Evidence map›Paper›PMID 28880957›Full record

ArticlePloS one2017

Mapping the STK4/Hippo signaling network in prostate cancer cell.

Damien Ready, Kader Yagiz, Pooneh Amin, Yuksel Yildiz, Vincent Funari, Serdar Bozdag, Bekir Cinar

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

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  12. The Hippo pathway: an emerging role in urologic cancers.American journal of clinical and experimental urology · 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

7 authors at 4 institutions in 2 countries.

Damien ReadyDepartment of Mathematics, Statistics, and Computer Science, Marquette University, Milwaukee, Wisconsin, United States of America.
Kader YagizDepartment of Medicine, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States of America.
Pooneh AminDepartment of Biological Sciences, the Center for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, Georgia, United States of America.
Yuksel YildizDepartment of Physiology, Adnan Menderes University, Aydin, Turkey.
Vincent FunariDepartment of Medicine and Division of Genetics, Cedars-Sinai Medical Center, Los Angeles, California, United States of America.
Serdar BozdagDepartment of Mathematics, Statistics, and Computer Science, Marquette University, Milwaukee, Wisconsin, United States of America.
Bekir CinarDepartment of Biological Sciences, the Center for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, Georgia, United States of America.ORCID http://orcid.org/0000-0002-4680-865X
Cedars-Sinai Medical Center · USCenter for Cancer Research · USMarquette University · USAdnan Menderes University · TR

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
Technologies/Resources for Core LaboratoriesG12MD007590 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2012 to 2018
$7.6M
NCATS NIH HHS UL1 TR000124NIMHD NIH HHS G12 MD007590
6 · The paper itself

Abstract

Dysregulation of MST1/STK4, a key kinase component of the Hippo-YAP pathway, is linked to the etiology of many cancers with poor prognosis. However, how STK4 restricts the emergence of aggressive cancer remains elusive. Here, we investigated the effects of STK4, primarily localized in the cytoplasm, lipid raft, and nucleus, on cell growth and gene expression in aggressive prostate cancer. We demonstrated that lipid raft and nuclear STK4 had superior suppressive effects on cell growth in vitro and in vivo compared with cytoplasmic STK4. Using RNA sequencing and bioinformatics analysis, we identified several differentially expressed (DE) genes that responded to ectopic STK4 in all three subcellular compartments. We noted that the number of DE genes observed in lipid raft and nuclear STK4 cells were much greater than cytoplasmic STK4. Our functional annotation clustering showed that these DE genes were commonly associated with oncogenic pathways such as AR, PI3K/AKT, BMP/SMAD, GPCR, WNT, and RAS as well as unique pathways such as JAK/STAT, which emerged only in nuclear STK4 cells. These findings indicate that MST1/STK4/Hippo signaling restricts aggressive tumor cell growth by intersecting with multiple molecular pathways, suggesting that targeting of the STK4/Hippo pathway may have important therapeutic implications for cancer.

Indexed as

AnimalsCell Line, TumorCell NucleusComputational BiologyCytoplasmFluorescent Antibody TechniqueHippo KinasesHippo Signaling PathwayHumansIntracellular Signaling Peptides and ProteinsMaleMiceProstateProstatic NeoplasmsProtein Serine-Threonine KinasesSignal TransductionHippo KinasesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesSTK4 protein, human

Identifiers

PMID28880957
PMCPMC5589252
OpenAlexW2753774840

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.