Evidence map›Paper›PMID 27488527›Full record

ArticleCancer research2016

Monocyte Induction of E-Selectin-Mediated Endothelial Activation Releases VE-Cadherin Junctions to Promote Tumor Cell Extravasation in the Metastasis Cascade.

Irina Häuselmann, Marko Roblek, Darya Protsyuk, Volker Huck, Lucia Knopfova, Sandra Grässle, Alexander T Bauer, Stefan W Schneider, Lubor Borsig

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

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 82 citations in OpenAlex.

  1. Trial
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  9. Glycosylation in Cancer.Handbook of experimental pharmacology · 2025
    Review
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  11. Article
  12. Review
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  14. Targeting inflammation as cancer therapy.Journal of hematology & oncology · 2024
    Review
  15. Article
  16. Review
  17. EarlyFrontiers in oncology · 2024
    Article
  18. Article
  19. Article
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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

9 authors at 3 institutions in 3 countries.

Irina HäuselmannInstitute of Physiology, University of Zürich and Zürich Center for Integrative Human Physiology, Zurich, Switzerland.
Marko RoblekInstitute of Physiology, University of Zürich and Zürich Center for Integrative Human Physiology, Zurich, Switzerland.
Darya ProtsyukInstitute of Physiology, University of Zürich and Zürich Center for Integrative Human Physiology, Zurich, Switzerland.
Volker HuckDepartment of Dermatology, Experimental Dermatology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Lucia KnopfovaInternational Clinical Research Center, Center for Biological and Cellular Engineering, St. Anne's University Hospital and Institute of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic.
Sandra GrässleDepartment of Dermatology, Experimental Dermatology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Alexander T BauerDepartment of Dermatology, Experimental Dermatology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Stefan W SchneiderDepartment of Dermatology, Experimental Dermatology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Lubor BorsigInstitute of Physiology, University of Zürich and Zürich Center for Integrative Human Physiology, Zurich, Switzerland. lborsig@access.uzh.ch.
Heidelberg University · DESwiss Integrative Center for Human Health · CHMasaryk University · CZ

Funding

Swiss National Science Foundation 152901
6 · The paper itself

Abstract

Tumor cells interact with blood constituents and these interactions promote metastasis. Selectins are vascular receptors facilitating interactions of tumor cells with platelets, leukocytes, and endothelium, but the role of endothelial E-selectin remains unclear. Here we show that E-selectin is a major receptor for monocyte recruitment to tumor cell-activated endothelium. Experimental and spontaneous lung metastasis using murine tumor cells, without E-selectin ligands, were attenuated in E-selectin-deficient mice. Tumor cell-derived CCL2 promoted endothelial activation, resulting in enhanced endothelial E-selectin expression. The recruitment of inflammatory monocytes to metastasizing tumor cells was dependent on the local endothelial activation and the presence of E-selectin. Monocytes promoted transendothelial migration of tumor cells through the induction of E-selectin-dependent endothelial retractions and a subsequent modulation of tight junctions through dephosphorylation of VE-cadherin. Thus, endothelial E-selectin shapes the tumor microenvironment through the recruitment, adhesion, and activation of monocytes that facilitate tumor cell extravasation and thereby metastasis. These findings provide evidence that endothelial E-selectin is a novel factor contributing to endothelial retraction required for efficient lung metastasis. Cancer Res; 76(18); 5302-12. ©2016 AACR.

Indexed as

AnimalsAntigens, CDCadherin 5CadherinsCell Line, TumorDisease Models, AnimalEndothelial CellsEndothelium, VascularE-SelectinFlow CytometryImmunoblottingImmunoprecipitationMiceMice, Mutant StrainsMonocytesNeoplasm InvasivenessAntigens, CDCadherin 5CadherinsE-Selectin

Identifiers

PMID27488527
PMCPMC6322653
OpenAlexW2495937874

What OpenQuestion holds

Textmetadata
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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.