Evidence map›Paper›PMID 16980632›Full record

ArticleMolecular and cellular biology2006

Locus-wide chromatin remodeling and enhanced androgen receptor-mediated transcription in recurrent prostate tumor cells.

Li Jia, Howard C Shen, Marcus Wantroba, Omar Khalid, Gangning Liang, Qingcai Wang, Elisabet Gentzschein, Jacek K Pinski, Frank Z Stanczyk, Peter A Jones and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Review
  3. Epigenetic Regulation in Prostate Cancer Progression.Current molecular biology reports · 2018
    Review
  4. Exploiting Epigenetic Alterations in Prostate Cancer.International journal of molecular sciences · 2017
    Review
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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

11 authors at 2 institutions in 2 countries.

Li JiaDepartment of Urology, Norris Cancer Center, USC Keck School of Medicine, Los Angeles, California, USA.
Howard C Shen
Marcus Wantroba
Omar Khalid
Gangning Liang
Qingcai Wang
Elisabet Gentzschein
Jacek K Pinski
Frank Z Stanczyk
Peter A Jones
Gerhard A Coetzee
General Department of Preventive Medicine · VNUSC Norris Comprehensive Cancer Center · US

Funding

VIRAL AND CHEMICAL CARCINOGENESIST32CA009320 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JONES, PETER A · 1985 to 2012
$2.5M
AR and RUNX2 target genes in prostate cancerR01CA109147 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI COETZEE, GERHARD A · 2006 to 2010
$1.3M
NCI NIH HHS R01 CA109147NCI NIH HHS R01CA109147NCI NIH HHS T32 CA009320NCI NIH HHS T32CA009320
6 · The paper itself

Abstract

Prostate cancers (PCas) become resistant to hormone withdrawal through increased androgen receptor (AR) signaling. Here we show increased AR-mediated transcription efficiency in PCa cells that have acquired the ability to grow in low concentrations of androgen. Compared to androgen-dependent PCa cells, these cells showed increased activity of transiently transfected reporters and increased mRNA synthesis relative to levels of AR occupancy of the prostate-specific antigen (PSA) gene. The locus also displayed up to 10-fold-higher levels of histone H3-K9/K14 acetylation and H3-K4 methylation across the entire body of the gene. Although similar increased mRNA expression and locus-wide histone acetylation were also observed at another kallikrein locus (KLK2), at a third AR target locus (TMPRSS2) increased gene expression and locus-wide histone acetylation were not seen in the absence of ligand. Androgen-independent PCa cells have thus evolved three distinctive alterations in AR-mediated transcription. First, increased RNA polymerase initiation and processivity contributed to increased gene expression. Second, AR signaling was more sensitive to ligand. Third, locus-wide chromatin remodeling conducive to the increased gene expression in the absence of ligand was apparent and depended on sustained AR activity. Therefore, increased AR ligand sensitivity as well as locus-specific chromatin alterations contribute to basal gene expression of a subpopulation of specific AR target genes in androgen-independent PCa cells. These features contribute to the androgen-independent phenotype of these cells.

Indexed as

Chromatin Assembly and DisassemblyTranscription, GeneticAcetylationAndrogensAnimalsChromatinDihydrotestosteroneGenes, ReporterHistonesHumansLigandsLuciferasesMaleMethylationMiceMice, NudeAndrogensAR protein, humanChromatinDihydrotestosteroneHistonesLigandsLuciferasesProstate-Specific AntigenReceptors, Androgen

Identifiers

PMID16980632
PMCPMC1592894
OpenAlexW1965000608

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.