Evidence map›Paper›PMID 18266956›Full record

ArticleJournal of cellular and molecular medicine2008

Decrease in stromal androgen receptor associates with androgen-independent disease and promotes prostate cancer cell proliferation and invasion.

Yirong Li, Caihong X Li, Huihui Ye, Fei Chen, Jonathan Melamed, Yi Peng, Jinsong Liu, Zhengxin Wang, Hui C Tsou, Jianjun Wei and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

55 citing papers in PubMed, 78 citations in OpenAlex.

  1. Crosstalk between protein lipidation and ubiquitination in tumor biology.Apoptosis : an international journal on programmed cell death · 2026
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  18. Ion Channel Profiling in Prostate Cancer: Toward Cell Population-Specific Screening.Reviews of physiology, biochemistry and pharmacology · 2021
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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

13 authors at 3 institutions in 1 country.

Yirong LiDepartment of Pathology, New York University School of Medicine, New York, NY 10010, USA.
Caihong X Li
Huihui Ye
Fei Chen
Jonathan Melamed
Yi Peng
Jinsong Liu
Zhengxin Wang
Hui C Tsou
Jianjun Wei
Paul Walden
Michael J Garabedian
Peng Lee
New York University · USThe University of Texas MD Anderson Cancer Center · USVA NY Harbor Healthcare System · US

Funding

UNIVERSITY OF TEXAS MD ANDERSON SPORE IN OVARIAN CANCERP50CA083639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BAST, ROBERT C · 1999 to 2015
$33.0M
RAS Signaling, Senescent Fibroblasts, and Ovarian Cancer ProgressionR01CA131183 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LIU, JINSONG · 2008 to 2012
$1.3M
REGULATION OF ANDROGEN RECEPTOR ACTIVITY IN THE PROSTATER01DK058024 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI GARABEDIAN, MICHAEL J · 2000 to 2003
$1.1M
NCI NIH HHS P50 CA083639NCI NIH HHS R01 CA131183NIDDK NIH HHS DK058024NIDDK NIH HHS R01 DK058024
6 · The paper itself

Abstract

Androgen receptor (AR) is expressed in both stromal and epithelial cells of the prostate. The majority of studies on AR expression and function in prostate cancer is focused on malignant epithelial cells rather than stromal cells. In this study, we examined the levels of stromal AR in androgen-dependent and -independent prostate cancer and the function of stromal AR in prostate cancer growth and invasion. We showed that stromal AR levels were decreased in the areas surrounding cancerous tissue, especially in androgen-independent cancer. Using two telomerase-immortalized human stromal cell lines, one AR-positive and the other AR-negative, we demonstrated that stromal cells lacking AR stimulated cell proliferation of co-cultured prostate cancer cells in vitro and enhanced tumour growth in vivo when co-injected with PC3 epithelial cells in nude mice. In contrast, stromal cells expressing AR suppressed prostate cancer growth in vitro and in vivo. In parallel with cancer growth, in vitro invasion assays revealed that stromal cells lacking AR increased the invasion ability of PC3 cell by one order of magnitude, while stromal cells expressing AR reduced this effect. These results indicate a negative regulation of prostate cancer growth and invasion by stromal AR. This provides potentially new mechanistic insights into the failure of androgen ablation therapy, and the reactivation of stromal AR could be a novel therapeutic approach for treating hormone refractory prostate cancer.

Indexed as

AgedAndrogensAnimalsCell ProliferationCell Transformation, NeoplasticHumansMaleMiceMiddle AgedNeoplasm InvasivenessProstatic NeoplasmsReceptors, AndrogenStromal CellsTelomeraseAndrogensAR protein, humanReceptors, AndrogenTelomeraseTERT protein, human

Identifiers

PMID18266956
PMCPMC3828892
OpenAlexW1967497738

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.