Evidence map›Paper›PMID 27384993›Full record

ArticleOncotarget2016

Dual tumor suppressing and promoting function of Notch1 signaling in human prostate cancer.

Karine Lefort, Paola Ostano, Maurizia Mello-Grand, Valérie Calpini, Maria Scatolini, Antonella Farsetti, G Paolo Dotto, Giovanna Chiorino

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 29 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

8 authors at 4 institutions in 4 countries.

Karine LefortDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland.
Paola OstanoLaboratory of Cancer Genomics, Fondazione "Edo ed Elvo Tempia Valenta", Biella, Italy.
Maurizia Mello-GrandLaboratory of Cancer Genomics, Fondazione "Edo ed Elvo Tempia Valenta", Biella, Italy.
Valérie CalpiniDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland.
Maria ScatoliniLaboratory of Molecular Oncology, Fondazione "Edo ed Elvo Tempia Valenta", Biella, Italy.
Antonella FarsettiInstitute of Cell Biology and Neurobiology, National Research Council, Rome, Italy.
G Paolo DottoDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland.
Giovanna ChiorinoLaboratory of Cancer Genomics, Fondazione "Edo ed Elvo Tempia Valenta", Biella, Italy.
Fondazione Edo ed Elvo Tempia · ITUniversity of Lausanne · CHInstitute of Cell Biology and Neurobiology · ITMassachusetts General Hospital · US

Funding

GROWTH DIFFERENTIATION CONTROL IN PRIMARY KERATINOCYTES.R01AR039190 · NIAMS · YALE UNIVERSITY · PI DOTTO, GIAN-PAOLO · 1988 to 2021
$9.5M
Dermal fibroblast/ATF3 control of skin homeostasisR01AR064786 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DOTTO, GIAN-PAOLO · 2014 to 2018
$1.9M
NIAMS NIH HHS R01 AR039190NIAMS NIH HHS R01 AR064786
6 · The paper itself

Abstract

Adenocarcinomas of the prostate arise as multifocal heterogeneous lesions as the likely result of genetic and epigenetic alterations and deranged cell-cell communication. Notch signaling is an important form of intercellular communication with a role in growth/differentiation control and tumorigenesis. Contrasting reports exist in the literature on the role of this pathway in prostate cancer (PCa) development. We show here that i) compared to normal prostate tissue, Notch1 expression is significantly reduced in a substantial fraction of human PCas while it is unaffected or even increased in others; ii) acute Notch activation both inhibits and induces process networks associated with prostatic neoplasms; iii) down-modulation of Notch1 expression and activity in immortalized normal prostate epithelial cells increases their proliferation potential, while increased Notch1 activity in PCa cells suppresses growth and tumorigenicity through a Smad3-dependent mechanism involving p21WAF1/CIP1; iv) prostate cancer cells resistant to Notch growth inhibitory effects retain Notch1-induced upregulation of pro-oncogenic genes, like EPAS1 and CXCL6, also overexpressed in human PCas with high Notch1 levels. Taken together, these results reconcile conflicting data on the role of Notch1 in prostate cancer.

Indexed as

AgedCarcinogenesisCell DifferentiationCell Line, TumorCell ProliferationGenes, Tumor SuppressorHumansMaleMiddle AgedProstatic NeoplasmsReceptor, Notch1Signal TransductionNOTCH1 protein, humanReceptor, Notch1Notchprostate cancer

Identifiers

PMID27384993
PMCPMC5216996
OpenAlexW2469107041

What OpenQuestion holds

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LicenceCC BY
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.