Evidence map›Paper›PMID 22277129›Full record

ArticleBMC cancer2012

Disruption of CTCF at the miR-125b1 locus in gynecological cancers.

Ernesto Soto-Reyes, Rodrigo González-Barrios, Fernanda Cisneros-Soberanis, Roberto Herrera-Goepfert, Víctor Pérez, David Cantú, Diddier Prada, Clementina Castro, Félix Recillas-Targa, Luis A Herrera

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. The microbiome and its impact on the epigenome in cancer.Frontiers in epigenetics and epigenomics · 2026
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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

10 authors at 2 institutions in 1 country.

Ernesto Soto-ReyesUnidad de Investigación Biomédica en Cáncer, Instituto Nacional de Cancerología (INCan), Universidad Nacional Autónoma de México (UNAM), México, DF, México.
Rodrigo González-Barrios
Fernanda Cisneros-Soberanis
Roberto Herrera-Goepfert
Víctor Pérez
David Cantú
Diddier Prada
Clementina Castro
Félix Recillas-Targa
Luis A Herrera
Universidad Nacional Autónoma de México · MXInstituto Nacional de Cardiología · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn cancer cells, transcriptional gene silencing has been associated with genetic and epigenetic defects. The disruption of DNA methylation patterns and covalent histone marks has been associated with cancer development. Until recently, microRNA (miRNA) gene silencing was not well understood. In particular, miR-125b1 has been suggested to be an miRNA with tumor suppressor activity, and it has been shown to be deregulated in various human cancers. In the present study, we evaluated the DNA methylation at the CpG island proximal to the transcription start site of miR-125b1 in cancer cell lines as well as in normal tissues and gynecological tumor samples. In addition, we analyzed the association of CTCF and covalent histone modifications at the miR-125b1 locus.

methodsTo assess the DNA methylation status of the miR-125b1, genomic DNA was transformed with sodium bisulfite, and then PCR-amplified with modified primers and sequenced. The miR-125b1 gene expression was analyzed by qRT-PCR using U6 as a control for constitutive gene expression. CTCF repressive histone marks abundance was evaluated by chromatin immunoprecipitation assays.

resultsThe disruption of CTCF in breast cancer cells correlated with the incorporation of repressive histone marks such H3K9me3 and H3K27me3 as well as with aberrant DNA methylation patterns. To determine the effect of DNA methylation at the CpG island of miR-125b1 on the expression of this gene, we performed a qRT-PCR assay. We observed a significant reduction on the expression of miR-125b1 in cancer cells in comparison with controls, suggesting that DNA methylation at the CpG island might reduce miR-125b1 expression. These effects were observed in other gynecological cancers, including ovarian and cervical tumors.

conclusionsA reduction of miR-125b1 expression in cancers, correlated with methylation, repressive histone marks and loss of CTCF binding at the promoter region.

Indexed as

Breast NeoplasmsCCCTC-Binding FactorCell Line, TumorCpG IslandsDNA MethylationDNA, NeoplasmEpigenesis, GeneticFemaleGene SilencingHistonesHumansMicroRNAsOvarian NeoplasmsRepressor ProteinsUterine Cervical NeoplasmsCCCTC-Binding FactorCTCF protein, humanDNA, NeoplasmHistonesMicroRNAsMIRN125 microRNA, humanRepressor Proteins

Identifiers

PMID22277129
PMCPMC3297514
OpenAlexW2134634618

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.