Evidence map›Paper›PMID 26407999›Full record

ArticleJournal of experimental & clinical cancer research : CR2015

Loss of the endothelial glycocalyx is associated with increased E-selectin mediated adhesion of lung tumour cells to the brain microvascular endothelium.

Srijana Rai, Zaynab Nejadhamzeeigilani, Nicholas J Gutowski, Jacqueline L Whatmore

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Biomarkers of endothelial glycocalyx dysfunction in pregnancy: a systematic review of clinical relevance and detection techniques.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Pooled it
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  12. The origin of brain malignancies at the blood-brain barrier.Cellular and molecular life sciences : CMLS · 2023
    Review
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  14. Receptor-Ligand Binding: Effect of Mechanical Factors.International journal of molecular sciences · 2023
    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

4 authors at 1 institution in 1 country.

Srijana RaiInstitute of Biomedical and Clinical Science, University of Exeter Medical School, St. Luke's campus, Exeter, EX1 2LU, UK. S.Rai@exeter.ac.uk.
Zaynab NejadhamzeeigilaniInstitute of Biomedical and Clinical Science, University of Exeter Medical School, St. Luke's campus, Exeter, EX1 2LU, UK. zaynabarya@gmail.com.
Nicholas J GutowskiInstitute of Biomedical and Clinical Science, University of Exeter Medical School, St. Luke's campus, Exeter, EX1 2LU, UK. N.J.Gutowski@exeter.ac.uk.
Jacqueline L WhatmoreInstitute of Biomedical and Clinical Science, University of Exeter Medical School, St. Luke's campus, Exeter, EX1 2LU, UK. J.L.Whatmore@exeter.ac.uk.
University of Exeter · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundArrest of metastasising lung cancer cells to the brain microvasculature maybe mediated by interactions between ligands on circulating tumour cells and endothelial E-selectin adhesion molecules; a process likely to be regulated by the endothelial glycocalyx. Using human cerebral microvascular endothelial cells and non-small cell lung cancer (NSCLC) cell lines, we describe how factors secreted by NSCLC cells i.e. cystatin C, cathepsin L, insulin-like growth factor-binding protein 7 (IGFBP7), vascular endothelial growth factor (VEGF) and tumour necrosis factor-alpha (TNF-α), damage the glycocalyx and enhance initial contacts between lung tumour and cerebral endothelial cells.

methodsEndothelial cells were treated with tumour secreted-proteins or lung tumour conditioned medium (CM). Surface levels of E-selectin were quantified by ELISA. Adhesion of A549 and SK-MES-1 cells was examined under flow conditions (1 dyne/cm(2)). Alterations in the endothelial glycocalyx were quantified by binding of fluorescein isothiocyanate-linked wheat germ agglutinin (WGA-FITC).

resultsA549 and SK-MES-1 CM and secreted-proteins significantly enhanced endothelial surface E-selectin levels after 30 min and 4 h and tumour cell adhesion after 30 min, 4 and 24 h. Both coincided with significant glycocalyx degradation; A549 and SK-MES-1 CM removing 55 ± 12 % and 58 ± 18.7 % of WGA-FITC binding, respectively. Inhibition of E-selectin binding by monoclonal anti-E-selectin antibody completely attenuated tumour cell adhesion.

conclusionThese data suggest that metastasising lung cancer cells facilitate their own adhesion to the brain endothelium by secreting factors that damage the endothelial glycocalyx, resulting in exposure of the previously shielded adhesion molecules and engagement of the E-selectin-mediated adhesion axis.

Indexed as

BrainBrain NeoplasmsCarcinoma, Non-Small-Cell LungCathepsin LCell AdhesionCell Adhesion MoleculesCell Line, TransformedCell Line, TumorCulture Media, ConditionedCystatin CEndothelial CellsEndothelium, VascularE-SelectinFlow CytometryGlycocalyxHumansCathepsin LCell Adhesion MoleculesCulture Media, ConditionedCystatin CE-Selectininsulin-like growth factor binding protein-related protein 1Insulin-Like Growth Factor Binding ProteinsSELE protein, humanTumor Necrosis Factor-alphaVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID26407999
PMCPMC4582832
OpenAlexW2117441339

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.