Evidence map›Paper›PMID 23538390›Full record

ArticleBritish journal of cancer2013

microRNA-183 is an oncogene targeting Dkk-3 and SMAD4 in prostate cancer.

K Ueno, H Hirata, V Shahryari, G Deng, Y Tanaka, Z L Tabatabai, Y Hinoda, R Dahiya

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
5.2field-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

79 citing papers in PubMed, 120 citations in OpenAlex.

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  16. Wnt-Signaling Regulated by Glucocorticoid-Induced miRNAs.International journal of molecular sciences · 2021
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  19. miR-183 promotes radioresistance of lung adenocarcinoma H1299 cells via epithelial-mesenchymal transition.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
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  20. Article

19 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

K UenoDepartment of Urology, San Francisco Veterans Affairs Medical Center, University of California at San Francisco, 4150 Clement Street, San Francisco, CA 94121, USA.
H Hirata
V Shahryari
G Deng
Y Tanaka
Z L Tabatabai
Y Hinoda
R Dahiya
San Francisco VA Medical Center · USYamaguchi University · JP

Funding

Wnt antagonist genes in kidney tumor progression and metastasisR01CA130860 · NCI · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI DAHIYA, RAJVIR · 2008 to 2012
$3.0M
MicroRNAs in the Progression and Metastisis of Prostate CancerR01CA138642 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAHIYA, RAJVIR · 2010 to 2014
$2.6M
Chemo-dietary prevention, miRNAs, epigenetic and prostate cancerR01CA160079 · NCI · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI DAHIYA, RAJVIR · 2011 to 2015
$2.2M
Role of genetic biomarkers in clinical assessment of prostate cancerIP1BX001604 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI DAHIYA, RAJVIR, LAU, YUN-FAI CHRIS · 2013 to 2016
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BLRD VA IP1 BX001604NCI NIH HHS R01 CA130860NCI NIH HHS R01CA130860NCI NIH HHS R01 CA138642NCI NIH HHS R01CA138642NCI NIH HHS R01 CA160079NCI NIH HHS R01CA160079
6 · The paper itself

Abstract

backgroundThe purpose of this study was to identify prostate cancer (PC) oncogenic microRNAs (miRs) based on miR microarray and to investigate whether these oncogenic miRs may be useful as PC biomarkers.

methodsInitially, we carried out miR microarray and real-time PCR using RWPE-1, PC-3, DU-145 and LNCaP cells. To investigate the function of miR-183, we used a miR-183 knockdown inhibitor in cell growth and wound-healing assays. We used several algorithms and confirmed that they are directly regulated by miR-183.

resultsWe identified three potential oncogenic miRs (miR-146a, miR-183 and miR-767-5P). The expression of miR-183 in PC cells (PC-3, DU-145 and LNCaP) was upregulated compared with RWPE-1 cells. MiR-183 expression was also significantly higher in PC tissues compared with that in matched normal prostate tissues. Additionally, miR-183 expression was correlated with higher prostate-specific antigen, higher pT and shorter overall survival. MiR-183 knockdown decreased cell growth and motility in PC cells and significantly decreased prostate tumour growth in in vivo nude mice experiments. We identified Dkk-3 and SMAD4 as potential target genes of miR-183.

conclusionOur data suggest that oncogenic miR-183 may be useful as a new PC biomarker and that inhibition of miR-183 expression may be therapeutically beneficial as a PC treatment.

Indexed as

Adaptor Proteins, Signal Transducingbeta CateninCell Growth ProcessesCell Line, TumorChemokinesGene Knockdown TechniquesHumansIn Situ HybridizationIntercellular Signaling Peptides and ProteinsMaleMicroRNAsProstatic NeoplasmsSmad4 ProteinTransfectionWnt ProteinsWnt Signaling PathwayAdaptor Proteins, Signal Transducingbeta CateninChemokinesCTNNB1 protein, humanDKK3 protein, humanIntercellular Signaling Peptides and ProteinsMicroRNAsMIRN183 microRNA, humanSmad4 ProteinSMAD4 protein, humanWnt Proteins

Identifiers

PMID23538390
PMCPMC3668476
OpenAlexW2017742278

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.