Evidence map›Paper›PMID 38236307›Full record

ArticleMolecular biology reports2024

Differential DNA methylation and CTCF binding between the ESR1 promoter a of MCF-7 and MDA-MB-231 breast cancer cells.

Edén Víctor Montes-de-Oca-Fuentes, Karina Jácome-López, Anaís Zarco-Mendoza, Georgina Guerrero, José Luis Ventura-Gallegos, Sergio Juárez-Méndez, Alberto Jose Cabrera-Quintero, Félix Recillas-Targa, Alejandro Zentella-Dehesa

Open access · hybridAbstract read
In one paragraph

Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. 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 4 institutions in 1 country.

Edén Víctor Montes-de-Oca-FuentesDepartamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México, 04510, México.
Karina Jácome-LópezUnidad de Bioquímica, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, 14080, México.
Anaís Zarco-MendozaDivisión de Investigación Básica, Laboratorio de Virus y Cancer, Secretaría de Salud, Instituto Nacional de Cancerología, Ciudad de México, 14080, México.
Georgina GuerreroDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad de México, 04510, México.
José Luis Ventura-GallegosDepartamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México, 04510, México.
Sergio Juárez-MéndezLaboratorio de Oncología Experimental, Secretaría de Salud, Instituto Nacional de Pediatría, Ciudad de México, 04530, México.
Alberto Jose Cabrera-QuinteroDepartamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México, 04510, México.
Félix Recillas-TargaDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad de México, 04510, México.
Alejandro Zentella-DehesaDepartamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México, 04510, México. azentell@iibiomedicas.unam.mx.ORCID http://orcid.org/0000-0002-5595-1466
Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MXUniversidad Nacional Autónoma de México · MXInstituto Nacional de Cancerología · MXInstituto Nacional de Pediatria · MX

Funding

Consejo Nacional de Ciencia y Tecnología 172558
6 · The paper itself

Abstract

backgroundESR1 is expressed by 60-70% of breast tumours. it's a good prognosis factor and the target of hormone therapy. Optimization of ESR1 reactivation therapy is currently ongoing. Here we probe if the transcription factor CTCF plays a role in the differential expression of ESR1 in the breast cancer cell lines MCF-7 (ESR1+) and MDA-MB-231 (ESR1-). METHODS AND

resultsKnockdown of CTCF in MCF-7 resulted in decreased ESR1 gene expression. CTCF binds to the promoter of ESR1 in MCF-7 but not in MDA-MB-231 cells. CTCF ESR1 binding sites are unmethylated in MCF7 but methylated in MDA-MB-231 cells.

conclusionESR1 expression in MCF7 cells is dependent on CTCF expression. CTCF can bind to specific regions of the promotor of ESR1 gene in MCF-7 cells but not in MDA-MB-231 cells, this correlates with the methylation status of these regions and could be involved in the transcriptional regulation of ESR1.

Indexed as

Breast NeoplasmsCCCTC-Binding FactorDNA MethylationEstrogen Receptor alphaDNAHumansMCF-7 CellsMDA-MB-231 CellsPromoter Regions, GeneticCCCTC-Binding FactorCTCF protein, humanDNAESR1 protein, humanEstrogen Receptor alphaBreast cancerCTCFDNA methylationESR1TNBC

Identifiers

PMID38236307
PMCPMC10796618
OpenAlexW4390972146

What OpenQuestion holds

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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.