Evidence map›Paper›PMID 25730905›Full record

ArticleOncotarget2015

Androgen receptor non-nuclear regulation of prostate cancer cell invasion mediated by Src and matriptase.

Jelani C Zarif, Laura E Lamb, Veronique V Schulz, Eric A Nollet, Cindy K Miranti

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 57 citations in OpenAlex.

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  11. Loss of CDCP1 triggers FAK activation in detached prostate cancer cells.American journal of clinical and experimental urology · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Non-nuclear AR Signaling in Prostate Cancer.Frontiers in chemistry · 2019
    Review
  19. Review
  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

5 authors at 3 institutions in 1 country.

Jelani C ZarifLaboratory of Integrin Signaling and Tumorigenesis, Van Andel Research Institute, Grand Rapids, MI 49503, USA.
Laura E LambDepartment of Urology, Beaumont Health System - Research Institute, Royal Oak, MI 48073, USA.
Veronique V SchulzLaboratory of Integrin Signaling and Tumorigenesis, Van Andel Research Institute, Grand Rapids, MI 49503, USA.
Eric A NolletLaboratory of Integrin Signaling and Tumorigenesis, Van Andel Research Institute, Grand Rapids, MI 49503, USA.
Cindy K MirantiLaboratory of Integrin Signaling and Tumorigenesis, Van Andel Research Institute, Grand Rapids, MI 49503, USA.
Van Andel Institute · USBeaumont Health · USMichigan State University · US

Funding

Role of alpha6 beta1 Integrin in Prostate CancerR01CA154835 · NCI · VAN ANDEL RESEARCH INSTITUTE · PI MIRANTI, CYNTHIA K · 2012 to 2017
$1.9M
NCI NIH HHS R01 CA154835NCI NIH HHS R01CA154835
6 · The paper itself

Abstract

Castration-resistant prostate cancers still depend on nuclear androgen receptor (AR) function despite their lack of dependence on exogenous androgen. Second generation anti-androgen therapies are more efficient at blocking nuclear AR; however resistant tumors still develop. Recent studies indicate Src is highly active in these resistant tumors. By manipulating AR activity in several different prostate cancer cell lines through RNAi, drug treatment, and the use of a nuclear-deficient AR mutant, we demonstrate that androgen acting on cytoplasmic AR rapidly stimulates Src tyrosine kinase via a non-genomic mechanism. Cytoplasmic AR, acting through Src enhances laminin integrin-dependent invasion. Active Matriptase, which cleaves laminin, is elevated within minutes after androgen stimulation, and is subsequently shed into the medium. Matriptase activation and shedding induced by cytoplasmic AR is dependent on Src. Concomitantly, CDCP1/gp140, a Matriptase and Src substrate that controls integrin-based migration, is activated. However, only inhibition of Matriptase, but not CDCP1, suppresses the AR/Src-dependent increase in invasion. Matriptase, present in conditioned medium from AR-stimulated cells, is sufficient to enhance invasion in the absence of androgen. Thus, invasion is stimulated by a rapid but sustained increase in Src activity, mediated non-genomically by cytoplasmic AR, leading to rapid activation and shedding of the laminin protease Matriptase.

Indexed as

Gene Expression Regulation, NeoplasticAndrogensCell Line, TumorCell MovementCell ShapeCulture Media, ConditionedCytoplasmHumansIntegrin alpha6beta1LamininMaleNeoplasm InvasivenessProstatic NeoplasmsReceptors, AndrogenRNA InterferenceRNA, Small InterferingAndrogensAR protein, humanCulture Media, ConditionedIntegrin alpha6beta1LamininReceptors, AndrogenRNA, Small InterferingSerine Endopeptidasessrc-Family KinasesST14 protein, humancastration-resistantmetastasisnongenomic AR signalingprostate cancerSrc

Identifiers

PMID25730905
PMCPMC4466655
OpenAlexW1541440885

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.