Evidence map›Paper›PMID 29867925›Full record

ArticleFrontiers in immunology2018

Breast Cancer-Derived Exosomes Alter Macrophage Polarization

Sunyoung Ham, Luize G Lima, Edna Pei Zhi Chai, Alexandra Muller, Richard J Lobb, Sophie Krumeich, Shu Wen Wen, Adrian P Wiegmans, Andreas Möller

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

134 citing papers in PubMed, 191 citations in OpenAlex.

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  13. Tumor-Associated Macrophage in Breast Tumor Microenvironment.International journal of molecular sciences · 2025
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74 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

9 authors at 3 institutions in 2 countries.

Sunyoung HamTumour Microenvironment Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Luize G LimaTumour Microenvironment Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Edna Pei Zhi ChaiTumour Microenvironment Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Alexandra MullerTumour Microenvironment Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Richard J LobbTumour Microenvironment Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Sophie KrumeichTumour Microenvironment Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Shu Wen WenCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, VIC, Australia.
Adrian P WiegmansTumour Microenvironment Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Andreas MöllerTumour Microenvironment Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
QIMR Berghofer Medical Research Institute · AUUniversity of Queensland · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-derived exosomes are being recognized as essential mediators of intercellular communication between cancer and immune cells. It is well established that bone marrow-derived macrophages (BMDMs) take up tumor-derived exosomes. However, the functional impact of these exosomes on macrophage phenotypes is controversial and not well studied. Here, we show that breast cancer-derived exosomes alter the phenotype of macrophages through the interleukin-6 (IL-6) receptor beta (glycoprotein 130, gp130)-STAT3 signaling pathway. Addition of breast cancer-derived exosomes to macrophages results in the activation of the IL-6 response pathway, including phosphorylation of the key downstream transcription factor STAT3. Exosomal gp130, which is highly enriched in cancer exosomes, triggers the secretion of IL-6 from BMDMs. Moreover, the exposure of BMDMs to cancer-derived exosomes triggers changes from a conventional toward a polarized phenotype often observed in tumor-associated macrophages. All of these effects can be inhibited through the addition of a gp130 inhibitor to cancer-derived exosomes or by blocking BMDMs exosome uptake. Collectively, this work demonstrates that breast cancer-derived exosomes are capable of inducing IL-6 secretion and a pro-survival phenotype in macrophages, partially

Indexed as

AnimalsAntineoplastic AgentsCell Line, TumorCoculture TechniquesCytokine Receptor gp130ExosomesFemaleHydrazinesInterleukin-6Macrophage ActivationMacrophagesMammary Neoplasms, ExperimentalMiceMice, Inbred C57BLPrimary Cell CultureQuinoxalinesAntineoplastic AgentsCytokine Receptor gp130HydrazinesIl6st protein, mouseInterleukin-6interleukin-6, mouseN'-(7-fluoroH-pyrrolo(1,2-a)quinoxalin-4-yl)pyrazine-2-carbohydrazideQuinoxalinesStat3 protein, mouseSTAT3 Transcription Factorbreast cancercancer-derived exosomesglycoprotein 130interleukin-6STAT3tumor-associated macrophages

Identifiers

PMID29867925
PMCPMC5951966
OpenAlexW2800494230

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.