Evidence map›Paper›PMID 21814574›Full record

ArticlePloS one2011

Cysteine-rich secretory protein-3 (CRISP3) is strongly up-regulated in prostate carcinomas with the TMPRSS2-ERG fusion gene.

Franclim R Ribeiro, Paula Paulo, Vera L Costa, João D Barros-Silva, João Ramalho-Carvalho, Carmen Jerónimo, Rui Henrique, Guro E Lind, Rolf I Skotheim, Ragnhild A Lothe and 1 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
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  6. Review
  7. Article
  8. Article
  9. Status ofProstate international · 2018
    Article
  10. Oncology letters · 2018
    Article
  11. Article
  12. ERG expression in prostate cancer: biological relevance and clinical implication.Journal of cancer research and clinical oncology · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. Article
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  19. Review
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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

11 authors at 4 institutions in 2 countries.

Franclim R RibeiroDepartment of Genetics, Portuguese Oncology Institute-Porto, Porto, Portugal.
Paula Paulo
Vera L Costa
João D Barros-Silva
João Ramalho-Carvalho
Carmen Jerónimo
Rui Henrique
Guro E Lind
Rolf I Skotheim
Ragnhild A Lothe
Manuel R Teixeira
Instituto Português de Oncologia Francisco Gentil · PTUniversity of Oslo · NOOslo University Hospital · NOUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large percentage of prostate cancers harbor TMPRSS2-ERG gene fusions, leading to aberrant overexpression of the transcription factor ERG. The target genes deregulated by this rearrangement, however, remain mostly unknown. To address this subject we performed genome-wide mRNA expression analysis on 6 non-malignant prostate samples and 24 prostate carcinomas with (n = 16) and without (n = 8) TMPRSS2-ERG fusion as determined by FISH. The top-most differentially expressed genes and their associations with ERG over-expression were technically validated by quantitative real-time PCR and biologically validated in an independent series of 200 prostate carcinomas. Several genes encoding metabolic enzymes or extracellular/transmembrane proteins involved in cell adhesion, matrix remodeling and signal transduction pathways were found to be co-expressed with ERG. Within those significantly over-expressed in fusion-positive carcinomas, CRISP3 showed more than a 50-fold increase when compared to fusion-negative carcinomas, whose expression levels were in turn similar to that of non-malignant samples. In the independent validation series, ERG and CRISP3 mRNA levels were strongly correlated (r(s) = 0.65, p<0.001) and both were associated with pT3 disease staging. Furthermore, immunohistochemistry results showed CRISP3 protein overexpression in 63% of the carcinomas and chromatin immunoprecipitation with an anti-ERG antibody showed that CRISP3 is a direct target of the transcription factor ERG. We conclude that ERG rearrangement is associated with significant expression alterations in genes involved in critical cellular pathways that define a subset of locally advanced PCa. In particular, we show that CRISP3 is a direct target of ERG that is strongly overexpressed in PCa with the TMPRSS2-ERG fusion gene.

Indexed as

Gene Expression Regulation, NeoplasticAgedBiomarkers, TumorBlotting, WesternCase-Control StudiesChromatin ImmunoprecipitationGene Expression ProfilingGenome, HumanHumansImmunoenzyme TechniquesIn Situ Hybridization, FluorescenceMaleMiddle AgedOligonucleotide Array Sequence AnalysisOncogene Proteins, FusionProstateBiomarkers, TumorCRISP3 protein, humanOncogene Proteins, FusionRNA, MessengerSalivary Proteins and PeptidesSeminal Plasma ProteinsTMPRSS2-ERG fusion protein, human

Identifiers

PMID21814574
PMCPMC3141037
OpenAlexW2082911875

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Registered trials

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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.