Evidence map›Paper›PMID 22210864›Full record

ArticleNucleic acids research2012

MicroRNA-1 is a candidate tumor suppressor and prognostic marker in human prostate cancer.

Robert S Hudson, Ming Yi, Dominic Esposito, Stephanie K Watkins, Arthur A Hurwitz, Harris G Yfantis, Dong H Lee, James F Borin, Michael J Naslund, Richard B Alexander and 4 more

Abstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

106 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Hyperglycemia and microRNAs in prostate cancer.Prostate cancer and prostatic diseases · 2025
    Article
  5. Article
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  9. Theranostics · 2023
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  12. Review
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  17. [microRNA-1 gene delivery mediated by exosomes suppresses CAL-27 cell proliferation].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021
    Article
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  19. Review
  20. Article

46 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

14 authors.

Robert S HudsonLaboratory of Human Carcinogenesis, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD, USA.
Ming Yi
Dominic Esposito
Stephanie K Watkins
Arthur A Hurwitz
Harris G Yfantis
Dong H Lee
James F Borin
Michael J Naslund
Richard B Alexander
Tiffany H Dorsey
Robert M Stephens
Carlo M Croce
Stefan Ambs

Funding

Maryland Prostate Cancer Case-Control StudyZIABC010499 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI AMBS, STEFAN · 2009 to 2025
$11.4M
MiRNAs/UCRs: biomarkers for cancer risk, tumor detection, progression & treatmentU01CA152758 · NCI · OHIO STATE UNIVERSITY · PI CROCE, CARLO M · 2010 to 2014
$1.8M
Non-coding RNAs as Prognostic and Diagnostic Markers in Prostate CancerZIABC010886 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI AMBS, STEFAN · 2009 to 2019
$1.6M
Intramural NIH HHSNCI NIH HHS U01 CA152758
6 · The paper itself

Abstract

We previously reported that miR-1 is among the most consistently down-regulated miRs in primary human prostate tumors. In this follow-up study, we further corroborated this finding in an independent data set and made the novel observation that miR-1 expression is further reduced in distant metastasis and is a candidate predictor of disease recurrence. Moreover, we performed in vitro experiments to explore the tumor suppressor function of miR-1. Cell-based assays showed that miR-1 is epigenetically silenced in human prostate cancer. Overexpression of miR-1 in these cells led to growth inhibition and down-regulation of genes in pathways regulating cell cycle progression, mitosis, DNA replication/repair and actin dynamics. This observation was further corroborated with protein expression analysis and 3'-UTR-based reporter assays, indicating that genes in these pathways are either direct or indirect targets of miR-1. A gene set enrichment analysis revealed that the miR-1-mediated tumor suppressor effects are globally similar to those of histone deacetylase inhibitors. Lastly, we obtained preliminary evidence that miR-1 alters the cellular organization of F-actin and inhibits tumor cell invasion and filipodia formation. In conclusion, our findings indicate that miR-1 acts as a tumor suppressor in prostate cancer by influencing multiple cancer-related processes and by inhibiting cell proliferation and motility.

Indexed as

Biomarkers, TumorCell CycleCell Line, TumorCell MovementCell ProliferationDNA RepairEpigenesis, GeneticGenes, Tumor SuppressorHistone Deacetylase InhibitorsHumansMaleMicroRNAsMitosisNeoplasm MetastasisNeoplasm Recurrence, LocalPrognosisBiomarkers, TumorHistone Deacetylase InhibitorsMicroRNAsMIRN1 microRNA, human

Identifiers

PMID22210864
PMCPMC3333883

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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.