Evidence map›Paper›PMID 32198489›Full record

ArticleScientific reports2020

Multifaceted Function of MicroRNA-299-3p Fosters an Antitumor Environment Through Modulation of Androgen Receptor and VEGFA Signaling Pathways in Prostate Cancer.

Kavya Ganapathy, Stephen Staklinski, Md Faqrul Hasan, Richard Ottman, Thomas Andl, Anders E Berglund, Jong Y Park, Ratna Chakrabarti

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

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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  11. Review
  12. Androgen Receptor-Related Non-coding RNAs in Prostate Cancer.Frontiers in cell and developmental biology · 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

8 authors at 2 institutions in 1 country.

Kavya GanapathyBurnett School of Biomedical Sciences, University of Central Florida, Orlando, FL, USA.
Stephen StaklinskiBurnett School of Biomedical Sciences, University of Central Florida, Orlando, FL, USA.
Md Faqrul HasanBurnett School of Biomedical Sciences, University of Central Florida, Orlando, FL, USA.
Richard OttmanBurnett School of Biomedical Sciences, University of Central Florida, Orlando, FL, USA.
Thomas AndlBurnett School of Biomedical Sciences, University of Central Florida, Orlando, FL, USA.
Anders E BerglundDepartment of Biostatistics and Bioinformatics, Moffitt Cancer Center, Tampa, FL, USA.ORCID http://orcid.org/0000-0002-0393-3530
Jong Y ParkDepartment of Cancer Epidemiology, Moffitt Cancer Center, Tampa, FL, USA.ORCID http://orcid.org/0000-0002-6384-6447
Ratna ChakrabartiBurnett School of Biomedical Sciences, University of Central Florida, Orlando, FL, USA. ratna.chakrabarti@ucf.edu.
University of Central Florida · USMoffitt Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is one of the most common cancers to affect men worldwide. Androgen receptor (AR) signaling is central to PCa and PCa therapy. MicroRNAs (miRNAs) play crucial roles in the regulation of prostate cancer through modulation of signaling pathways. In the present study, we illustrate the functional significance and therapeutic benefit of miR-299-3p, an AR targeting microRNA, in PCa progression. We noted loss of expression of miR-299-3p in prostate tumors compared to noncancerous prostate tissues. Replenishment of miR-299-3p in C4-2B, 22Rv-1 and PC-3 cells contributed to cell cycle arrest, reduced proliferation, migration and increased expression of apoptotic markers. Additionally, overexpression of miR-299-3p induced a reduction of AR, PSA and VEGFA expression. AGO-RNA pulldown experiment showed enrichment of AR, VEGFA and miR-299-3p in C4-2B cells overexpressing miR-299-3p. miR-299-3p overexpression also inhibited epithelial mesenchymal transition, expression of Slug, TGF-β3, phospho-AKT and phospho-PRAS40, but increased expression of E-cadherin. Furthermore, miR-299 overexpression resulted in reduced tumor growth in xenograft models and increased drug sensitivity. Overall, this study has identified novel mechanisms of antitumor and antimigration function of miR-299-3p through modulation of AR and VEGFA signaling pathways which lead to improved drug sensitivity of PCa.

Indexed as

Cell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionHumansMaleMicroRNAsProstatic NeoplasmsReceptors, AndrogenSignal TransductionVascular Endothelial Growth Factor AAR protein, humanMicroRNAsMIRN299 microRNA, humanReceptors, AndrogenVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID32198489
PMCPMC7083835
OpenAlexW3012422550

What OpenQuestion holds

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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.