Evidence map›Paper›PMID 20041160›Full record

ArticlePloS one2009

MiR-24 tumor suppressor activity is regulated independent of p53 and through a target site polymorphism.

Prasun J Mishra, Bo Song, Pravin J Mishra, Yuan Wang, Rita Humeniuk, Debabrata Banerjee, Glenn Merlino, Jingfang Ju, Joseph R Bertino

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. MicroRNAs: The Link between the Metabolic Syndrome and Oncogenesis.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. miR-15a and miR-24-1 as putative prognostic microRNA signatures for pediatric pilocytic astrocytomas and ependymomas.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Review
  17. Article
  18. Circulating miRNAs as biomarkers for endocrine disorders.Journal of endocrinological investigation · 2016
    Review
  19. Article
  20. Article
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

9 authors at 5 institutions in 1 country.

Prasun J MishraLaboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Bo Song
Pravin J Mishra
Yuan Wang
Rita Humeniuk
Debabrata Banerjee
Glenn Merlino
Jingfang Ju
Joseph R Bertino
National Institutes of Health · USRutgers Cancer Institute of New JerseyStony Brook University · USRutgers, The State University of New Jersey · USStony Brook University Hospital · US

Funding

Genetically Engineered Mouse Models to Study RTK Function in MelanomaZIABC008756 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MERLINO, GLENN T. · 2009 to 2024
$17.7M
Novel Method for Isolating Actively Translated mRNAsR21CA114043 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI JU, JINGFANG · 2006 to 2007
$259k
Intramural NIH HHSNCI NIH HHS CA0810NCI NIH HHS CA114043NCI NIH HHS R21 CA114043PHS HHS C5IL039280
6 · The paper itself

Abstract

MicroRNAs (miRNAs) are predicted to regulate approximately 30% of all human genes; however, only a few miRNAs have been assigned their targets and specific functions. Here we demonstrate that miR-24, a ubiquitously expressed miRNA, has an anti-proliferative effect independent of p53 function. Cell lines with differential p53 status were used as a model to study the effects of miR-24 on cell proliferation, cell cycle control, gene regulation and cellular transformation. Overexpression of miR-24 in six different cell lines, independent of p53 function, inhibited cell proliferation and resulted in G2/S cell cycle arrest. MiR-24 over expression in cells with wt-p53 upregulated TP53 and p21 protein; however, in p53-null cells miR-24 still induced cell cycle arrest without the involvement of p21. We show that miR-24 regulates p53-independent cellular proliferation by regulating an S-phase enzyme, dihydrofolate reductase (DHFR) a target of the chemotherapeutic drug methotrexate (MTX). Of interest, we found that a miR-24 target site polymorphism in DHFR 3' UTR that results in loss of miR-24-function and high DHFR levels in the cell imparts a growth advantage to immortalized cells and induces neoplastic transformation. Of clinical significance, we found that miR-24 is deregulated in human colorectal cancer tumors and a subset of tumors has reduced levels of miR-24. A novel function for miR-24 as a p53-independent cell cycle inhibitory miRNA is proposed.

Indexed as

3' Untranslated RegionsAnimalsCell AdhesionCell Cycle ProteinsCell DifferentiationCell Line, TumorCell ProliferationCell ShapeColorectal NeoplasmsDown-RegulationDrug Resistance, NeoplasmG2 PhaseGene Expression Regulation, NeoplasticHumansMethotrexateMice3' Untranslated RegionsCell Cycle ProteinsMethotrexateMicroRNAsMIRN24 microRNA, humanTetrahydrofolate DehydrogenaseTumor Suppressor Protein p53

Identifiers

PMID20041160
PMCPMC2794546
OpenAlexW1972346050

What OpenQuestion holds

Textmetadata
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.