Evidence map›Paper›PMID 23893956›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2013

Targeting stromal androgen receptor suppresses prolactin-driven benign prostatic hyperplasia (BPH).

Kuo-Pao Lai, Chiung-Kuei Huang, Lei-Ya Fang, Kouji Izumi, Chi-Wen Lo, Ronald Wood, Jon Kindblom, Shuyuan Yeh, Chawnshang Chang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Antioxidants (Basel, Switzerland) · 2022
    Article
  8. Review
  9. Animal models of benign prostatic hyperplasia.Prostate cancer and prostatic diseases · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. CombinedFrontiers in pharmacology · 2019
    Article
  15. Article
  16. Article
  17. Compounds fromEvidence-based complementary and alternative medicine : eCAM · 2017
    Article
  18. Article
  19. Article
  20. Article
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 3 countries.

Kuo-Pao LaiGeorge Whipple Distinguished University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, New York 14642. chang@urmc.rochester.edu.
Chiung-Kuei Huang
Lei-Ya Fang
Kouji Izumi
Chi-Wen Lo
Ronald Wood
Jon Kindblom
Shuyuan Yeh
Chawnshang Chang
University of Rochester Medical Center · USUniversity of Gothenburg · SE

Funding

New Mice Models for Studies of Androgen Receptor in Prostate CancerR01CA127300 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2008 to 2012
$1.6M
Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
NCI NIH HHS CA127300NCI NIH HHS CA156700NCI NIH HHS R01 CA127300NCI NIH HHS R01 CA156700
6 · The paper itself

Abstract

Stromal-epithelial interaction plays a pivotal role to mediate the normal prostate growth, the pathogenesis of benign prostatic hyperplasia (BPH), and prostate cancer development. Until now, the stromal androgen receptor (AR) functions in the BPH development, and the underlying mechanisms remain largely unknown. Here we used a genetic knockout approach to ablate stromal fibromuscular (fibroblasts and smooth muscle cells) AR in a probasin promoter-driven prolactin transgenic mouse model (Pb-PRL tg mice) that could spontaneously develop prostate hyperplasia to partially mimic human BPH development. We found Pb-PRL tg mice lacking stromal fibromuscular AR developed smaller prostates, with more marked changes in the dorsolateral prostate lobes with less proliferation index. Mechanistically, prolactin mediated hyperplastic prostate growth involved epithelial-stromal interaction through epithelial prolactin/prolactin receptor signals to regulate granulocyte macrophage-colony stimulating factor expression to facilitate stromal cell growth via sustaining signal transducer and activator of transcription-3 activity. Importantly, the stromal fibromuscular AR could modulate such epithelial-stromal interacting signals. Targeting stromal fibromuscular AR with the AR degradation enhancer, ASC-J9(®), led to the reduction of prostate size, which could be used in future therapy.

Indexed as

Androgen-Binding ProteinAnimalsCell ProliferationCells, CulturedCurcuminDisease Models, AnimalEpithelial CellsEpithelial-Mesenchymal TransitionFibroblastsGene ExpressionGranulocyte-Macrophage Colony-Stimulating FactorMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, Smooth MuscleAndrogen-Binding ProteinASC-J9 compoundCurcuminGranulocyte-Macrophage Colony-Stimulating FactorprobasinProlactinReceptors, AndrogenStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID23893956
PMCPMC3787128
OpenAlexW2124330457

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.