Evidence map›Paper›PMID 34099864›Full record

ArticleJournal of human genetics2021

Mapping genetic variability in mature miRNAs and miRNA binding sites in prostate cancer.

Bongyong Lee, Jian-Liang Li, John Marchica, Mark Mercola, Vipul Patel, Ranjan J Perera

Open access · greenAbstract read
In one paragraph

Article in Journal of human genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
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

6 authors at 3 institutions in 1 country.

Bongyong LeeDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Jian-Liang LiIntegrative Bioinformatics, National Institute of Environmental Health Sciences, Durham, NC, USA.ORCID http://orcid.org/0000-0002-6487-081X
John MarchicaJohns Hopkins All Children's Hospital, St. Petersburg, FL, USA.ORCID http://orcid.org/0000-0003-3463-6210
Mark MercolaDepartment Medicine, Stanford University, Palo Alto, CA, USA.
Vipul PatelAdventHealth 410 Celebration Pl Suite 200, Kissimmee, FL, USA.
Ranjan J PereraDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, School of Medicine, Johns Hopkins University, Baltimore, MD, USA. jperera2@jh.edu.ORCID http://orcid.org/0000-0002-5926-3687
Johns Hopkins University · USNational Institute of Environmental Health Sciences · USStanford University · US

Funding

Tumor Microenvironment and Cancer ImmunologyP30CA030199 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI ELENA B PASQUALE · 1985 to 2026
$107.2M
NCI NIH HHS P30 CA030199
6 · The paper itself

Abstract

MicroRNAs (miRNAs) regulate diverse cancer hallmarks through sequence-specific regulation of gene expression, so genetic variability in their seed sequences or target sites could be responsible for cancer initiation or progression. While several efforts have been made to predict the locations of single nucleotide variants (SNVs) at miRNA target sites and associate them with cancer risk and susceptibility, there have been few direct assessments of SNVs in both mature miRNAs and their target sites to assess their impact on miRNA function in cancers. Using genome-wide target capture of miRNAs and miRNA-binding sites followed by deep sequencing in prostate cancer cell lines, here we identified prostate cancer-specific SNVs in mature miRNAs and their target binding sites. SNV rs9860655 in the mature sequence of miR-570 was not present in benign prostate hyperplasia (BPH) tissue or cell lines but was detectable in clinical prostate cancer tissue samples and adjacent normal tissue. SLC45A3 (prostein), a putative oncogene target of miR-1178, was highly upregulated in PC3 cells harboring an miR-1178 seed sequence SNV. Finally, systematic assessment of losses and gains of miRNA targets through 3'UTR SNVs revealed SNV-associated changes in target oncogene and tumor suppressor gene expression that might be associated with prostate carcinogenesis. Further work is required to systematically assess the functional effects of miRNA SNVs.

Indexed as

Binding SitesCarcinogenesisCell Line, TumorGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGenetic VariationHigh-Throughput Nucleotide SequencingHumansMaleMicroRNAsMonosaccharide Transport ProteinsPolymorphism, Single NucleotideProstatic NeoplasmsRNA-Binding ProteinsMicroRNAsMIRN1178 microRNA, humanMonosaccharide Transport ProteinsRNA-Binding ProteinsSLC45a3 protein, human

Identifiers

PMID34099864
PMCPMC11849141
OpenAlexW3166736630

What OpenQuestion holds

Textmetadata
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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.