Evidence map›Paper›PMID 21700680›Full record

ArticleMolecular cancer research : MCR2011

BRCA1 loss induces GADD153-mediated doxorubicin resistance in prostate cancer.

Paola De Luca, Elba S Vazquez, Cristian P Moiola, Florencia Zalazar, Javier Cotignola, Geraldine Gueron, Kevin Gardner, Adriana De Siervi

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  16. Prostate tumor growth is impaired by CtBP1 depletion in high-fat diet-fed mice.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
    Article
  17. Review
  18. A human XPC protein interactome--a resource.International journal of molecular sciences · 2013
    Article
  19. BRCA1 and p53 regulate critical prostate cancer pathways.Prostate cancer and prostatic diseases · 2013
    Article
  20. Article
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

8 authors at 3 institutions in 2 countries.

Paola De LucaLaboratory of Cancer and Apoptosis, Department of Biological Chemistry, School of Scences, University of Buenos Aires, CONICET, Buenos Aires, Argentina.
Elba S Vazquez
Cristian P Moiola
Florencia Zalazar
Javier Cotignola
Geraldine Gueron
Kevin Gardner
Adriana De Siervi
University of Buenos Aires · ARConsejo Nacional de Investigaciones Científicas y Técnicas · ARNational Cancer Institute · US

Funding

Molecular linkages between epigenetic regulation and metabolism in breast cancerZIABC010847 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GARDNER, KEVIN · 2009 to 2017
$7.7M
Intramural NIH HHS ZIA BC010847
6 · The paper itself

Abstract

BRCA1 plays numerous roles in the regulation of genome integrity and chemoresistance. Although BRCA1 interaction with key proteins involved in DNA repair is well known, its role as a coregulator in the transcriptional response to DNA damage remains poorly understood. In this study, we show that BRCA1 plays a central role in the transcriptional response to genotoxic stress in prostate cancer. BRCA1 expression mediates apoptosis, cell-cycle arrest, and decreased viability in response to doxorubicin treatment. Xenograft studies using human prostate carcinoma PC3 cells show that BRCA1 depletion results in increased tumor growth. A focused survey of BRCA1-regulated genes in prostate carcinoma reveals that multiple regulators of genome stability and cell-cycle control, including BLM, FEN1, DDB2, H3F3B, BRCA2, CCNB2, MAD2L1, and GADD153, are direct transcriptional targets of BRCA1. Furthermore, we show that BRCA1 targets GADD153 promoter to increase its transcription in response to DNA damage. Finally, GADD153 depletion significantly abrogates BRCA1 influence on cell-cycle progression and cell death in response to doxorubicin treatment. These findings define a novel transcriptional pathway through which BRCA1 orchestrates cell fate decisions in response to genotoxic insults, and suggest that BRCA1 status should be considered for new chemotherapeutic treatment strategies in prostate cancer.

Indexed as

AnimalsAntibiotics, AntineoplasticBRCA1 ProteinCarcinomaCell Cycle CheckpointsCell Line, TumorDNA DamageDoxorubicinDrug Resistance, NeoplasmGenomic InstabilityHumansMaleMiceProstatic NeoplasmsTranscription Factor CHOPAntibiotics, AntineoplasticBRCA1 ProteinDoxorubicinTranscription Factor CHOP

Identifiers

PMID21700680
PMCPMC6959536
OpenAlexW2138388674

What OpenQuestion holds

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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.