Evidence map›Paper›PMID 23435425›Full record

ArticleOncogene2014

ELF3 is a repressor of androgen receptor action in prostate cancer cells.

A Shatnawi, J D Norris, C Chaveroux, J S Jasper, A B Sherk, D P McDonnell, V Giguère

Abstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Unique transcriptional signatures of sleep loss across independently evolved cavefish populations.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2020
    Article
  8. Article
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  12. Review
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  15. Moonlighting proteins in cancer.Cancer letters · 2016
    Review
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 4 institutions in 2 countries.

A ShatnawiGoodman Cancer Research Centre, McGill University, Montréal, Québec, Canada.
J D NorrisDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA.
C ChaverouxGoodman Cancer Research Centre, McGill University, Montréal, Québec, Canada.
J S JasperDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA.
A B SherkDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA.
D P McDonnellDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA.
V Giguère1] Goodman Cancer Research Centre, McGill University, Montréal, Québec, Canada. [2] Departments of Biochemistry, Medicine and Oncology, McGill University, Montréal, Québec, Canada.
Duke Medical Center · USMcGill University Health Centre · CADuke University Hospital · USMcGill University · CA

Funding

Molecular Determinants of Androgen Receptor PharmacologyR01CA139818 · NCI · DUKE UNIVERSITY · PI MCDONNELL, DONALD P · 2009 to 2013
$1.7M
CIHR MOP-64275NCI NIH HHS 5R01 CA139818NCI NIH HHS R01 CA139818
6 · The paper itself

Abstract

The androgen receptor (AR) has a critical role in the development and progression of prostate cancer (PC) and is a major therapeutic target in this disease. The transcriptional activity of AR is modulated by the coregulators with which it interacts, and consequently deregulation of cofactor expression and/or activity impacts the expression of genes whose products can have a role in PC pathogenesis. Here we report that E74-like factor 3 (ELF3), a member of the ETS family of transcription factors, is a repressor of AR transcriptional activity. Exogenous expression of ELF3 represses AR transcriptional activity when assessed using reporter-based transfection assays or when evaluated on endogenous AR target genes. Conversely, ELF3 knock down increases the AR transcriptional activity. Biochemical dissection of this activity indicates that it results from the physical interaction between ELF3 and AR and that this interaction inhibits the recruitment of AR to specific androgen response elements within target gene promoters. Significantly, we observed that depletion of ELF3 expression in LNCaP cells promotes cell migration, whereas increased ELF3 expression severely inhibits tumor growth in vitro and in a mouse xenograft model. Taken together, these results suggest that modulation of ELF3 expression and/or AR/ELF3 interaction may have utility in the treatment of PC.

Indexed as

AnimalsCell Line, TumorCell MovementDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred NODMice, SCIDNeoplasm TransplantationProstatic NeoplasmsProtein BindingProtein Interaction Domains and MotifsProto-Oncogene ProteinsProto-Oncogene Proteins c-etsDNA-Binding ProteinsELF3 protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-etsReceptors, AndrogenRepressor ProteinsTranscription Factors

Identifiers

PMID23435425
PMCPMC4103030
OpenAlexW2067356799

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.