Evidence map›Paper›PMID 25595908›Full record

ArticleOncotarget2015

Specific and redundant activities of ETV1 and ETV4 in prostate cancer aggressiveness revealed by co-overexpression cellular contexts.

Diana Mesquita, João D Barros-Silva, Joana Santos, Rolf I Skotheim, Ragnhild A Lothe, Paula Paulo, Manuel R Teixeira

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
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  5. Article
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  7. Article
  8. Review
  9. Article
  10. Androgen-Driven Fusion Genes and Chimeric Transcripts in Prostate Cancer.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Article
  13. Strong cytoplasmic ETV1 expression has a negative impact on prostate cancer outcome.Virchows Archiv : an international journal of pathology · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Oncogenic mechanisms ofOncoscience · 2016
    Article
  19. 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

7 authors at 3 institutions in 2 countries.

Diana MesquitaDepartment of Genetics and Cancer Genetics Group - CI-IPOP, Portuguese Oncology Institute, Porto, Portugal.
João D Barros-SilvaDepartment of Genetics and Cancer Genetics Group - CI-IPOP, Portuguese Oncology Institute, Porto, Portugal.
Joana SantosDepartment of Genetics and Cancer Genetics Group - CI-IPOP, Portuguese Oncology Institute, Porto, Portugal.
Rolf I SkotheimDepartment of Cancer Prevention, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Nydalen, Oslo, Norway.
Ragnhild A LotheDepartment of Cancer Prevention, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Nydalen, Oslo, Norway.
Paula PauloDepartment of Genetics and Cancer Genetics Group - CI-IPOP, Portuguese Oncology Institute, Porto, Portugal.
Manuel R TeixeiraDepartment of Genetics and Cancer Genetics Group - CI-IPOP, Portuguese Oncology Institute, Porto, Portugal.
Instituto Português de Oncologia Francisco Gentil · PTOslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic rearrangements involving ETS transcription factors are found in 50-70% of prostate carcinomas. While the large majority of the rearrangements involve ERG, around 10% involve members of the PEA3 subfamily (ETV1, ETV4 and ETV5). Using a panel of prostate cancer cell lines we found co-overexpression of ETV1 and ETV4 in two cell line models of advanced prostate cancer (MDA-PCa-2b and PC3) and questioned whether these PEA3 family members would cooperate in the acquisition of oncogenic properties or show functional redundancy. Using shRNAs we found that ETV1 and ETV4 have partially overlapping functions, with ETV1 being more relevant for cell invasion and ETV4 for anchorage-independent growth. In vitro expression signatures revealed the regulation of both specific and shared candidate targets that may resemble cellular mechanisms in vivo by interaction with the same intermediate partners. By combining the phenotypic impact data and the gene expression profiles of in vitro models with clinico-pathological features and gene expression profiles of ETS-subtyped tumors, we identified a set of eight genes associated with advanced stage and a set of three genes associated with higher Gleason score, supporting an oncogenic role of ETV1 and ETV4 overexpression and revealing gene sets that may be useful as prognostic markers.

Indexed as

Adenovirus E1A ProteinsApoptosisBiomarkers, TumorBlotting, WesternCell AdhesionCell MovementCell ProliferationDNA-Binding ProteinsFlow CytometryGene Expression ProfilingGene Regulatory NetworksHumansImmunoenzyme TechniquesIn Situ Hybridization, FluorescenceMaleOligonucleotide Array Sequence AnalysisAdenovirus E1A ProteinsBiomarkers, TumorDNA-Binding ProteinsETV1 protein, humanETV4 protein, humanOncogene Proteins, FusionProto-Oncogene ProteinsProto-Oncogene Proteins c-etsRNA, MessengerTranscription FactorsETV1 and ETV4 co-overexpressiononcogenic rolePEA3-positive tumorsprostate cancertarget genes

Identifiers

PMID25595908
PMCPMC4467144
OpenAlexW1533091649

What OpenQuestion holds

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LicenceCC BY
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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.