Evidence map›Paper›PMID 27294523›Full record

ArticleThe Journal of clinical investigation2016

Notch promotes tumor metastasis in a prostate-specific Pten-null mouse model.

Oh-Joon Kwon, Li Zhang, Jianghua Wang, Qingtai Su, Qin Feng, Xiang H F Zhang, Sendurai A Mani, Robia Paulter, Chad J Creighton, Michael M Ittmann and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 79 citations in OpenAlex.

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  10. Epithelial and mesenchymal fate decisions in Wolffian duct development.Trends in endocrinology and metabolism: TEM · 2023
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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 2 countries.

Oh-Joon Kwon
Li Zhang
Jianghua Wang
Qingtai Su
Qin Feng
Xiang H F Zhang
Sendurai A Mani
Robia Paulter
Chad J Creighton
Michael M Ittmann
Li Xin
Baylor College of Medicine · USMichael E. DeBakey VA Medical Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Virology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BUTEL, JANET S · 1994 to 2015
$21.7M
Role of FGFR1 signaling in distinct cell lineages in prostate cancer progresssionU01CA141497 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ITTMANN, MICHAEL M · 2009 to 2013
$3.4M
The Notch Signaling in Prostate Homeostasis and CarcinogenesisR01CA190378 · NCI · UNIVERSITY OF WASHINGTON · PI XIN, LI · 2015 to 2019
$1.9M
BD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430k
Reprogramming of Prostate Stromal Cells by Prostate InflammationR21CA196570 · NCI · BAYLOR COLLEGE OF MEDICINE · PI XIN, LI · 2016 to 2017
$408k
NCI NIH HHS P30 CA125123NCI NIH HHS R01 CA190378NCI NIH HHS R21 CA196570NCI NIH HHS U01 CA141497NCRR NIH HHS S10 RR024574NIAID NIH HHS P30 AI036211
6 · The paper itself

Abstract

Although Notch signaling is deregulated in prostate cancer, the role of this pathway in disease development and progression is not fully understood. Here, we analyzed 2 human prostate cancer data sets and found that higher Notch signaling correlates with increased metastatic potential and worse disease survival rates. We used the Pten-null mouse prostate cancer model to investigate the function of Notch signaling in the initiation and progression of prostate cancer. Disruption of the transcription factor RBPJ in Pten-null mice revealed that endogenous canonical Notch signaling is not required for disease initiation and progression. However, augmentation of Notch activity in this model promoted both proliferation and apoptosis of prostate epithelial cells, which collectively reduced the primary tumor burden. The increase in cellular apoptosis was linked to DNA damage-induced p53 activation. Despite a reduced primary tumor burden, Notch activation in Pten-null mice promoted epithelial-mesenchymal transition and FOXC2-dependent tumor metastases but did not confer resistance to androgen deprivation. Notch activation also resulted in transformation of seminal vesicle epithelial cells in Pten-null mice. Our study highlights a multifaceted role for Notch signaling in distinct aspects of prostate cancer biology and supports Notch as a potential therapeutic target for metastatic prostate cancer.

Indexed as

Neoplasm MetastasisAnimalsApoptosisCell Line, TumorCell ProliferationDisease Models, AnimalDisease ProgressionEpithelial CellsEpithelial-Mesenchymal TransitionForkhead Transcription FactorsGene Expression Regulation, NeoplasticGenotypeMagnetic Resonance ImagingMaleMiceMice, Inbred C57BLForkhead Transcription Factorsmesenchyme fork head 1 proteinNOTCH1 protein, humanNotch1 protein, mousePTEN PhosphohydrolasePTEN protein, humanPten protein, mouseReceptor, Notch1Receptors, Notch

Identifiers

PMID27294523
PMCPMC4922719
OpenAlexW2416137753

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.