Evidence map›Paper›PMID 23878190›Full record

ArticleCancer research2013

Infiltrating macrophages promote prostate tumorigenesis via modulating androgen receptor-mediated CCL4-STAT3 signaling.

Lei-Ya Fang, Kouji Izumi, Kuo-Pao Lai, Liang Liang, Lei Li, Hiroshi Miyamoto, Wen-Jye Lin, Chawnshang Chang

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
10.7field-weighted citation impact, top 1% 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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.

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34 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

8 authors at 3 institutions in 2 countries.

Lei-Ya FangAuthors' Affiliations: George Whipple Lab for Cancer Research, Departments of Pathology, Urology, and Radiation Oncology, The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, New York; Immunology Research Center, National Health Research Institutes, Zhunan, Miaoli County, and Sex Hormone Research Center, China Medical University and Hospital, Taichung, Taiwan.
Kouji Izumi
Kuo-Pao Lai
Liang Liang
Lei Li
Hiroshi Miyamoto
Wen-Jye Lin
Chawnshang Chang
National Health Research Institutes · TWUniversity of Rochester Medical Center · USChina Medical University · TW

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

Infiltrating macrophages are a key component of inflammation during tumorigenesis, but the direct evidence of such linkage remains unclear. We report here that persistent coculturing of immortalized prostate epithelial cells with macrophages, without adding any carcinogens, induces prostate tumorigenesis and that induction involves the alteration of signaling of macrophage androgen receptor (AR)-inflammatory chemokine CCL4-STAT3 activation as well as epithelial-to-mesenchymal transition and downregulation of p53/PTEN tumor suppressors. In vivo studies further showed that PTEN(+/-) mice lacking macrophage AR developed far fewer prostatic intraepithelial neoplasia (PIN) lesions, supporting an in vivo role for macrophage AR during prostate tumorigenesis. CCL4-neutralizing antibody effectively blocked macrophage-induced prostate tumorigenic signaling and targeting AR via an AR-degradation enhancer, ASC-J9, reduced CCL4 expression, and xenografted tumor growth in vivo. Importantly, CCL4 upregulation was associated with increased Snail expression and downregulation of p53/PTEN in high-grade PIN and prostate cancer. Together, our results identify the AR-CCL4-STAT3 axis as key regulators during prostate tumor initiation and highlight the important roles of infiltrating macrophages and inflammatory cytokines for the prostate tumorigenesis.

Indexed as

AnimalsAntibodies, MonoclonalCells, CulturedCell Transformation, NeoplasticChemokine CCL4CurcuminCytokinesEnzyme-Linked Immunosorbent AssayEpithelial-Mesenchymal TransitionHumansImmunoenzyme TechniquesMacrophagesMaleMiceMice, KnockoutProstateAntibodies, MonoclonalASC-J9 compoundChemokine CCL4CurcuminCytokinesPTEN PhosphohydrolasePten protein, mouseReceptors, AndrogenSTAT3 Transcription Factor

Identifiers

PMID23878190
PMCPMC3833080
OpenAlexW2129040096

What OpenQuestion holds

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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.