Evidence map›Paper›PMID 25886373›Full record

ArticleBMC cancer2015

The tumour-promoting receptor tyrosine kinase, EphB4, regulates expression of integrin-β8 in prostate cancer cells.

Inga Mertens-Walker, Bruno C Fernandini, Mohanan S N Maharaj, Anja Rockstroh, Colleen C Nelson, Adrian C Herington, Sally-Anne Stephenson

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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  8. Article
  9. EphrinB2-EphB4 Signaling in Neurooncological Disease.International journal of molecular sciences · 2022
    Review
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  15. Current Advances inFrontiers in pharmacology · 2021
    Review
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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

7 authors at 3 institutions in 1 country.

Inga Mertens-WalkerInstitute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia. inga.mertenswalker@qut.edu.au.
Bruno C FernandiniInstitute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia. fern0082@uni.flinders.edu.au.
Mohanan S N MaharajInstitute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia. mohanan.maharaj@hdr.qut.edu.au.
Anja RockstrohAustralian Prostate Cancer Research Centre - Queensland, Princess Alexandra Hospital, Woolloongabba, Queensland, 4102, Australia. anja.rockstroh@qut.edu.au.
Colleen C NelsonInstitute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia. colleen.nelson@qut.edu.au.
Adrian C HeringtonInstitute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia. a.herington@qut.edu.au.
Sally-Anne StephensonInstitute of Health and Biomedical Innovation, Queensland University of Technology, Translational Research Institute, 37 Kent Street, Woolloongabba, Queensland, 4102, Australia. s.stephenson@qut.edu.au.
Queensland University of Technology · AUTranslational Research Institute · AUPrincess Alexandra Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe EphB4 receptor tyrosine kinase is overexpressed in many cancers including prostate cancer. The molecular mechanisms by which this ephrin receptor influences cancer progression are complex as there are tumor-promoting ligand-independent mechanisms in place as well as ligand-dependent tumor suppressive pathways.

methodsWe employed transient knockdown of EPHB4 in prostate cancer cells, coupled with gene microarray analysis, to identify genes that were regulated by EPHB4 and may represent linked tumor-promoting factors. We validated target genes using qRT-PCR and employed functional assays to determine their role in prostate cancer migration and invasion.

resultsWe discovered that over 500 genes were deregulated upon EPHB4 siRNA knockdown, with integrin β8 (ITGB8) being the top hit (29-fold down-regulated compared to negative non-silencing siRNA). Gene ontology analysis found that the process of cell adhesion was highly deregulated and two other integrin genes, ITGA3 and ITGA10, were also differentially expressed. In parallel, we also discovered that over-expression of EPHB4 led to a concomitant increase in ITGB8 expression. In silico analysis of a prostate cancer progression microarray publically available in the Oncomine database showed that both EPHB4 and ITGB8 are highly expressed in prostatic intraepithelial neoplasia, the precursor to prostate cancer. Knockdown of ITGB8 in PC-3 and 22Rv1 prostate cancer cells in vitro resulted in significant reduction of cell migration and invasion.

conclusionsThese results reveal that EphB4 regulates integrin β8 expression and that integrin β8 plays a hitherto unrecognized role in the motility of prostate cancer cells and thus targeting integrin β8 may be a new treatment strategy for prostate cancer.

Indexed as

Gene Expression Regulation, NeoplasticCell Line, TumorHumansIntegrin beta ChainsMaleProstatic NeoplasmsReceptor, EphB4Receptor Protein-Tyrosine Kinasesintegrin beta8Integrin beta ChainsReceptor, EphB4Receptor Protein-Tyrosine Kinases

Identifiers

PMID25886373
PMCPMC4389669
OpenAlexW2071146832

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.