Evidence map›Paper›PMID 26988912›Full record

ArticleOncotarget2016

Loss of miR-449a in ERG-associated prostate cancer promotes the invasive phenotype by inducing SIRT1.

Parameet Kumar, Shashwat Sharad, Gyorgy Petrovics, Ahmed Mohamed, Albert Dobi, Taduru L Sreenath, Shiv Srivastava, Roopa Biswas

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 24 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

8 authors at 1 institution in 1 country.

Parameet KumarDepartment of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814 USA.
Shashwat SharadDepartment of Surgery and Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814 USA.
Gyorgy PetrovicsDepartment of Surgery and Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814 USA.
Ahmed MohamedDepartment of Surgery and Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814 USA.
Albert DobiDepartment of Surgery and Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814 USA.
Taduru L SreenathDepartment of Surgery and Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814 USA.
Shiv SrivastavaDepartment of Surgery and Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814 USA.
Roopa BiswasDepartment of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD, 20814 USA.
Uniformed Services University of the Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic regulation by SIRT1, a multifaceted NAD+-dependent protein deacetylase, is one of the most common factors modulating cellular processes in a broad range of diseases, including prostate cancer (CaP). SIRT1 is over-expressed in CaP cells, however the associated mechanism is not well understood. To identify whether specific microRNAs might mediate this linkage, we have screened a miRNA library for differential expression in ERG-associated CaP tissues. Of 20 differentially and significantly expressed miRNAs that distinguish ERG-positive tumors from ERG-negative tumors, we find miR-449a is highly suppressed in ERG-positive tumors. We establish that SIRT1 is a direct target of miR-449a and is also induced by ERG in ERG-associated CaP. Our data suggest that attenuation of miR-449a promotes the invasive phenotype of the ERG-positive CaP in part by inducing the expression of SIRT1 in prostate cancer cells. Furthermore, we also find that suppression of SIRT1 results in a significant reduction in ERG expression in ERG-positive CaP cells, indicating a feed-back regulatory loop associated with ERG, miR-449a and SIRT1. We also report that ERG suppresses p53 acetylation perhaps through miR-449a-SIRT1 axis in CaP cells. Our findings provide new insight into the function of miRNAs in regulating ERG-associated CaP. Thus, miR-449a activation or SIRT1 suppression may represent new therapeutic opportunity for ERG-associated CaP.

Indexed as

Cell Line, TumorGene Expression Regulation, NeoplasticHumansMaleMicroRNAsNeoplasm InvasivenessPhenotypeProstatic NeoplasmsSirtuin 1Transcriptional Regulator ERGERG protein, humanMicroRNAsMIRN449 microRNA, humanSIRT1 protein, humanSirtuin 1Transcriptional Regulator ERGERGmicroRNAmiR-449aprostate cancerSIRT1

Identifiers

PMID26988912
PMCPMC5008401
OpenAlexW2330936054

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.