Evidence map›Paper›PMID 25884570›Full record

ArticleBMC cancer2015

Androgen receptor and chemokine receptors 4 and 7 form a signaling axis to regulate CXCL12-dependent cellular motility.

Jordy J Hsiao, Brandon H Ng, Melinda M Smits, Jiahui Wang, Rohini J Jasavala, Harryl D Martinez, Jinhee Lee, Jhullian J Alston, Hiroaki Misonou, James S Trimmer and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. A Spatiotemporal Atlas of the Androgen Receptor Proximal Interactome.bioRxiv : the preprint server for biology · 2026
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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

11 authors at 3 institutions in 2 countries.

Jordy J HsiaoDepartment of Molecular Physiology & Biophysics, The University of Iowa, Carver College of Medicine, 51 Newton Road, Iowa City, Iowa, 52242, USA. jordy-hsiao@uiowa.edu.
Brandon H NgDepartment of Molecular Physiology & Biophysics, The University of Iowa, Carver College of Medicine, 51 Newton Road, Iowa City, Iowa, 52242, USA. ng.brandonh@gmail.com.
Melinda M SmitsDepartment of Molecular Physiology & Biophysics, The University of Iowa, Carver College of Medicine, 51 Newton Road, Iowa City, Iowa, 52242, USA. melinda-smits@uiowa.edu.
Jiahui WangDepartment of Molecular Physiology & Biophysics, The University of Iowa, Carver College of Medicine, 51 Newton Road, Iowa City, Iowa, 52242, USA. jiahui-wang@uiowa.edu.
Rohini J JasavalaDepartment of Pharmacology, Davis Genome Center, University of California Davis School of Medicine, One Shields Avenue, Davis, California, 95616, USA. rjasavala@gmail.com.
Harryl D MartinezDepartment of Molecular Physiology & Biophysics, The University of Iowa, Carver College of Medicine, 51 Newton Road, Iowa City, Iowa, 52242, USA. harryl.martinez@gmail.com.
Jinhee LeeDepartment of Molecular Physiology & Biophysics, The University of Iowa, Carver College of Medicine, 51 Newton Road, Iowa City, Iowa, 52242, USA. jinhee-lee@uiowa.edu.
Jhullian J AlstonDepartment of Molecular Physiology & Biophysics, The University of Iowa, Carver College of Medicine, 51 Newton Road, Iowa City, Iowa, 52242, USA. jhu2@umbc.edu.
Hiroaki MisonouGraduate School of Brain Science, Doshisha University, Kyoto, Japan. hmisono@mail.doshisha.ac.jp.
James S TrimmerDepartment of Neurobiology, Physiology and Behavior and Department of Physiology and Membrane Biology, University of California Davis, School of Medicine, One Shields Avenue, Davis, California, 95616, USA. jtrimmer@ucdavis.edu.
Michael E WrightDepartment of Molecular Physiology & Biophysics, The University of Iowa, Carver College of Medicine, 51 Newton Road, Iowa City, Iowa, 52242, USA. michael-e-wright@uiowa.edu.
University of Iowa · USUniversity of California, Davis · USDoshisha University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIdentifying cellular signaling pathways that become corrupted in the presence of androgens that increase the metastatic potential of organ-confined tumor cells is critical to devising strategies capable of attenuating the metastatic progression of hormone-naïve, organ-confined tumors. In localized prostate cancers, gene fusions that place ETS-family transcription factors under the control of androgens drive gene expression programs that increase the invasiveness of organ-confined tumor cells. C-X-C chemokine receptor type 4 (CXCR4) is a downstream target of ERG, whose upregulation in prostate-tumor cells contributes to their migration from the prostate gland. Recent evidence suggests that CXCR4-mediated proliferation and metastasis of tumor cells is regulated by CXCR7 through its scavenging of chemokine CXCL12. However, the role of androgens in regulating CXCR4-mediated motility with respect to CXCR7 function in prostate-cancer cells remains unclear.

methodsImmunocytochemistry, western blot, and affinity-purification analyses were used to study how androgens influenced the expression, subcellular localization, and function of CXCR7, CXCR4, and androgen receptor (AR) in LNCaP prostate-tumor cells. Moreover, luciferase assays and quantitative polymerase chain reaction (qPCR) were used to study how chemokines CXCL11 and CXCL12 regulate androgen-regulated genes (ARGs) in LNCaP prostate-tumor cells. Lastly, cell motility assays were carried out to determine how androgens influenced CXCR4-dependent motility through CXCL12.

resultsHere we show that, in the LNCaP prostate-tumor cell line, androgens coordinate the expression of CXCR4 and CXCR7, thereby promoting CXCL12/CXCR4-mediated cell motility. RNA interference experiments revealed functional interactions between AR and CXCR7 in these cells. Co-localization and affinity-purification experiments support a physical interaction between AR and CXCR7 in LNCaP cells. Unexpectedly, CXCR7 resided in the nuclear compartment and modulated AR-mediated transcription. Moreover, androgen-mediated cell motility correlated positively with the co-localization of CXCR4 and CXCR7 receptors, suggesting that cell migration may be linked to functional CXCR4/CXCR7 heterodimers. Lastly, CXCL12-mediated cell motility was CXCR7-dependent, with CXCR7 expression required for optimal expression of CXCR4 protein.

conclusionsOverall, our results suggest that inhibition of CXCR7 function might decrease the metastatic potential of organ-confined prostate cancers.

Indexed as

AndrogensCell Line, TumorCell MovementCell ProliferationChemokine CXCL11Chemokine CXCL12Gene Expression Regulation, NeoplasticHumansMaleProstatic NeoplasmsReceptors, AndrogenReceptors, CXCRReceptors, CXCR4RNA InterferenceSignal TransductionACKR3 protein, humanAndrogensChemokine CXCL11Chemokine CXCL12CXCL11 protein, humanCXCL12 protein, humanReceptors, AndrogenReceptors, CXCRReceptors, CXCR4

Identifiers

PMID25884570
PMCPMC4393632
OpenAlexW2005805066

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.