Evidence map›Paper›PMID 28680152›Full record

ArticleScientific reports2017

Exosomes from metastatic cancer cells transfer amoeboid phenotype to non-metastatic cells and increase endothelial permeability: their emerging role in tumor heterogeneity.

Odessa Schillaci, Simona Fontana, Francesca Monteleone, Simona Taverna, Maria Antonietta Di Bella, Dolores Di Vizio, Riccardo Alessandro

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
20.6field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 432 citations in OpenAlex.

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  5. The role of exosomes in bladder cancer immunotherapy.Journal of the National Cancer Center · 2025
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6 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

7 authors at 3 institutions in 2 countries.

Odessa SchillaciDepartment of Biopathology and Medical Biotechnologies, University of Palermo, Palermo, Italy.
Simona FontanaDepartment of Biopathology and Medical Biotechnologies, University of Palermo, Palermo, Italy. simona.fontana@unipa.it.ORCID 0000-0003-4681-2170
Francesca MonteleoneDepartment of Biopathology and Medical Biotechnologies, University of Palermo, Palermo, Italy.
Simona TavernaInstitute of Biomedicine and Molecular Immunology (IBIM), National Research Council, Palermo, Italy.
Maria Antonietta Di BellaDepartment of Biopathology and Medical Biotechnologies, University of Palermo, Palermo, Italy.
Dolores Di VizioDivision of Cancer Biology and Therapeutics, Departments of Surgery, Biomedical Sciences and Pathology and Laboratory Medicine, Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA, USA.
Riccardo AlessandroDepartment of Biopathology and Medical Biotechnologies, University of Palermo, Palermo, Italy.
University of Palermo · ITIstituto di Biomedicina e di Immunologia Molecolare Alberto Monroy · ITSamueli Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The goal of this study was to understand if exosomes derived from high-metastatic cells may influence the behavior of less aggressive cancer cells and the properties of the endothelium. We found that metastatic colon cancer cells are able to transfer their amoeboid phenotype to isogenic primary cancer cells through exosomes, and that this morphological transition is associated with the acquisition of a more aggressive behavior. Moreover, exosomes from the metastatic line (SW620Exos) exhibited higher ability to cause endothelial hyperpermeability than exosomes from the non metastatic line (SW480Exos). SWATH-based quantitative proteomic analysis highlighted that SW620Exos are significantly enriched in cytoskeletal-associated proteins including proteins activating the RhoA/ROCK pathway, known to induce amoeboid properties and destabilization of endothelial junctions. In particular, thrombin was identified as a key mediator of the effects induced by SW620Exos in target cells, in which we also found a significant increase of RhoA activity. Overall, our results demonstrate that in a heterogeneous context exosomes released by aggressive sub-clones can contribute to accelerate tumor progression by spreading malignant properties that affect both the tumor cell plasticity and the endothelial cell behavior.

Indexed as

Cell Line, TumorCell PlasticityColonic NeoplasmsEndotheliumExosomesHumansHuman Umbilical Vein Endothelial CellsPermeabilityPhenotypeProteomicsrhoA GTP-Binding Proteinrho-Associated KinasesSignal TransductionThrombinrhoA GTP-Binding ProteinRHOA protein, humanrho-Associated KinasesThrombin

Identifiers

PMID28680152
PMCPMC5498501
OpenAlexW2726771639

What OpenQuestion holds

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LicenceCC BY
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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.