Evidence map›Paper›PMID 19789348›Full record

ArticleCancer research2009

Induction of prostatic intraepithelial neoplasia and modulation of androgen receptor by ETS variant 1/ETS-related protein 81.

Sook Shin, Tae-Dong Kim, Fang Jin, Jan M van Deursen, Scott M Dehm, Donald J Tindall, Joseph P Grande, Jan-Marie Munz, George Vasmatzis, Ralf Janknecht

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 83 citations in OpenAlex.

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  13. ETS factors in prostate cancer.Cancer letters · 2022
    Review
  14. Sumoylation of transcription factor ETV1 modulates its oncogenic potential in prostate cancer.International journal of clinical and experimental pathology · 2021
    Article
  15. Article
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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

10 authors at 2 institutions in 1 country.

Sook ShinDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.
Tae-Dong Kim
Fang Jin
Jan M van Deursen
Scott M Dehm
Donald J Tindall
Joseph P Grande
Jan-Marie Munz
George Vasmatzis
Ralf Janknecht
Mayo Clinic · USUniversity of Oklahoma Health Sciences Center · US

Funding

Utility of serum and Tissue Biomarkers for Predicting Response to Androgen DeprivP50CA091956 · NCI · MAYO CLINIC ROCHESTER · PI TINDALL, DONALD J. · 2001 to 2010
$23.4M
Coregulators in Androgen-Refractory Prostate CancerR01CA121277 · NCI · MAYO CLINIC ROCHESTER · PI TINDALL, DONALD J. · 2006 to 2010
$1.3M
Androgenic Inactivation of FOXO1 in Prostate CancerR01CA125747 · NCI · MAYO CLINIC ROCHESTER · PI TINDALL, DONALD J. · 2007 to 2011
$1.3M
NCI NIH HHS P50 CA091956NCI NIH HHS R01 CA121277NCI NIH HHS R01 CA125747
6 · The paper itself

Abstract

ETS variant 1 (ETV1), also known as ETS-related protein 81, is overexpressed in prostate tumors, but whether and how this transcription factor affects tumorigenesis has remained elusive. Here, we show that ETV1 is primarily overexpressed in the most aggressive human prostate tumors. Transgenic ETV1 mice developed prostatic intraepithelial neoplasia as well as hyperplasia/neoplasia in seminal vesicles. Moreover, ETV1 cooperated with the androgen receptor (AR) to bind to the prostate-specific antigen enhancer and stimulate gene transcription. Consistent with its ability to physically interact with AR, ETV1 rendered an ETV1 binding site-driven reporter androgen inducible, and, on the other hand, ETV1 super-induced transcription from an AR binding site on androgen stimulation. In conclusion, our study substantiates that ETV1 overexpression is an underlying cause in the development of prostate and possibly also seminal vesicle cancer. Its interaction with and activation of AR provides a molecular mechanism on how ETV1 exerts its deleterious function. Thus, inhibiting ETV1 or blocking its interaction with AR may represent novel strategies in prostate cancer therapy.

Indexed as

AndrogensAnimalsBinding SitesBlotting, WesternCell Line, TumorChromatin ImmunoprecipitationDNA-Binding ProteinsElectrophoretic Mobility Shift AssayEnhancer Elements, GeneticFemaleGene Expression Regulation, NeoplasticHumansImmunoprecipitationLasersLuciferasesMaleAndrogensAR protein, humanDNA-Binding ProteinsETV1 protein, humanLuciferasesProstate-Specific AntigenReceptors, AndrogenRNA, MessengerRNA, Small InterferingTranscription Factors

Identifiers

PMID19789348
PMCPMC3947560
OpenAlexW1982956833

What OpenQuestion holds

Textmetadata
LicenceTDM
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.