Evidence map›Paper›PMID 22874998›Full record

ArticleCell death & disease2012

PPARγ isoforms differentially regulate metabolic networks to mediate mouse prostatic epithelial differentiation.

D W Strand, M Jiang, T A Murphy, Y Yi, K C Konvinse, O E Franco, Y Wang, J D Young, S W Hayward

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

40 citing papers in PubMed, 56 citations in OpenAlex.

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  11. Review
  12. Transcriptional networks controlling stromal cell differentiation.Nature reviews. Molecular cell biology · 2021
    Review
  13. Cancers · 2021
    Article
  14. 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

9 authors at 2 institutions in 1 country.

D W StrandDepartment of Urologic Surgery, Vanderbilt-Ingram Comprehensive Cancer Center, Vanderbilt University School of Engineering, and Vanderbilt University Medical Center, Nashville, TN 37232-2765, USA.
M Jiang
T A Murphy
Y Yi
K C Konvinse
O E Franco
Y Wang
J D Young
S W Hayward
Vanderbilt University Medical Center · USVanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
MULTIDISCIPLINARY BASIC RESEARCH TRAINING IN CANCERT32CA009592 · NCI · VANDERBILT UNIVERSITY · PI Justin M Balko, Julie A Rhoades (Sterling) · 1987 to 2026
$10.4M
Paracrine Regulation of BPH PathogenesisR01DK067049 · NIDDK · VANDERBILT UNIVERSITY · PI HAYWARD, SIMON W · 2004 to 2013
$2.6M
PPAR-gamma and BPH/LUTSP20DK090874 · NIDDK · VANDERBILT UNIVERSITY · PI HAYWARD, SIMON W · 2010 to 2011
$868k
Role of Glutaminolysis in the Myc-induced Metabolic Phenotype of Tumor CellsR21CA155964 · NCI · VANDERBILT UNIVERSITY · PI YOUNG, JAMEY D. · 2011 to 2012
$261k
NCI NIH HHS P30 CA068485NCI NIH HHS P30 CA68485NCI NIH HHS R21 CA155964NCI NIH HHS T32 CA009592NEI NIH HHS P30 EY008126NEI NIH HHS P30 EY08126NIDDK NIH HHS 2R01 DK067049NIDDK NIH HHS P20 DK090874NIDDK NIH HHS P30 DK058404NIDDK NIH HHS P30 DK58404NIDDK NIH HHS R01 DK067049
6 · The paper itself

Abstract

Recent observations indicate prostatic diseases are comorbidities of systemic metabolic dysfunction. These discoveries revealed fundamental questions regarding the nature of prostate metabolism. We previously showed that prostate-specific ablation of PPARγ in mice resulted in tumorigenesis and active autophagy. Here, we demonstrate control of overlapping and distinct aspects of prostate epithelial metabolism by ectopic expression of individual PPARγ isoforms in PPARγ knockout prostate epithelial cells. Expression and activation of either PPARγ 1 or 2 reduced de novo lipogenesis and oxidative stress and mediated a switch from glucose to fatty acid oxidation through regulation of genes including Pdk4, Fabp4, Lpl, Acot1 and Cd36. Differential effects of PPARγ isoforms included decreased basal cell differentiation, Scd1 expression and triglyceride fatty acid desaturation and increased tumorigenicity by PPARγ1. In contrast, PPARγ2 expression significantly increased basal cell differentiation, Scd1 expression and AR expression and responsiveness. Finally, in confirmation of in vitro data, a PPARγ agonist versus high-fat diet (HFD) regimen in vivo confirmed that PPARγ agonization increased prostatic differentiation markers, whereas HFD downregulated PPARγ-regulated genes and decreased prostate differentiation. These data provide a rationale for pursuing a fundamental metabolic understanding of changes to glucose and fatty acid metabolism in benign and malignant prostatic diseases associated with systemic metabolic stress.

Indexed as

Metabolic Networks and PathwaysAnimalsCell DifferentiationCell LineCell Transformation, NeoplasticDiet, High-FatDown-RegulationEpithelial CellsFatty AcidsGene Expression RegulationGene Knockout TechniquesGlucoseLipogenesisMaleMiceOxidative StressFatty AcidsGlucosePPAR gammaProtein IsoformsScd1 protein, mouseStearoyl-CoA DesaturaseThiazolidinediones

Identifiers

PMID22874998
PMCPMC3434663
OpenAlexW2027104066

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.