Evidence map›Paper›PMID 28553931›Full record

ArticleOncogenesis2017

The immunosuppressive cytokine interleukin-4 increases the clonogenic potential of prostate stem-like cells by activation of STAT6 signalling.

G Nappo, F Handle, F R Santer, R V McNeill, R I Seed, A T Collins, G Morrone, Z Culig, N J Maitland, H H H Erb

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

67 citing papers in PubMed, 93 citations in OpenAlex.

  1. Phase I/II Study of the Aurora Kinase A Inhibitor Alisertib and Pembrolizumab in Refractory, Rb-Deficient Head and Neck Squamous Cell Carcinomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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  19. Metabolic changes during prostate cancer development and progression.Journal of cancer research and clinical oncology · 2023
    Review
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7 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

10 authors at 7 institutions in 4 countries.

G NappoThe Cancer Research Unit, Department of Biology, University of York, York, UK.
F HandleDivision of Experimental Urology, Department of Urology, Medical University of Innsbruck, Innsbruck, Austria.
F R SanterDivision of Experimental Urology, Department of Urology, Medical University of Innsbruck, Innsbruck, Austria.
R V McNeillJack Birch Unit for Molecular Carcinogenesis, Department of Biology, University of York, York, UK.
R I SeedThe Cancer Research Unit, Department of Biology, University of York, York, UK.
A T CollinsThe Cancer Research Unit, Department of Biology, University of York, York, UK.
G MorroneDepartment of Experimental and Clinical Medicine, Laboratory of Molecular Haematopoiesis and Stem Cell Biology, Magna Graecia University, Catanzaro, Italy.
Z CuligDivision of Experimental Urology, Department of Urology, Medical University of Innsbruck, Innsbruck, Austria.
N J MaitlandThe Cancer Research Unit, Department of Biology, University of York, York, UK.
H H H ErbThe Cancer Research Unit, Department of Biology, University of York, York, UK.
Magna Graecia University · ITUniversität Innsbruck · ATUniversity of York · GBHull York Medical School · GBInnsbruck Medical University · ATUniversity Medical Center of the Johannes Gutenberg University Mainz · DEYorkshire Cancer Research · GB

Funding

Austrian Science Fund FWF P 26799
6 · The paper itself

Abstract

Interleukin-4 plays a critical role in the regulation of immune responses and has been detected at high levels in the tumour microenvironment of cancer patients, where concentrations correlate with the grade of malignancy. In prostate cancer, interleukin-4 has been associated with activation of the androgen receptor, increased proliferation and activation of survival pathways such as Akt and NF-κB. However, its role in therapy resistance has not yet been determined. Here we investigate the influence of interleukin-4 on primary epithelial cells from prostate cancer patients. Our data demonstrate an increase in the clonogenic potential of these cells when cultured in the presence of interleukin-4. In addition, a Phospho-Kinase Array revealed that in contrast to previously published work, signal transducer and activator of transcription6 (STAT6) is the only signalling molecule activated after interleukin-4 treatment. Using the STAT6-specific inhibitor AS1517499 we could confirm the role of STAT6 in increasing colony-forming frequency. However, clonogenic recovery assays revealed that interleukin-4 does not rescue the effects of either irradiation or docetaxel treatment. We therefore propose that although the interleukin-4/STAT6 axis does not appear to be involved in therapy resistance, it does play a crucial role in the colony-forming abilities of the basal cell population in prostate cancer. IL-4 may therefore contribute to disease relapse by providing a niche that is favourable for the clonogenic growth of prostate cancer stem cells.

Identifiers

PMID28553931
PMCPMC5523058
OpenAlexW2615281074

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.