Evidence map›Paper›PMID 22209699›Full record

ArticleThe American journal of pathology2012

PTEN regulates PDGF ligand switch for β-PDGFR signaling in prostate cancer.

M Katie Conley-LaComb, Wei Huang, Shihua Wang, Dongping Shi, Young Suk Jung, Abdo Najy, Rafael Fridman, R Daniel Bonfil, Michael L Cher, Yong Q Chen and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

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  14. Targeting the PDGF signaling pathway in tumor treatment.Cell communication and signaling : CCS · 2013
    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 3 institutions in 1 country.

M Katie Conley-LaCombDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan.
Wei HuangDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan.
Shihua WangDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, North Carolina.
Dongping ShiDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan.
Young Suk JungDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan.
Abdo NajyDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan.
Rafael FridmanDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan.
R Daniel BonfilDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan; Department of Urology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan.
Michael L CherDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan; Department of Urology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan.
Yong Q ChenDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, North Carolina. Electronic address: yqchen@wfubmc.edu.
Hyeong-Reh Choi KimDepartment of Pathology, Barbara Ann Karmanos Cancer Institute, Wayne State University, School of Medicine, Detroit, Michigan. Electronic address: hrckim@med.wayne.edu.
The Barbara Ann Karmanos Cancer Institute · USWake Forest University · USWayne State University · US

Funding

TRAINING PROGRAM IN THE BIOLOGY OF CANCERT32CA009531 · NCI · WAYNE STATE UNIVERSITY · PI Larry H Matherly · 1985 to 2026
$5.3M
Phospholipid Signaling in Fish oil-induced Growth Inhibition of Prostate CancerP01CA106742 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHEN, YONG Q · 2006 to 2010
$5.0M
PDGF D AND PROSTATE CANCER BONE METASTASISR01CA123362 · NCI · WAYNE STATE UNIVERSITY · PI KIM, HYEONG-REH CHOI · 2010 to 2020
$3.1M
Mechanisms of Fish Oil Supplement in Prevention of Pros*R01CA107668 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHEN, YONG Q · 2004 to 2014
$2.9M
Omega-3 PUFA-gene interaction in prostate cancerR01CA163273 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHEN, YONG Q · 2012 to 2016
$1.8M
PDGF Regulation of Cell Growth and DeathR01CA064139 · NCI · WAYNE STATE UNIVERSITY · PI KIM, HYEONG-REH CHOI · 2002 to 2006
$1.3M
The MT1-MMP/RANKL/RANK Axis in Prostate Cancer Bone MetastasisR01CA137280 · NCI · WAYNE STATE UNIVERSITY · PI CHER, MICHAEL L, FRIDMAN, RAFAEL A. · 2009 to 2010
$910k
ELUCIDATING THE FUNCTION OF MATRIPTASE-ACTIVATED PDGF D IN BONE METASTATIC PROSTAF32CA142038 · NCI · WAYNE STATE UNIVERSITY · PI NAJY, ABDO JAMAL · 2010 to 2012
$160k
NCI NIH HHS F32 CA142038NCI NIH HHS P01 CA106742NCI NIH HHS P01CA106742NCI NIH HHS R01 CA064139NCI NIH HHS R01CA064139NCI NIH HHS R01 CA107668NCI NIH HHS R01CA107668NCI NIH HHS R01 CA123362NCI NIH HHS R01CA123362NCI NIH HHS R01 CA137280NCI NIH HHS R01CA137280NCI NIH HHS R01 CA163273NCI NIH HHS T32 CA009531NCI NIH HHS T32-CA009531
6 · The paper itself

Abstract

Platelet-derived growth factor (PDGF) family members are potent growth factors that regulate cell proliferation, migration, and transformation. Clinical studies have shown that both PDGF receptor β (β-PDGFR) and its ligand PDGF D are up-regulated in primary prostate cancers and bone metastases, whereas PDGF B, a classic ligand for β-PDGFR, is not frequently detected in clinical samples. In this study, we examined the role of the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) in the regulation of PDGF expression levels using both a prostate-specific, conditional PTEN-knockout mouse model and mouse prostate epithelial cell lines established from these mice. We found an increase in PDGF D and β-PDGFR expression levels in PTEN-null tumor cells, accompanied by a decrease in PDGF B expression. Among Akt isoforms, increased Akt3 expression was most prominent in mouse PTEN-null cells, and phosphatidylinositol 3-kinase/Akt activity was essential for the maintenance of increased PDGF D and β-PDGFR expression. In vitro deletion of PTEN resulted in a PDGF ligand switch from PDGF B to PDGF D in normal mouse prostate epithelial cells, further demonstrating that PTEN regulates this ligand switch. Similar associations between PTEN status and PDGF isoforms were noted in human prostate cancer cell lines. Taken together, these results suggest a mechanism by which loss of PTEN may promote prostate cancer progression via PDGF D/β-PDGFR signal transduction.

Indexed as

AMP-Activated Protein KinasesAnimalsHumansLigandsMaleMAP Kinase Signaling SystemMiceMice, KnockoutPhosphatidylinositol 3-KinasesPlatelet-Derived Growth FactorProstatic NeoplasmsPTEN PhosphohydrolaseReceptor, Platelet-Derived Growth Factor betaTumor Cells, CulturedUp-RegulationAMP-Activated Protein KinasesLigandsPhosphatidylinositol 3-KinasesPlatelet-Derived Growth FactorPTEN PhosphohydrolasePTEN protein, humanPten protein, mouseReceptor, Platelet-Derived Growth Factor beta

Identifiers

PMID22209699
PMCPMC3349886
OpenAlexW2025344254

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.