Evidence map›Paper›PMID 24616504›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Protective role of miR-155 in breast cancer through RAD51 targeting impairs homologous recombination after irradiation.

Pierluigi Gasparini, Francesca Lovat, Matteo Fassan, Lucia Casadei, Luciano Cascione, Naduparambil K Jacob, Stefania Carasi, Dario Palmieri, Stefan Costinean, Charles L Shapiro and 2 more

RetractedErratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 119 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 3 pooled it
10.4field-weighted citation impact, top 1% 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

119 citing papers in PubMed, 3 syntheses or guidelines pooled it, 221 citations in OpenAlex.

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  19. Molecular medicine reports · 2023
    Article
  20. Application of nano-radiosensitizers in combination cancer therapy.Bioengineering & translational medicine · 2023
    Review

59 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Pierluigi GaspariniDepartment of Molecular Virology, Immunology and Medical Genetics, Wexner Medical Center and Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210.
Francesca Lovat
Matteo Fassan
Lucia Casadei
Luciano Cascione
Naduparambil K Jacob
Stefania Carasi
Dario Palmieri
Stefan Costinean
Charles L Shapiro
Kay Huebner
Carlo M Croce
The Ohio State University · USThe Ohio State University Wexner Medical Center · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
Identifying non-coding RNAs for early detection and prevention of lung cancerU01CA166905 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M, PASS, HARVEY IRA · 2013 to 2017
$4.5M
MicroRNA profiles of TN breast cancer to define subgroups and targets for therapyU01CA154200 · NCI · OHIO STATE UNIVERSITY · PI HUEBNER, KAY · 2010 to 2014
$2.3M
MiRNAs/UCRs: biomarkers for cancer risk, tumor detection, progression & treatmentU01CA152758 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M · 2010 to 2014
$1.8M
Wwox as a Critical Signal Mediator in Breast CancerR01CA120516 · NCI · OHIO STATE UNIVERSITY · PI HUEBNER, KAY · 2006 to 2013
$1.3M
NCI NIH HHS CA120516NCI NIH HHS CA152758NCI NIH HHS CA154200NCI NIH HHS CA166905NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA120516NCI NIH HHS U01 CA152758NCI NIH HHS U01 CA154200NCI NIH HHS U01 CA166905
6 · The paper itself

Abstract

Cell survival after DNA damage relies on DNA repair, the abrogation of which causes genomic instability and development of cancer. However, defective DNA repair in cancer cells can be exploited for cancer therapy using DNA-damaging agents. DNA double-strand breaks are the major lethal lesions induced by ionizing radiation (IR) and can be efficiently repaired by DNA homologous recombination, a system that requires numerous factors including the recombinase RAD51 (RAD51). Therapies combined with adjuvant radiotherapy have been demonstrated to improve the survival of triple-negative breast cancer patients; however, such therapy is challenged by the emergence of resistance in tumor cells. It is, therefore, essential to develop novel therapeutic strategies to overcome radioresistance and improve radiosensitivity. In this study we show that overexpression of microRNA 155 (miR-155) in human breast cancer cells reduces the levels of RAD51 and affects the cellular response to IR. miR-155 directly targets the 3'-untranslated region of RAD51. Overexpression of miR-155 decreased the efficiency of homologous recombination repair and enhanced sensitivity to IR in vitro and in vivo. High miR-155 levels were associated with lower RAD51 expression and with better overall survival of patients in a large series of triple-negative breast cancers. Taken together, our findings indicate that miR-155 regulates DNA repair activity and sensitivity to IR by repressing RAD51 in breast cancer. Testing for expression levels of miR-155 may be useful in the identification of breast cancer patients who will benefit from an IR-based therapeutic approach.

Indexed as

Breast NeoplasmsFemaleHomologous RecombinationHumansMCF-7 CellsMicroRNAsModels, BiologicalPrognosisRad51 RecombinaseRadiation ToleranceMicroRNAsMIRN155 microRNA, humanRAD51 protein, humanRad51 Recombinasegamma-raysnoncoding RNATNBC

Identifiers

PMID24616504
PMCPMC3970505
OpenAlexW2007138966

What OpenQuestion holds

Textmetadata
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.