Evidence map›Paper›PMID 16983333›Full record

ArticleOncogene2007

Nitric oxide-mediated inhibition of androgen receptor activity: possible implications for prostate cancer progression.

M V Cronauer, Y Ince, R Engers, L Rinnab, W Weidemann, C V Suschek, M Burchardt, H Kleinert, J Wiedenmann, H Sies and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Testosterone in COVID-19: An Adversary Bane or Comrade Boon.Frontiers in cellular and infection microbiology · 2021
    Review
  11. Review
  12. Article
  13. Alterations of tumor microenvironment by nitric oxide impedes castration-resistant prostate cancer growth.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. Article
  15. Article
  16. Review
  17. 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

12 authors at 4 institutions in 1 country.

M V CronauerDepartment of Urology, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Y Ince
R Engers
L Rinnab
W Weidemann
C V Suschek
M Burchardt
H Kleinert
J Wiedenmann
H Sies
R Ackermann
K-D Kröncke
Heinrich Heine University Düsseldorf · DEUniversität Ulm · DEJohannes Gutenberg University Mainz · DEUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation increases the risk of cancer and many cancers, including prostate cancer, arise at sites of chronic inflammation. Inducible nitric oxide synthase (iNOS) is an enzyme dominantly expressed during inflammatory reactions. Although synthesis of high amounts of nitric oxide (NO) by iNOS has been demonstrated in pathophysiological processes, such as acute or chronic inflammation, autoimmune diseases or tumorigenesis, the role of iNOS activity in most of these diseases is poorly understood. Analysing prostate cancer biopsies by immunohistochemistry we found iNOS protein expression in tumor cells strongly paralleled by nitrotyrosine suggesting that iNOS is fully active. In vitro, NO inhibits androgen receptor-dependent promoter activity and prostate specific antigen production as well as DNA-binding activity of the androgen receptor (AR) in a concentration-dependent manner. Inhibition of the activity of androgen receptor-dependent reporter constructs is neither owing to diminished AR protein levels nor owing to an inhibition of its nuclear import. In addition, NO inhibits the proliferation of androgen receptor-positive prostate cancer cells significantly more efficiently than proliferation of androgen receptor-negative prostate cancer cells. In summary, our findings suggest that intratumoral iNOS activity favors development of prostate cancer cells that are able to proliferate androgen receptor-independently, thereby promoting prostate tumor progression.

Indexed as

Androgen Receptor AntagonistsCell Line, TumorDisease ProgressionHumansImmunohistochemistryMaleNitric OxideNitric Oxide Synthase Type IIProstatic NeoplasmsReceptors, AndrogenReverse Transcriptase Polymerase Chain ReactionAndrogen Receptor AntagonistsNitric OxideNitric Oxide Synthase Type IIReceptors, Androgen

Identifiers

PMID16983333
OpenAlexW2055131998

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.