Evidence map›Paper›PMID 19465936›Full record

ArticleOncogene2009

Aryl hydrocarbon receptor inhibition downregulates the TGF-beta/Smad pathway in human glioblastoma cells.

D Gramatzki, G Pantazis, J Schittenhelm, G Tabatabai, C Köhle, W Wick, M Schwarz, M Weller, I Tritschler

Abstract read
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In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

76 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
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  4. Article
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  6. Article
  7. Review
  8. Article
  9. Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Metformin attenuates V-domain Ig suppressor of T-cell activation through the aryl hydrocarbon receptor pathway in Melanoma: In Vivo and In Vitro Studies.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

16 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

D GramatzkiLaboratory of Molecular Neuro-Oncology, Department of General Neurology and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany.
G Pantazis
J Schittenhelm
G Tabatabai
C Köhle
W Wick
M Schwarz
M Weller
I Tritschler
University of Tübingen · DEHertie Institute for Clinical Brain Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dioxin/aryl hydrocarbon receptor (AhR) is a transcription factor, which has been attributed a role in human cancerogenesis, cell cycle progression and transforming growth factor-beta (TGF-beta) signaling. As TGF-beta is an important mediator of the malignant phenotype of human gliomas, we studied AhR expression and function in glioma cells. AhR was not only expressed in glioma cells in vitro, but was also detected in human gliomas in vivo by immunohistochemistry, with a predominantly nuclear staining in glioblastomas. The AhR agonist, 3-methylcholanthrene, induced AhR nuclear translocation and upregulated mRNA levels of the AhR target gene, cytochrome P450 1A1 (CYP1A1). Conversely, pharmacological inhibition of AhR using the novel AhR antagonist, CH-223191, or AhR gene silencing using small interfering RNA showed that constitutive AhR activity positively controls TGF-beta1, TGF-beta2 and latent TGF-beta-binding protein-1 protein levels in malignant glioma cells. Moreover, antagonism of AhR reduced clonogenic survival and invasiveness of glioma cells. In contrast, AhR regulates TGF-beta signaling negatively in non-neoplastic astrocytes. Thus, the pathogenesis of glioma formation may involve altered AhR regulation of the TGF-beta/Smad pathway, and AhR may represent a promising target for the treatment of human malignant gliomas and other diseases associated with pathological TGF-beta activity.

Indexed as

Down-RegulationBrain NeoplasmsCell Line, TumorGene SilencingGlioblastomaHumansImmunohistochemistryPolymerase Chain ReactionReceptors, Aryl HydrocarbonRNA, MessengerSmad ProteinsTransforming Growth Factor betaReceptors, Aryl HydrocarbonRNA, MessengerSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID19465936
OpenAlexW2047874826

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.