Evidence map›Paper›PMID 27623747›Full record

ArticleScientific reports2016

Refinement of the androgen response element based on ChIP-Seq in androgen-insensitive and androgen-responsive prostate cancer cell lines.

Stephen Wilson, Jianfei Qi, Fabian V Filipp

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 2 pooled it
9.7field-weighted citation impact, top 1% 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

88 citing papers in PubMed, 2 syntheses or guidelines pooled it, 131 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Sex Steroid Hormone Regulation of T-Cell Function and Antitumor Immunity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
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  9. Androgens modulate endometrial function.Medical molecular morphology · 2025
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28 more citing papers are in PubMed but not listed here.

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.

Stephen WilsonSystems Biology and Cancer Metabolism, Program for Quantitative Systems Biology, University of California Merced, 2500 North Lake Road, Merced, CA 95343, USA.
Jianfei QiMarlene and Stewart Greenebaum Cancer Center, Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore MD 21201, USA.
Fabian V FilippSystems Biology and Cancer Metabolism, Program for Quantitative Systems Biology, University of California Merced, 2500 North Lake Road, Merced, CA 95343, USA.
University of California, Merced · USUniversity of Maryland, Baltimore · US

Funding

Tumor pyruvate kinase as key regulator of cancer metabolismR00CA154887 · NCI · UNIVERSITY OF CALIFORNIA, MERCED · PI FILIPP, FABIAN VOLKER · 2012 to 2014
$725k
Role of JMJD1A in hypoxia-induced EMT and prostate cancer stem cellsR00CA154888 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI QI, JIANFEI · 2013 to 2015
$685k
Molecular mechanisms controlling cell proliferation during tissue turnover and caR21CA176114 · NCI · UNIVERSITY OF CALIFORNIA, MERCED · PI OVIEDO, NESTOR J · 2014 to 2015
$361k
Role of Jmjd1a in hypoxia-induced EMT and prostate cancer stem cellsK99CA154888 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI QI, JIANFEI · 2011 to 2012
$215k
Tumor pyruvate kinase as key regulator of cancer metabolismK99CA154887 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI FILIPP, FABIAN VOLKER · 2011 to 2012
$177k
NCI NIH HHS K99 CA154887NCI NIH HHS K99 CA154888NCI NIH HHS R00 CA154887NCI NIH HHS R00 CA154888NCI NIH HHS R21 CA176114
6 · The paper itself

Abstract

Sequence motifs are short, recurring patterns in DNA that can mediate sequence-specific binding for proteins such as transcription factors or DNA modifying enzymes. The androgen response element (ARE) is a palindromic, dihexameric motif present in promoters or enhancers of genes targeted by the androgen receptor (AR). Using chromatin immunoprecipitation sequencing (ChIP-Seq) we refined AR-binding and AREs at a genome-scale in androgen-insensitive and androgen-responsive prostate cancer cell lines. Model-based searches identified more than 120,000 ChIP-Seq motifs allowing for expansion and refinement of the ARE. We classified AREs according to their degeneracy and their transcriptional involvement. Additionally, we quantified ARE utilization in response to somatic copy number amplifications, AR splice-variants, and steroid treatment. Although imperfect AREs make up 99.9% of the motifs, the degree of degeneracy correlates negatively with validated transcriptional outcome. Weaker AREs, particularly ARE half sites, benefit from neighboring motifs or cooperating transcription factors in regulating gene expression. Taken together, ARE full sites generate a reliable transcriptional outcome in AR positive cells, despite their low genome-wide abundance. In contrast, the transcriptional influence of ARE half sites can be modulated by cooperating factors.

Indexed as

AndrogensBinding SitesCell Line, TumorChromatin ImmunoprecipitationDNA-Binding ProteinsHumansMaleNeoplasm Recurrence, LocalNucleotide MotifsPromoter Regions, GeneticProstatic NeoplasmsProtein BindingReceptors, AndrogenResponse ElementsAndrogensAR protein, humanDNA-Binding ProteinsReceptors, Androgen

Identifiers

PMID27623747
PMCPMC5021938
OpenAlexW2518980159

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.