Evidence map›Paper›PMID 21656830›Full record

ArticleThe Prostate2011

Reactivation of embryonic nodal signaling is associated with tumor progression and promotes the growth of prostate cancer cells.

Mitchell G Lawrence, Naira V Margaryan, Daniela Loessner, Angus Collins, Kris M Kerr, Megan Turner, Elisabeth A Seftor, Carson R Stephens, John Lai, APC BioResource and 3 more

Abstract readComparative Study
In one paragraph

Article in The Prostate, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 104 citations in OpenAlex.

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  10. TGFB1/INHBA Homodimer/Nodal-SMAD2/3 Signaling Network: A Pivotal Molecular Target in PDAC Treatment.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Review
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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

13 authors at 4 institutions in 3 countries.

Mitchell G LawrenceAustralian Prostate Cancer Research Centre-Queensland, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia.
Naira V Margaryan
Daniela Loessner
Angus Collins
Kris M Kerr
Megan Turner
Elisabeth A Seftor
Carson R Stephens
John Lai
APC BioResource
Lynne-Marie Postovit
Judith A Clements
Mary J C Hendrix
Northwestern University · USQueensland University of Technology · AUSullivan Nicolaides Pathology · AUWestern University · CA

Funding

Epigenetic Effect of the Microenvironment on Stem Cell Plasticity and FunctionR01CA121205 · NCI · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI HENDRIX, MARY J.C. · 2007 to 2011
$2.1M
NCI NIH HHS CA121205NCI NIH HHS R01 CA121205
6 · The paper itself

Abstract

backgroundNodal is a member of the transforming growth factor β (TGFβ) superfamily that directs embryonic patterning and promotes the plasticity and tumorigenicity of tumor cells, but its role in the prostate is unknown. The goal of this study was to characterize the expression and function of Nodal in prostate cancer and determine whether, like other TGFβ ligands, it modulates androgen receptor (AR) activity.

methodsNodal expression was investigated using immunohistochemistry of tissue microarrays and Western blots of prostate cell lines. The functional role of Nodal was examined using Matrigel and soft agar growth assays. Cross-talk between Nodal and AR signaling was assessed with luciferase reporter assays and expression of endogenous androgen regulated genes.

resultsSignificantly increased Nodal expression was observed in cancer compared with benign prostate specimens. Nodal was only expressed by DU145 and PC3 cells. All cell lines expressed Nodal's co-receptor, Cripto-1, but lacked Lefty, a critical negative regulator of Nodal signaling. Recombinant human Nodal triggered downstream Smad2 phosphorylation in DU145 and LNCaP cells, and stable transfection of pre-pro-Nodal enhanced the growth of LNCaP cells in Matrigel and soft agar. Finally, Nodal attenuated AR signaling, reducing the activity of a PSA promoter construct in luciferase assays and down-regulating the endogenous expression of androgen regulated genes.

conclusionsAn aberrant Nodal signaling pathway is re-expressed and functionally active in prostate cancer cells.

Indexed as

Disease ProgressionGene Expression Regulation, NeoplasticHumansMaleNodal ProteinProstatic NeoplasmsReceptors, AndrogenSignal TransductionTransforming Growth Factor betaTumor Cells, CulturedNodal ProteinNODAL protein, humanReceptors, AndrogenTransforming Growth Factor beta

Identifiers

PMID21656830
PMCPMC3234312
OpenAlexW1990402395

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.