Evidence map›Paper›PMID 27966446›Full record

ArticleOncotarget2017

VE-cadherin RGD motifs promote metastasis and constitute a potential therapeutic target in melanoma and breast cancers.

Rubén A Bartolomé, Sofía Torres, Soledad Isern de Val, Beatriz Escudero-Paniagua, Eva Calviño, Joaquín Teixidó, J Ignacio Casal

Open access · diamondAbstract read
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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
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

29 citing papers in PubMed, 39 citations in OpenAlex.

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  12. Exosomes and organ-specific metastasis.Molecular therapy. Methods & clinical development · 2021
    Review
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  15. The Overexpression ofFrontiers in oncology · 2021
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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

7 authors at 1 institution in 1 country.

Rubén A BartoloméDepartment of Cellular and Molecular Medicine, Centro de Investigaciones Biológicas (CIB-CSIC), Ramiro de Maeztu, Madrid, Spain.
Sofía TorresDepartment of Cellular and Molecular Medicine, Centro de Investigaciones Biológicas (CIB-CSIC), Ramiro de Maeztu, Madrid, Spain.
Soledad Isern de ValDepartment of Cellular and Molecular Medicine, Centro de Investigaciones Biológicas (CIB-CSIC), Ramiro de Maeztu, Madrid, Spain.
Beatriz Escudero-PaniaguaDepartment of Cellular and Molecular Medicine, Centro de Investigaciones Biológicas (CIB-CSIC), Ramiro de Maeztu, Madrid, Spain.
Eva CalviñoDepartment of Cellular and Molecular Medicine, Centro de Investigaciones Biológicas (CIB-CSIC), Ramiro de Maeztu, Madrid, Spain.
Joaquín TeixidóDepartment of Cellular and Molecular Medicine, Centro de Investigaciones Biológicas (CIB-CSIC), Ramiro de Maeztu, Madrid, Spain.
J Ignacio CasalDepartment of Cellular and Molecular Medicine, Centro de Investigaciones Biológicas (CIB-CSIC), Ramiro de Maeztu, Madrid, Spain.
Centro de Investigaciones Biológicas Margarita Salas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have investigated the role of vascular-endothelial (VE)-cadherin in melanoma and breast cancer metastasis. We found that VE-cadherin is expressed in highly aggressive melanoma and breast cancer cell lines. Remarkably, inactivation of VE-cadherin triggered a significant loss of malignant traits (proliferation, adhesion, invasion and transendothelial migration) in melanoma and breast cancer cells. These effects, except transendothelial migration, were induced by the VE-cadherin RGD motifs. Co-immunoprecipitation experiments demonstrated an interaction between VE-cadherin and α2β1 integrin, with the RGD motifs found to directly affect β1 integrin activation. VE-cadherin-mediated integrin signaling occurred through specific activation of SRC, ERK and JNK, including AKT in melanoma. Knocking down VE-cadherin suppressed lung colonization capacity of melanoma or breast cancer cells inoculated in mice, while pre-incubation with VE-cadherin RGD peptides promoted lung metastasis for both cancer types. Finally, an in silico study revealed the association of high VE-cadherin expression with poor survival in a subset of melanoma patients and breast cancer patients showing low CD34 expression. These findings support a general role for VE-cadherin and other RGD cadherins as critical regulators of lung and liver metastasis in multiple solid tumours. These results pave the way for cadherin-specific RGD targeted therapies to control disseminated metastasis in multiple cancers.

Indexed as

OligopeptidesProtein Interaction Domains and MotifsAnimalsAntigens, CDAntineoplastic AgentsBreast NeoplasmsCadherin 5CadherinsCell AdhesionCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalFemaleGene ExpressionHeterograftsAntigens, CDAntineoplastic Agentsarginyl-glycyl-aspartic acidCadherin 5CadherinsIntegrinsOligopeptidesbreast cancermelanomametastasisRGD motifVE-cadherin

Identifiers

PMID27966446
PMCPMC5352113
OpenAlexW2559933726

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.