Evidence map›Paper›PMID 28533486›Full record

ArticleOncotarget2017

Galectin-3 acts as an angiogenic switch to induce tumor angiogenesis via Jagged-1/Notch activation.

Sofia Nascimento Dos Santos, Helen Sheldon, Jonathas Xavier Pereira, Christopher Paluch, Esther M Bridges, Márcia Curry El-Cheikh, Adrian L Harris, Emerson Soares Bernardes

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

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
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  13. BAP31 Promotes Angiogenesis via Galectin-3 Upregulation in Neuroblastoma.International journal of molecular sciences · 2024
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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

8 authors at 5 institutions in 2 countries.

Sofia Nascimento Dos SantosRadiopharmacy Department, Nuclear Energy Research Institute, São Paulo, Brazil.
Helen SheldonDepartment of Medical Oncology, Molecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Jonathas Xavier PereiraDepartment of Pathology, Faculty of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Christopher PaluchT-cell Biology Group, Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Esther M BridgesDepartment of Medical Oncology, Molecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Márcia Curry El-CheikhInstitute for Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Adrian L HarrisDepartment of Medical Oncology, Molecular Oncology Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.
Emerson Soares BernardesRadiopharmacy Department, Nuclear Energy Research Institute, São Paulo, Brazil.
University of Oxford · GBUniversidade Federal do Rio de Janeiro · BRInstituto de Pesquisas Energéticas e Nucleares · BRMRC Weatherall Institute of Molecular Medicine · GBNuclear Engineering Institute · BR

Funding

Cancer Research UK 11359Cancer Research UK 16466Cancer Research UK 18974Medical Research Council G0300648
6 · The paper itself

Abstract

Angiogenesis is a coordinated process tightly regulated by the balance between Delta-like-4 (DLL4) and Jagged-1 (JAG1) in endothelial cells. Here we show that galectin-3 (gal-3), a glycan-binding protein secreted by cancer cells under hypoxic conditions, triggers sprouting angiogenesis, assisted by hypoxic changes in the glycosylation status of endothelial cells that enhance binding to gal-3. Galectin-3's proangiogenic functions were found to be predominantly dependent on the Notch ligand JAG1. Differential direct binding to JAG1 was shown by surface plasmon resonance assay. Upon binding to Notch ligands, gal-3 preferentially increased JAG1 protein half-life over DLL4 and preferentially activated JAG1/Notch-1 signaling in endothelial cells. JAG1 overexpression in Lewis lung carcinoma cells accelerated tumor growth in vivo, but this effect was prevented in Lgals3-/- mice. Our findings establish gal-3 as a molecular regulator of the JAG1/Notch-1 signaling pathway and have direct implications for the development of strategies aimed at controlling tumor angiogenesis.

Indexed as

AnimalsBlood ProteinsDisease Models, AnimalEndothelial CellsGalectin 3GalectinsHumansHypoxiaIntracellular Signaling Peptides and ProteinsJagged-1 ProteinLigandsMembrane ProteinsMiceMice, KnockoutModels, BiologicalNeoplasmsBlood Proteinsdelta proteinGalectin 3GalectinsIntracellular Signaling Peptides and ProteinsJagged-1 ProteinLGALS3 protein, humanLigandsMembrane ProteinsReceptors, Notchangiogenesiscancergalectin-3Jagged-1Notch

Identifiers

PMID28533486
PMCPMC5564783
OpenAlexW2613903695

What OpenQuestion holds

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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.