Evidence map›Paper›PMID 29808619›Full record

ArticleMolecular oncology2018

Loss of androgen receptor signaling in prostate cancer-associated fibroblasts (CAFs) promotes CCL2- and CXCL8-mediated cancer cell migration.

Bianca Cioni, Ekaterina Nevedomskaya, Monique H M Melis, Johan van Burgsteden, Suzan Stelloo, Emma Hodel, Daniele Spinozzi, Jeroen de Jong, Henk van der Poel, Jan Paul de Boer and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
10.4field-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

64 citing papers in PubMed, 113 citations in OpenAlex.

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  8. Enzalutamide-Resistant STEAP4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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4 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

13 authors at 3 institutions in 1 country.

Bianca CioniDivision of Oncogenomics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Ekaterina NevedomskayaDivision of Oncogenomics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Monique H M MelisDivision of Molecular Genetics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Johan van BurgstedenDivision of Molecular Genetics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Suzan StellooDivision of Oncogenomics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Emma HodelDivision of Molecular Genetics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Daniele SpinozziDivision of Molecular Genetics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Jeroen de JongDivision of Pathology, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Henk van der PoelDivision of Urology, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Jan Paul de BoerDivision of Oncogenomics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Lodewyk F A WesselsDivision of Molecular Carcinogenesis, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Wilbert ZwartDivision of Oncogenomics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
Andries M BergmanDivision of Oncogenomics, The Netherlands Cancer Institute (NKI), Amsterdam, The Netherlands.
The Netherlands Cancer Institute · NLOncode Institute · NLDelft University of Technology · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblasts are abundantly present in the prostate tumor microenvironment (TME), including cancer-associated fibroblasts (CAFs) which play a key role in cancer development. Androgen receptor (AR) signaling is the main driver of prostate cancer (PCa) progression, and stromal cells in the TME also express AR. High-grade tumor and poor clinical outcome are associated with low AR expression in the TME, which suggests a protective role of AR signaling in the stroma against PCa development. However, the mechanism of this relation is not clear. In this study, we isolated AR-expressing CAF-like cells. Testosterone (R1881) exposure did not affect CAF-like cell morphology, proliferation, or motility. PCa cell growth was not affected by culturing in medium from R1881-exposed CAF-like cells; however, migration of PCa cells was inhibited. AR chromatin immune precipitation sequencing (ChIP-seq) was performed and motif search suggested that AR in CAF-like cells bound the chromatin through AP-1-elements upon R1881 exposure, inducing enhancer-mediated AR chromatin interactions. The vast majority of chromatin binding sites in CAF-like cells were unique and not shared with AR sites observed in PCa cell lines or tumors. AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.

Indexed as

Cell MovementSignal TransductionAgedCancer-Associated FibroblastsChemokine CCL2HumansInterleukin-8MaleMiddle AgedProstateProstatic NeoplasmsReceptors, AndrogenCCL2 protein, humanChemokine CCL2CXCL8 protein, humanInterleukin-8Receptors, Androgenandrogen receptorcancer-associated fibroblastscancer cell migrationCCL2CXCL8EMTprostate cancer

Identifiers

PMID29808619
PMCPMC6068356
OpenAlexW2805802928

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.