Evidence map›Paper›PMID 23383207›Full record

ArticlePloS one2013

MicroRNA-182-5p promotes cell invasion and proliferation by down regulating FOXF2, RECK and MTSS1 genes in human prostate cancer.

Hiroshi Hirata, Koji Ueno, Varahram Shahryari, Guoren Deng, Yuichiro Tanaka, Z Laura Tabatabai, Yuji Hinoda, Rajvir Dahiya

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 3 pooled it
5.9field-weighted citation impact, top 3% 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

89 citing papers in PubMed, 3 syntheses or guidelines pooled it, 146 citations in OpenAlex.

  1. Pooled it
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  11. miRNA in Molecular Diagnostics.Bioengineering (Basel, Switzerland) · 2022
    Review
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29 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 3 institutions in 2 countries.

Hiroshi HirataDepartment of Urology, San Francisco Veterans Affairs Medical Center and University of California San Francisco, San Francisco, California, United States of America.
Koji Ueno
Varahram Shahryari
Guoren Deng
Yuichiro Tanaka
Z Laura Tabatabai
Yuji Hinoda
Rajvir Dahiya
San Francisco VA Medical Center · USUniversity of California, San Francisco · 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

Recently miR-182 has been reported to be over-expressed in prostate cancer (PC) tissues, however detailed functional analysis of miR-182-5p has not been carried out. The purpose of this study was to: 1. analyze the function of miR-182-5p in prostate cancer, 2. assess its usefulness as a tumor marker, 3. identify miR-182-5p target genes in PC, 4. investigate the potential for miR-182-5p inhibitor to be used in PC treatment. Initially we found that miR-182-5p expression was significantly higher in prostate cancer tissues and cell lines compared to normal prostate tissues and cells. Moreover high miR-182-5p expression was associated with shorter overall survival in PC patients. To study the functional significance of miR-182-5p, we knocked down miR-182-5p with miR-182-5p inhibitor. After miR-182-5p knock-down, prostate cancer cell proliferation, migration and invasion were decreased. We identified FOXF2, RECK and MTSS1 as potential target genes of miR-182-5p using several algorithms which was confirmed by 3'UTR luciferase assay and Western analysis. Knock-down of miR-182-5p also significantly decreased in vivo prostate tumor growth. In conclusion this is the first report documenting that over-expression of miR-182-5p is associated with prostate cancer progression and potentially useful as a prognostic biomarker. Also knock down of miR-182-5p in order to increase expression of tumor suppressor genes FOXF2, RECK and MTSS1 may be of therapeutic benefit in prostate cancer treatment.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell Line, TumorCell MovementCell SurvivalForkhead Transcription FactorsGene Knockdown TechniquesGPI-Linked ProteinsHumansMaleMiceMice, NudeMicrofilament ProteinsMicroRNAsNeoplasm InvasivenessNeoplasm ProteinsForkhead Transcription FactorsFOXF2 protein, humanGPI-Linked ProteinsMicrofilament ProteinsMicroRNAsMirn182 microRNA, humanMTSS1 protein, humanNeoplasm ProteinsRECK protein, human

Identifiers

PMID23383207
PMCPMC3559583
OpenAlexW2045406164

What OpenQuestion holds

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LicenceCC0
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.