Evidence map›Paper›PMID 23472063›Full record

ArticlePloS one2013

5' UTR control of native ERG and of Tmprss2:ERG variants activity in prostate cancer.

Francesca Zammarchi, George Boutsalis, Luca Cartegni

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 54 citations in OpenAlex.

  1. Regulation of translation by upstream translation initiation codons of surfactant protein A1 splice variants.American journal of physiology. Lung cellular and molecular physiology · 2015
    Trial
  2. Case Report: A heterozygous loss-of-function variant of theFrontiers in cardiovascular medicine · 2025
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  20. Alternative splicing programs in prostate cancer.International journal of cell biology · 2013
    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

3 authors at 2 institutions in 1 country.

Francesca ZammarchiDepartment of Molecular Pharmacology and Chemistry, Memorial Sloan-Kettering Cancer Center, New York, New York, USA.
George Boutsalis
Luca Cartegni
Memorial Sloan Kettering Cancer Center · USCornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ERG, a member of the ETS transcription factor family, is frequently overexpressed in prostate cancer as a result of its fusion to the androgen-responsive Tmprss2 gene. Different genomic rearrangements and alternative splicing events around the junction region lead to multiple combination of Tmprss2:ERG fusion transcripts that correlate with different tumor aggressiveness, but their specific functions and biological activities are still unclear. The complexity of ERG expression pattern is compounded by the use of alternative promoters, splice sites, polyadenylation sites and translation initiation sites in both the native and fusion contexts. Our systematic characterization of native ERG and Tmprss2:ERG variants reveals that their different oncogenic potential is impacted by the status of the Ets domain and the configuration of the 5' UTR region. In particular, expression and activity of functional ERG and Tmprss2:ERG variants are influenced both by translation initiation signals within the different isoforms and by inhibitory upstream Open Reading Frames (uORF) in their 5' UTRs. Stable expression of ERG and Tmprss2:ERG variants promoted cell migration/invasion, induced a block of proliferation and induced a senescence-like state, suggesting a role for these variants in the prostate tumorigenesis process. In addition to Tmprss2:ERG fusion products, a group of related native ERG isoforms is also highly over-expressed in fusion-carrying prostate cancers, and share the same translation initiation site (in ERG exon 4) with the commonly observed Tmprss2 exon1 joined to ERG exon 4 (T1:E4) fusion-derived variant. Usage of this ATG can be preferentially down-regulated by directed antisense-based compounds, possibly representing the basis of a targeted approach that distinguishes between tumor-associated and normal ERG.

Indexed as

5' Untranslated RegionsGene Expression Regulation, NeoplasticAlternative SplicingAnimalsCell DeathCell Line, TumorGenetic VariationHeLa CellsHumansMaleMiceNIH 3T3 CellsOpen Reading FramesPromoter Regions, GeneticProstatic NeoplasmsProtein Biosynthesis5' Untranslated RegionsERG protein, humanProtein IsoformsSerine EndopeptidasesTMPRSS2 protein, humanTrans-ActivatorsTranscriptional Regulator ERG

Identifiers

PMID23472063
PMCPMC3589450
OpenAlexW2045698719

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.