Evidence map›Paper›PMID 26701805›Full record

ArticleCancer research2016

SOX4 Is Essential for Prostate Tumorigenesis Initiated by PTEN Ablation.

Birdal Bilir, Adeboye O Osunkoya, W Guy Wiles, Soma Sannigrahi, Veronique Lefebvre, Daniel Metzger, Demetri D Spyropoulos, W David Martin, Carlos S Moreno

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 89 citations in OpenAlex.

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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 4 institutions in 2 countries.

Birdal BilirDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
Adeboye O OsunkoyaDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia. Department of Urology, Emory University, Atlanta, Georgia. Winship Cancer Institute, Emory University, Atlanta, Georgia.
W Guy WilesWinship Cancer Institute, Emory University, Atlanta, Georgia.
Soma SannigrahiDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia. Hubert Department of Global Health Infectious Diseases, Rollins School of Public Health, Emory University, Atlanta, Georgia.
Veronique LefebvreDepartment of Cellular and Molecular Medicine, Cleveland Clinic, Cleveland, Ohio.
Daniel MetzgerDepartment of Functional Genomics and Cancer, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Institut National de Santé et de Recherche Médicale (INSERM) U964/Centre National de Recherche Scientifique (CNRS) UMR 7104/Université de Strasbourg, Illkirch, France.
Demetri D SpyropoulosDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina.
W David MartinWinship Cancer Institute, Emory University, Atlanta, Georgia.
Carlos S MorenoDepartment of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia. Winship Cancer Institute, Emory University, Atlanta, Georgia. cmoreno@emory.edu.
Emory University · USCentre National de la Recherche Scientifique · FRCleveland Clinic · USMedical University of South Carolina · US

Funding

Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5M
Systematic discovery of neomorph protein-protein interactions in cancer for oncogenic pathway perturbationU01CA217875 · NCI · EMORY UNIVERSITY · PI FU, HAIAN · 2017 to 2021
$4.5M
HIGH THROUGHPUT PROTEIN-PROTEIN INTERACTION INTERROGATION IN CANCERU01CA168449 · NCI · EMORY UNIVERSITY · PI FU, HAIAN · 2012 to 2016
$4.2M
Developmental Transcription Factors in Prostate CancerR01CA106826 · NCI · EMORY UNIVERSITY · PI MORENO, CARLOS SANCHEZ · 2005 to 2013
$2.6M
NCI NIH HHS P30 CA138292NCI NIH HHS P30CA138292NCI NIH HHS R01 CA106826NCI NIH HHS R01CA106826NCI NIH HHS U01 CA168449NCI NIH HHS U01 CA217875
6 · The paper itself

Abstract

Understanding remains incomplete of the mechanisms underlying initiation and progression of prostate cancer, the most commonly diagnosed cancer in American men. The transcription factor SOX4 is overexpressed in many human cancers, including prostate cancer, suggesting it may participate in prostate tumorigenesis. In this study, we investigated this possibility by genetically deleting Sox4 in a mouse model of prostate cancer initiated by loss of the tumor suppressor Pten. We found that specific homozygous deletion of Sox4 in the adult prostate epithelium strongly inhibited tumor progression initiated by homozygous loss of Pten. Mechanistically, Sox4 ablation reduced activation of AKT and β-catenin, leading to an attenuated invasive phenotype. Furthermore, SOX4 expression was induced by Pten loss as a result of the activation of PI3K-AKT-mTOR signaling, suggesting a positive feedback loop between SOX4 and PI3K-AKT-mTOR activity. Collectively, our findings establish that SOX4 is a critical component of the PTEN/PI3K/AKT pathway in prostate cancer, with potential implications for combination-targeted therapies against both primary and advanced prostate cancers.

Indexed as

Animalsbeta CateninCarcinogenesisCell Line, TumorHumansMaleMicePhosphatidylinositol 3-KinasesProstatic NeoplasmsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionSOXC Transcription FactorsTOR Serine-Threonine Kinasesbeta CateninPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanSOX4 protein, humanSOXC Transcription FactorsTOR Serine-Threonine Kinases

Identifiers

PMID26701805
PMCPMC4779598
OpenAlexW2257673337

What OpenQuestion holds

Textmetadata
LicenceTDM
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.