when constitutively active AhR is suppressed by transfection with an AhR repressor plasmid (AhRR); (5) AhRR transfection significantly increases background levels of endogenous c-myc mRNA and c-Myc protein. These results suggest that the AhR influences the expression of c-Myc, a protein critical to malignant transformation.

Indexed as

Breast NeoplasmsCell Transformation, NeoplasticFemaleGenes, mycGenes, ReporterHumansPlasmidsPromoter Regions, GeneticProto-Oncogene Proteins c-mycReceptors, Aryl HydrocarbonTransfectionTumor Cells, CulturedProto-Oncogene Proteins c-mycReceptors, Aryl Hydrocarbon

Identifiers

PMID16091746
OpenAlexW1975091600

What OpenQuestion holds

Textmetadata
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.