Evidence map›Paper›PMID 32764667›Full record

ArticleScientific reports2020

PRMT1-dependent methylation of BRCA1 contributes to the epigenetic defense of breast cancer cells against ionizing radiation.

María F Montenegro, Rebeca González-Guerrero, Luis Sánchez-Del-Campo, Antonio Piñero-Madrona, Juan Cabezas-Herrera, José Neptuno Rodríguez-López

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

29 citing papers in PubMed, 34 citations in OpenAlex.

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  15. Role of PRMT1 and PRMT5 in Breast Cancer.International journal of molecular sciences · 2024
    Review
  16. 8-Cl-Ado and 8-NHLeukemia · 2024
    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

6 authors at 1 institution in 1 country.

María F Montenegro *Department of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, Spain. fermontenegro@um.es.
Rebeca González-Guerrero *Department of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, Spain.
Luis Sánchez-Del-CampoDepartment of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, Spain.
Antonio Piñero-MadronaDepartment of Surgery, University Hospital Virgen de la Arrixaca, IMIB, Murcia, Spain.
Juan Cabezas-HerreraMolecular Therapy and Biomarkers Research Group, University Hospital Virgen de la Arrixaca, IMIB, Murcia, Spain.
José Neptuno Rodríguez-LópezDepartment of Biochemistry and Molecular Biology A, School of Biology, University of Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB), Murcia, Spain. neptuno@um.es.
Instituto Murciano de Investigación Biosanitaria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The therapeutic effect of irradiation is thought to come from DNA damage that affects rapidly proliferating cancer cells; however, resistant cells rapidly initiate mechanisms to repair such damage. While DNA repair mechanisms responsible for cancer cell survival following DNA damage are understood, less is known about the epigenetic mechanisms resulting in resistance to radiotherapy. Although changes in DNA methylation are related to mechanisms of long-term resistance, it is more likely that the methylation state of a series of proteins could be responsible for the first-line of defense of cancer cells against irradiation. In this study, we observed that irradiation of breast cancer cells was accompanied by an overproduction in S-adenosylmethionine, which increases the activity of cellular methylases. We found that by activating PRMT1, irradiation triggers a BRCA1-dependent program that results in efficient DNA repair and inhibition of apoptosis. Depletion of PRMT1 in irradiated cells resulted in a switch of BRCA1 functions from repair and survival in the nucleus to activation of cell death signals in the cytoplasm. We conclude that by modulating the cellular localization of BRCA1, PRMT1 is an important regulator of the oncogenic functions of BRCA1, contributing to the epigenetic defense of breast cancer cells against ionizing radiation.

Indexed as

Radiation ToleranceAnimalsBRCA1 ProteinBreast NeoplasmsCell Line, TumorCell NucleusCell SurvivalCytoplasmDNA RepairEpigenesis, GeneticFemaleHumansMCF-7 CellsMiceProtein-Arginine N-MethyltransferasesRadiation, IonizingBRCA1 ProteinBRCA1 protein, humanPRMT1 protein, humanProtein-Arginine N-MethyltransferasesRepressor ProteinsS-Adenosylmethionine

Identifiers

PMID32764667
PMCPMC7413540
OpenAlexW3047604913

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.