Evidence map›Paper›PMID 25980494›Full record

ArticleOncotarget2015

Cyr61 as mediator of Src signaling in triple negative breast cancer cells.

María Pilar Sánchez-Bailón, Annarica Calcabrini, Víctor Mayoral-Varo, Agnese Molinari, Kay-Uwe Wagner, Jesús Pérez Losada, Sergio Ciordia, Juan Pablo Albar, Jorge Martín-Pérez

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  4. TargetingInternational journal of molecular sciences · 2020
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  14. Dual roles of CCN proteins in breast cancer progression.Journal of cell communication and signaling · 2016
    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 6 institutions in 3 countries.

María Pilar Sánchez-BailónDepartamento de Biología del Cáncer, Instituto de Investigaciones Biomédicas A. Sols (CSIC/UAM), Madrid 28029, Spain.
Annarica CalcabriniDepartamento de Biología del Cáncer, Instituto de Investigaciones Biomédicas A. Sols (CSIC/UAM), Madrid 28029, Spain.
Víctor Mayoral-VaroDepartamento de Biología del Cáncer, Instituto de Investigaciones Biomédicas A. Sols (CSIC/UAM), Madrid 28029, Spain.
Agnese MolinariDipartimento Tecnologie e Salute, Istituto Superiore di Sanità, Roma 00161, Italy.
Kay-Uwe WagnerEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198-6805, USA.
Jesús Pérez LosadaCentro de Investigación del Cáncer (CSIC/USAL), Campus Unamuno, Salamanca 37007, Spain.
Sergio CiordiaServicio de Proteómica, Centro Nacional de Biotecnología (CSIC), Madrid 28049, Spain.
Juan Pablo AlbarServicio de Proteómica, Centro Nacional de Biotecnología (CSIC), Madrid 28049, Spain.
Jorge Martín-PérezDepartamento de Biología del Cáncer, Instituto de Investigaciones Biomédicas A. Sols (CSIC/UAM), Madrid 28029, Spain.
Centro Nacional de Biotecnología · ESInstituto de Investigaciones Biomédicas Sols-Morreale · ESUniversidad Autónoma de Madrid · ESCentro de Investigación del Cáncer · ESIstituto Superiore di Sanità · ITUniversity of Nebraska Medical Center · US

Funding

Growth-Regulatory Signaling Networks in Breast CancerR01CA117930 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WAGNER, KAY-UWE · 2006 to 2016
$2.5M
NCI NIH HHS R01 CA117930
6 · The paper itself

Abstract

SFKs are involved in tumorigenesis and metastasis. Here we analyzed c-Src contribution to initial steps of metastasis by tetracycline-dependent expression of a specific shRNA-c-Src, which suppressed c-Src mRNA and protein levels in metastatic MDA-MB-231 cells. c-Src suppression did not alter cell proliferation or survival, but it significantly reduced anchorage-independent growth. Concomitantly with diminished tyrosine-phosphorylation/activation of Fak, caveolin-1, paxillin and p130CAS, c-Src depletion also inhibited cellular migration, invasion and transendothelial migration. Quantitative proteomic analyses of the secretome showed that Cyr61 levels, which were detected in the exosomal fraction, were diminished upon shRNA-c-Src expression. In contrast, Cyr61 expression was unaltered inside cells. Cyr61 partially colocalized with cis-Golgi gp74 marker and with exosomal marker CD63, but c-Src depletion did not alter their cellular distribution. In SUM159PT cells, transient c-Src suppression also reduced secreted exosomal Cyr61 levels. Furthermore, conditional expression of a c-Src dominant negative mutant (SrcDN, c-Src-K295M/Y527F) in MDA-MB-231 and in SUM159PT diminished secreted Cyr61 as well. Cyr61 transient suppression in MDA-MB-231 inhibited invasion and transendothelial migration. Finally, in both MDA-MB-231 and SUM159PT, a neutralizing Cyr61 antibody restrained migration. Collectively, these results suggest that c-Src regulates secreted proteins, including the exosomal Cyr61, which are involved in modulating the metastatic potential of triple negative breast cancer cells.

Indexed as

Biomarkers, TumorCell Line, TumorCell MovementCell ProliferationCSK Tyrosine-Protein KinaseCysteine-Rich Protein 61FemaleHumansProteomicsRNA, MessengerSignal Transductionsrc-Family KinasesTriple Negative Breast NeoplasmsBiomarkers, TumorCCN1 protein, humanCSK protein, humanCSK Tyrosine-Protein KinaseCysteine-Rich Protein 61RNA, Messengersrc-Family Kinasesc-SrcCyr61invasionmigrationtriple negative breast cancer

Identifiers

PMID25980494
PMCPMC4537031
OpenAlexW1590055389

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.