Evidence map›Paper›PMID 30813351›Full record

ArticleInternational journal of molecular sciences2019

BCAS2 Enhances Carcinogenic Effects of Estrogen Receptor Alpha in Breast Cancer Cells.

Ángel Salmerón-Hernández, María Yamilet Noriega-Reyes, Albert Jordan, Noemi Baranda-Avila, Elizabeth Langley

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.1field-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

11 citing papers in PubMed, 31 citations in OpenAlex.

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  10. Genome-Wide DNA Methylation Profiles in Community Members Exposed to the World Trade Center Disaster.International journal of environmental research and public health · 2020
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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

5 authors at 3 institutions in 2 countries.

Ángel Salmerón-HernándezDepartamento de Investigación Básica, Instituto Nacional de Cancerología, Av. San Fernando No. 22, Col. Sección XVI, 14080 Mexico City, Mexico. angel.salher@yahoo.com.mx.
María Yamilet Noriega-ReyesDepartamento de Investigación Básica, Instituto Nacional de Cancerología, Av. San Fernando No. 22, Col. Sección XVI, 14080 Mexico City, Mexico. yamilet_noriega@hotmail.com.
Albert JordanInstitut de Biología Molecular de Barcelona (IBMB-CSIC) Parc Científic de Barcelona, Barcelona, 08028 Cataluña, Spain. ajvbmc@ibmb.csic.es.
Noemi Baranda-AvilaDepartamento de Investigación Básica, Instituto Nacional de Cancerología, Av. San Fernando No. 22, Col. Sección XVI, 14080 Mexico City, Mexico. mimi19481@yahoo.com.mx.
Elizabeth LangleyDepartamento de Investigación Básica, Instituto Nacional de Cancerología, Av. San Fernando No. 22, Col. Sección XVI, 14080 Mexico City, Mexico. langleyemx@gmail.com.
Instituto Nacional de Cancerología · MXInstitut de Biologia Molecular de Barcelona · ESUniversidad Nacional Autónoma de México · MX

Funding

Consejo Nacional de Ciencia y Tecnología 33831-M and 182189Instituto Nacional de Cancerología s/nPrograma de Apoyo a Proyectos de Investigación e Inovación Tecnológica, Dirección General de Asuntos del Personal Academico, UNAM s/n
6 · The paper itself

Abstract

Estrogen receptor alpha (ERα) has an established role in breast cancer biology. Transcriptional activation by ERα is a multistep process modulated by coactivator and corepressor proteins. Breast Cancer Amplified Sequence 2 (BCAS2), is a poorly studied ERα coactivator. In this work, we characterize some of the mechanisms through which this protein increases ERα activity and how this promotes carcinogenic processes in breast cancer cells. Using protein-protein interaction and luciferase assays we show that BCAS2 interacts with ERα both in vitro and in vivo and upregulates transcriptional activation of ERα directly through its N-terminal region (AF-1) and indirectly through its C-terminal (AF-2) region, acting in concert with AF-2 interacting coactivators. Elevated expression of BCAS2 positively affects proliferation, clonogenicity and migration of breast cancer cells and directly activates ERα regulated genes which have been shown to play a role in tumor growth and progression. Finally, we used signal transduction pathway inhibitors to elucidate how BCAS2 is regulated in these cells and observed that BCAS2 is preferentially regulated by the PI3K/AKT signaling pathway. BCAS2 is an AF-1 coactivator of ERα whose overexpression promotes carcinogenic processes, suggesting an important role in the development of estrogen-receptor positive breast cancer.

Indexed as

Breast NeoplasmsCarcinogenesisCell Line, TumorCell MovementCell ProliferationEstradiolEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHumansNeoplasm ProteinsPromoter Regions, GeneticProtein BindingSignal TransductionTranscription, GeneticTumor Stem Cell AssayBCAS2 protein, humanESR1 protein, humanEstradiolEstrogen Receptor alphaNeoplasm ProteinsBCAS2breast cancercoactivatorsestrogen receptor

Identifiers

PMID30813351
PMCPMC6412365
OpenAlexW2915630557

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.