Evidence map›Paper›PMID 31739170›Full record

ArticleiScience2019

E6AP Promotes a Metastatic Phenotype in Prostate Cancer.

Cristina Gamell, Ivona Bandilovska, Twishi Gulati, Arielle Kogan, Syer Choon Lim, Zaklina Kovacevic, Elena A Takano, Clelia Timpone, Arjelle D Agupitan, Cassandra Litchfield and 13 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 13 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

23 authors at 7 institutions in 3 countries.

Cristina GamellTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
Ivona BandilovskaTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
Twishi GulatiSir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC 3010, Australia.
Arielle KoganTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
Syer Choon LimDepartment of Pathology and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia.
Zaklina KovacevicDepartment of Pathology and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia.
Elena A TakanoDepartment of Pathology, Peter MacCallum Cancer Centre, Melbourne 3000, Australia.
Clelia TimponeTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
Arjelle D AgupitanTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
Cassandra LitchfieldTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
Giovanni BlandinoIRCCS Regina Elena National Cancer Institute, Rome, Italy.
Lisa G HorvathThe Chris O'Brien Lifehouse, Sydney, NSW 2050, Australia; Garvan Institute of Medical Research, Sydney, NSW 2010, Australia.
Stephen B FoxSir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC 3010, Australia; Department of Pathology, Peter MacCallum Cancer Centre, Melbourne 3000, Australia.
Scott G WilliamsDivision of Radiation Oncology and Cancer Imaging, Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia.
Andrea RussoIRCCS Regina Elena National Cancer Institute, Rome, Italy.
Enzo GalloIRCCS Regina Elena National Cancer Institute, Rome, Italy.
Piotr J PaulTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia.
Catherine MitchellDepartment of Pathology, Peter MacCallum Cancer Centre, Melbourne 3000, Australia.
Shahneen SandhuSir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC 3010, Australia.
Simon P KeamTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC 3010, Australia.
Sue HauptTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC 3010, Australia.
Des R RichardsonDepartment of Pathology and Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia; Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Ygal HauptTumour Suppression Laboratory, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, VIC 3000, Australia; Department of Pathology, Peter MacCallum Cancer Centre, Melbourne 3000, Australia; Department of Clinical Pathology, University of Melbourne, Parkville, VIC 3010, Australia; Department of Biochemistry and Molecular Biology, Monash University, Melbourne 3800, Australia. Electronic address: ygal.haupt@petermac.org.
Peter MacCallum Cancer Centre · AUIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Melbourne · AURobert Bosch (Australia) · AUChris O’Brien Lifehouse · AUMonash University · AUUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although primary prostate cancer is largely curable, progression to metastatic disease is associated with very poor prognosis. E6AP is an E3 ubiquitin ligase and a transcriptional co-factor involved in normal prostate development. E6AP drives prostate cancer when overexpressed. Our study exposed a role for E6AP in the promotion of metastatic phenotype in prostate cells. We revealed that elevated levels of E6AP in primary prostate cancer correlate with regional metastasis and demonstrated that E6AP promotes acquisition of mesenchymal features, migration potential, and ability for anchorage-independent growth. We identified the metastasis suppressor NDRG1 as a target of E6AP and showed it is key in E6AP induction of mesenchymal phenotype. We showed that treatment of prostate cancer cells with pharmacological agents upregulated NDRG1 expression suppressed E6AP-induced cell migration. We propose that the E6AP-NDRG1 axis is an attractive therapeutic target for the treatment of E6AP-driven metastatic prostate cancer.

Indexed as

Biological SciencesCancerCell Biology

Identifiers

PMID31739170
PMCPMC6864340
OpenAlexW2983217620

What OpenQuestion holds

Textmetadata
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.