Evidence map›Paper›PMID 26945682›Full record

ArticleJournal of cellular physiology2016

The Androgen Receptor Regulates PPARγ Expression and Activity in Human Prostate Cancer Cells.

Emuejevoke Olokpa, Adrienne Bolden, LaMonica V Stewart

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

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  16. The role of androgen and its related signals in PCOS.Journal of cellular and molecular medicine · 2021
    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

3 authors at 1 institution in 1 country.

Emuejevoke OlokpaDepartment of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, Tennessee.
Adrienne BoldenDepartment of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, Tennessee.
LaMonica V StewartDepartment of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, Tennessee.
Meharry Medical College · US

Funding

The RCMI Program in Health Disparities Research at Meharry Medical College - SupplementU54MD007586 · NIMHD · MEHARRY MEDICAL COLLEGE · PI Samuel Evans Adunyah, JAMES E HILDRETH · 2017 to 2026
$48.2M
VANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7M
THE MEHARRY RISE INITIATIVER25GM059994 · NIGMS · MEHARRY MEDICAL COLLEGE · PI MOTLEY-JOHNSON, EVANGELINE D · 1999 to 2021
$23.0M
Meharry RCMI Program in Women's Health ResearchG12MD007586 · NIMHD · MEHARRY MEDICAL COLLEGE · PI HILDRETH, JAMES E · 2012 to 2016
$7.8M
Minority Institution Research Training ProgramT32HL007735 · NHLBI · MEHARRY MEDICAL COLLEGE · PI ADUNYAH, SAMUEL EVANS · 1992 to 2014
$2.9M
Regulation of Prostate Cancer Growth by PPARg LigandsK01CA114253 · NCI · MEHARRY MEDICAL COLLEGE · PI STEWART, LAMONICA VANETTE · 2006 to 2010
$792k
NCI NIH HHS K01 CA114253NCRR NIH HHS UL1 RR024975NHLBI NIH HHS T32 HL007735NIGMS NIH HHS R25 GM059994NIMHD NIH HHS G12 MD007586NIMHD NIH HHS U54 MD007586
6 · The paper itself

Abstract

The peroxisome proliferator activated receptor gamma (PPARγ) is a ligand-activated transcription factor that regulates growth and differentiation within normal prostate and prostate cancers. However the factors that control PPARγ within the prostate cancers have not been characterized. The goal of this study was to examine whether the androgen receptor (AR) regulates PPARγ expression and function within human prostate cancer cells. qRT-PCR and Western blot analyses revealed nanomolar concentrations of the AR agonist dihydrotestosterone (DHT) decrease PPARγ mRNA and protein within the castration-resistant, AR-positive C4-2 and VCaP human prostate cancer cell lines. The AR antagonists bicalutamide and enzalutamide blocked the ability of DHT to reduce PPARγ levels. In addition, siRNA mediated knockdown of AR increased PPARγ protein levels and ligand-induced PPARγ transcriptional activity within the C4-2 cell line. Furthermore, proteasome inhibitors that interfere with AR function increased the level of basal PPARγ and prevented the DHT-mediated suppression of PPARγ. These data suggest that AR normally functions to suppress PPARγ expression within AR-positive prostate cancer cells. To determine whether increases in AR protein would influence PPARγ expression and activity, we used lipofectamine-based transfections to overexpress AR within the AR-null PC-3 cells. The addition of AR to PC-3 cells did not significantly alter PPARγ protein levels. However, the ability of the PPARγ ligand rosiglitazone to induce activation of a PPARγ-driven luciferase reporter and induce expression of FABP4 was suppressed in AR-positive PC-3 cells. Together, these data indicate AR serves as a key modulator of PPARγ expression and function within prostate tumors. J. Cell. Physiol. 231: 2664-2672, 2016. © 2016 Wiley Periodicals, Inc.

Indexed as

AndrogensCell Line, TumorDihydrotestosteroneGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMalePPAR gammaProstatic NeoplasmsProteasome InhibitorsReceptors, AndrogenRNA, MessengerTranscription, GeneticAndrogensAR protein, humanDihydrotestosteronePPAR gammaProteasome InhibitorsReceptors, AndrogenRNA, Messenger

Identifiers

PMID26945682
PMCPMC5132088
OpenAlexW2291633071

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.