Evidence map›Paper›PMID 26735887›Full record

ArticleOncotarget2016

RUNX1 and FOXP3 interplay regulates expression of breast cancer related genes.

María Sol Recouvreux, Esteban Nicolás Grasso, Pablo Christian Echeverria, Luciana Rocha-Viegas, Lucio Hernán Castilla, Carolina Schere-Levy, Johanna Melisa Tocci, Edith Claudia Kordon, Natalia Rubinstein

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

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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 Sol RecouvreuxInstituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-UBA-CONICET), Buenos Aires, Argentina.
Esteban Nicolás GrassoInstituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-UBA-CONICET), Buenos Aires, Argentina.
Pablo Christian EcheverriaDepartment of Biologie Cellulaire, Universite de Geneve Sciences III, Geneve, Switzerland.
Luciana Rocha-ViegasInstituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-UBA-CONICET), Buenos Aires, Argentina.
Lucio Hernán CastillaDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, USA.
Carolina Schere-LevyInstituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-UBA-CONICET), Buenos Aires, Argentina.
Johanna Melisa TocciInstituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-UBA-CONICET), Buenos Aires, Argentina.
Edith Claudia KordonInstituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-UBA-CONICET), Buenos Aires, Argentina.
Natalia RubinsteinInstituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-UBA-CONICET), Buenos Aires, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARInstituto de Neurología de Buenos Aires · ARFundación Ciencias Exactas y Naturales · ARInstituto de Química y Fisicoquímica Biológicas · ARUniversity of Geneva · CHUniversity of Massachusetts Chan Medical School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Runx1 participation in epithelial mammary cells is still under review. Emerging data indicates that Runx1 could be relevant for breast tumor promotion. However, to date no studies have specifically evaluated the functional contribution of Runx1 to control gene expression in mammary epithelial tumor cells. It has been described that Runx1 activity is defined by protein context interaction. Interestingly, Foxp3 is a breast tumor suppressor gene. Here we show that endogenous Runx1 and Foxp3 physically interact in normal mammary cells and this interaction blocks Runx1 transcriptional activity. Furthermore we demonstrate that Runx1 is able to bind to R-spondin 3 (RSPO3) and Gap Junction protein Alpha 1 (GJA1) promoters. This binding upregulates Rspo3 oncogene expression and downregulates GJA1 tumor suppressor gene expression in a Foxp3-dependent manner. Moreover, reduced Runx1 transcriptional activity decreases tumor cell migration properties. Collectively, these data provide evidence of a new mechanism for breast tumor gene expression regulation, in which Runx1 and Foxp3 physically interact to control mammary epithelial cell gene expression fate. Our work suggests for the first time that Runx1 could be involved in breast tumor progression depending on Foxp3 availability.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAnimalsApoptosisBlotting, WesternBreast NeoplasmsCell MovementCell ProliferationChromatin ImmunoprecipitationConnexin 43Core Binding Factor Alpha 2 SubunitFemaleFluorescent Antibody TechniqueForkhead Transcription FactorsHumansImmunoenzyme TechniquesConnexin 43Core Binding Factor Alpha 2 SubunitForkhead Transcription FactorsFOXP3 protein, humanGJA1 protein, humanRSPO3 protein, humanR-SpondinsRUNX1 protein, humanThrombospondinsFoxp3gene expression regulationGJA1Rspo3Runx1

Identifiers

PMID26735887
PMCPMC4872732
OpenAlexW2299263021

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.