Evidence map›Paper›PMID 22665497›Full record

ArticleMolecular and cellular biology2012

The stress response mediator ATF3 represses androgen signaling by binding the androgen receptor.

Hongbo Wang, Ming Jiang, Hongmei Cui, Mengqian Chen, Ralph Buttyan, Simon W Hayward, Tsonwin Hai, Zhengxin Wang, Chunhong Yan

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.9field-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

26 citing papers in PubMed, 41 citations in OpenAlex.

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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

9 authors at 5 institutions in 1 country.

Hongbo WangCenter for Cell Biology and Cancer Research, Albany Medical College, Albany, New York, USA.
Ming Jiang
Hongmei Cui
Mengqian Chen
Ralph Buttyan
Simon W Hayward
Tsonwin Hai
Zhengxin Wang
Chunhong Yan
Albany Medical Center Hospital · USVanderbilt University · USColumbia College - South Carolina · USThe Ohio State University · USThe University of Texas MD Anderson Cancer Center · US

Funding

Paracrine Regulation of BPH PathogenesisR01DK067049 · NIDDK · VANDERBILT UNIVERSITY · PI HAYWARD, SIMON W · 2004 to 2013
$2.6M
The Role of ATF3 in the DNA Damage ResponseR01CA139107 · NCI · AUGUSTA UNIVERSITY · PI YAN, CHUNHONG · 2010 to 2015
$1.2M
ATF3 in Beta cell signaling, expression &destructionR01DK059605 · NIDDK · OHIO STATE UNIVERSITY · PI HAI, TSONWIN · 2003 to 2006
$1.2M
ATF3, a stress-inducible gene, in tumorigenesis and metastasisR01CA118306 · NCI · OHIO STATE UNIVERSITY · PI HAI, TSONWIN · 2008 to 2011
$1.0M
Screening Assays for Small Molecules Targeting Oncogenic eIF4E ExpressionR01CA164006 · NCI · AUGUSTA UNIVERSITY · PI YAN, CHUNHONG · 2012 to 2014
$832k
NCI NIH HHS R01 CA118306NCI NIH HHS R01 CA139107NCI NIH HHS R01CA139107NCI NIH HHS R01 CA164006NCI NIH HHS R01CA164006NIDDK NIH HHS R01 DK059605NIDDK NIH HHS R01 DK067049NIDDK NIH HHS R01DK067049
6 · The paper itself

Abstract

Activating transcription factor 3 (ATF3) is a common mediator of cellular stress response signaling and is often aberrantly expressed in prostate cancer. We report here that ATF3 can directly bind the androgen receptor (AR) and consequently repress AR-mediated gene expression. The ATF3-AR interaction requires the leucine zipper domain of ATF3 that independently binds the DNA-binding and ligand-binding domains of AR, and the interaction prevents AR from binding to cis-acting elements required for expression of androgen-dependent genes while inhibiting the AR N- and C-terminal interaction. The functional consequences of the loss of ATF3 expression include increased transcription of androgen-dependent genes in prostate cancer cells that correlates with increased ability to grow in low-androgen-containing medium and increased proliferative activity of the prostate epithelium in ATF3 knockout mice that is associated with prostatic hyperplasia. Our results thus demonstrate that ATF3 is a novel repressor of androgen signaling that can inhibit AR functions, allowing prostate cells to restore homeostasis and maintain integrity in the face of a broad spectrum of intrinsic and environmental insults.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionActivating Transcription Factor 3AnimalsCell Line, TumorCell ProliferationEpitheliumGene Expression RegulationHomeostasisHumansMaleMiceMice, KnockoutModels, BiologicalProstateProstatic NeoplasmsActivating Transcription Factor 3ATF3 protein, humanAtf3 protein, mouseReceptors, Androgen

Identifiers

PMID22665497
PMCPMC3434546
OpenAlexW2169073049

What OpenQuestion holds

Textmetadata
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.