Evidence map›Paper›PMID 28881308›Full record

ArticleNeoplasia (New York, N.Y.)2017

Overexpression of Exportin-5 Overrides the Inhibitory Effect of miRNAs Regulation Control and Stabilize Proteins via Posttranslation Modifications in Prostate Cancer.

Naseruddin Höti, Shuang Yang, Paul Aiyetan, Binod Kumar, Yingwei Hu, David Clark, Arife Unal Eroglu, Punit Shah, Tamara Johnson, Wasim H Chowdery and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

5 citing papers in PubMed, 11 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

12 authors at 2 institutions in 1 country.

Naseruddin HötiBrady Urological Institute, Department of Urology, Johns Hopkins School of Medicine, Baltimore, MD; Department of Pathology, Division of Clinical Chemistry, Johns Hopkins School of Medicine, Baltimore, MD. Electronic address: nhoti1@jhmi.edu.
Shuang YangDepartment of Pathology, Division of Clinical Chemistry, Johns Hopkins School of Medicine, Baltimore, MD.
Paul AiyetanDepartment of Pathology, Division of Clinical Chemistry, Johns Hopkins School of Medicine, Baltimore, MD.
Binod KumarBrady Urological Institute, Department of Urology, Johns Hopkins School of Medicine, Baltimore, MD.
Yingwei HuDepartment of Pathology, Division of Clinical Chemistry, Johns Hopkins School of Medicine, Baltimore, MD.
David ClarkDepartment of Pathology, Division of Clinical Chemistry, Johns Hopkins School of Medicine, Baltimore, MD.
Arife Unal ErogluDepartment of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD.
Punit ShahDepartment of Pathology, Division of Clinical Chemistry, Johns Hopkins School of Medicine, Baltimore, MD.
Tamara JohnsonBrady Urological Institute, Department of Urology, Johns Hopkins School of Medicine, Baltimore, MD.
Wasim H ChowderyDepartment of Urology, The University of Texas Health Science Center at San Antonio, San Antonio, TX.
Hui ZhangDepartment of Pathology, Division of Clinical Chemistry, Johns Hopkins School of Medicine, Baltimore, MD.
Ronald RodriguezDepartment of Urology, The University of Texas Health Science Center at San Antonio, San Antonio, TX.
Johns Hopkins University · USThe University of Texas Health Science Center at San Antonio · US

Funding

Glycoprotein biomarkers for the early detection of aggressive prostate cancerU01CA152813 · NCI · JOHNS HOPKINS UNIVERSITY · PI ZHANG, HUI · 2010 to 2021
$6.2M
Development of Highly Targeted, Imageable Adenoviral Vectors for Prostate CancerR01CA121153 · NCI · JOHNS HOPKINS UNIVERSITY · PI RODRIGUEZ, RONALD · 2007 to 2011
$1.5M
NCI NIH HHS R01 CA121153NCI NIH HHS U01 CA152813
6 · The paper itself

Abstract

Although XPO5 has been characterized to have tumor-suppressor features in the miRNA biogenesis pathway, the impact of altered expression of XPO5 in cancers is unexplored. Here we report a novel "oncogenic" role of XPO5 in advanced prostate cancer. Using prostate cancer models, we found that excess levels of XPO5 override the inhibitory effect of the canoncial miRNA-mRNA regulation, resulting in a global increase in proteins expression. Importantly, we found that decreased expression of XPO5 could promote an increase in proteasome degradation, whereas overexpression of XPO5 leads to altered protein posttranslational modification via hyperglycosylation, resulting in cellular protein stability. We evaluated the therapeutic advantage of targeting XPO5 in prostate cancer and found that knocking down XPO5 in prostate cancer cells suppressed cellular proliferation and tumor development without significantly impacting normal fibroblast cells survival. To our knowledge, this is the first report describing the oncogenic role of XPO5 in overriding the miRNAs regulation control. Furthermore, we believe that these findings will provide an explanation as to why, in some cancers that express higher abundance of mature miRNAs, fail to suppress their potential protein targets.

Indexed as

Gene ExpressionRNA InterferenceAnimalsCell Line, TumorCell ProliferationCluster AnalysisGene Expression ProfilingGene Knockdown TechniquesHumansKaryopherinsMaleMicroRNAsProstatic NeoplasmsProtein Processing, Post-TranslationalProtein StabilityProteomeKaryopherinsMicroRNAsProteomeReceptors, AndrogenXPO5 protein, human

Identifiers

PMID28881308
PMCPMC5587889
OpenAlexW2751377341

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.