Evidence map›Paper›PMID 27924948›Full record

ArticleScientific reports2016

FOXA1, GATA3 and PPARɣ Cooperate to Drive Luminal Subtype in Bladder Cancer: A Molecular Analysis of Established Human Cell Lines.

Joshua I Warrick, Vonn Walter, Hironobu Yamashita, Eunah Chung, Lauren Shuman, Vasty Osei Amponsa, Zongyu Zheng, Wilson Chan, Tiffany L Whitcomb, Feng Yue and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
10.7field-weighted citation impact, top 1% 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

100 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

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40 more citing papers are in PubMed but not listed here.

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

17 authors at 4 institutions in 2 countries.

Joshua I WarrickDepartment of Pathology, Pennsylvania State University Milton S. Hershey Medical Center, Hershey, PA, USA.
Vonn WalterDepartment of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, PA, USA.
Hironobu YamashitaDepartment of Pathology, Pennsylvania State University Milton S. Hershey Medical Center, Hershey, PA, USA.
Eunah ChungDivision of Pediatric Urology and Developmental Biology, Cincinnati Children's Hospital Medical Center, OH, USA.
Lauren ShumanDepartment of Pathology, Pennsylvania State University Milton S. Hershey Medical Center, Hershey, PA, USA.
Vasty Osei AmponsaDepartment of Pathology, Pennsylvania State University Milton S. Hershey Medical Center, Hershey, PA, USA.
Zongyu ZhengDepartment of Pathology, Pennsylvania State University Milton S. Hershey Medical Center, Hershey, PA, USA.
Wilson ChanDepartment of Pathology, Pennsylvania State University Milton S. Hershey Medical Center, Hershey, PA, USA.
Tiffany L WhitcombDepartment of Comparative Medicine, Pennsylvania State University College of Medicine, PA, USA.
Feng YueDepartment of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, PA, USA.
Tejaswi IyyankiDepartment of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, PA, USA.
Yuka I KawasawaDepartment of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, PA, USA.
Matthew KaagDepartment of Surgery, Division of Urology, Pennsylvania State University College of Medicine, PA, USA.
Wansong GuoDepartment of Surgery, Division of Urology, Changchun Central Hospital, Changchun, China.
Jay D RamanDepartment of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, PA, USA.
Joo-Seop ParkDivision of Pediatric Urology and Developmental Biology, Cincinnati Children's Hospital Medical Center, OH, USA.
David J DeGraffDepartment of Pathology, Pennsylvania State University Milton S. Hershey Medical Center, Hershey, PA, USA.
Pennsylvania State University · USPenn State Milton S. Hershey Medical Center · USCincinnati Children's Hospital Medical Center · USChangchun Obstetrics and Gynecology Hospital · CN

Funding

Cell Fate Regulation of Nephron ProgenitorsR01DK100315 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI PARK, JOO-SEOP · 2014 to 2018
$1.7M
Mechanisms of Urothelial Metaplasia and TumorigenesisR00CA172122 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI DEGRAFF, DAVID J. · 2014 to 2016
$727k
Mechanisms of Urothelial Metaplasia and TumorigenesisK99CA172122 · NCI · VANDERBILT UNIVERSITY · PI DEGRAFF, DAVID J. · 2013 to 2013
$94k
NCI NIH HHS K99 CA172122NCI NIH HHS R00 CA172122NIDDK NIH HHS R01 DK100315
6 · The paper itself

Abstract

Discrete bladder cancer molecular subtypes exhibit differential clinical aggressiveness and therapeutic response, which may have significant implications for identifying novel treatments for this common malignancy. However, research is hindered by the lack of suitable models to study each subtype. To address this limitation, we classified bladder cancer cell lines into molecular subtypes using publically available data in the Cancer Cell Line Encyclopedia (CCLE), guided by genomic characterization of bladder cancer by The Cancer Genome Atlas (TCGA). This identified a panel of bladder cancer cell lines which exhibit genetic alterations and gene expression patterns consistent with luminal and basal molecular subtypes of human disease. A subset of bladder cancer cell lines exhibit in vivo histomorphologic patterns consistent with luminal and basal subtypes, including papillary architecture and squamous differentiation. Using the molecular subtype assignments, and our own RNA-seq analysis, we found overexpression of GATA3 and FOXA1 cooperate with PPARɣ activation to drive transdifferentiation of a basal bladder cancer cells to a luminial phenotype. In summary, our analysis identified a set of human cell lines suitable for the study of molecular subtypes in bladder cancer, and furthermore indicates a cooperative regulatory network consisting of GATA3, FOXA1, and PPARɣ drive luminal cell fate.

Indexed as

AnimalsBase SequenceBiomarkers, TumorCell Line, TumorGATA3 Transcription FactorGene Expression Regulation, NeoplasticGene Regulatory NetworksGenetic Association StudiesHepatocyte Nuclear Factor 3-alphaHumansPPAR gammaRatsRegulatory Sequences, Nucleic AcidSequence Analysis, RNAUrinary Bladder NeoplasmsUrotheliumBiomarkers, TumorFOXA1 protein, humanGATA3 protein, humanGATA3 Transcription FactorHepatocyte Nuclear Factor 3-alphaPPAR gamma

Identifiers

PMID27924948
PMCPMC5141480
OpenAlexW2560018230

What OpenQuestion holds

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Registered trials

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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.