Evidence map›Paper›PMID 19088023›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2008

miR-192 Regulates dihydrofolate reductase and cellular proliferation through the p53-microRNA circuit.

Bo Song, Yuan Wang, Kenji Kudo, Elaine J Gavin, Yaguang Xi, Jingfang Ju

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.

  1. Pooled it
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  6. Serum-Circulating microRNAs in Sporadic Inclusion Body Myositis.International journal of molecular sciences · 2023
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  7. Review
  8. Development of 5-FU-modified tumor suppressor microRNAs as a platform for novel microRNA-based cancer therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
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28 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

6 authors at 4 institutions in 2 countries.

Bo SongTranslational Research Laboratory, Department of Pathology, Stony Brook University Medical Center, Stony Brook, New York 11794-8691, USA.
Yuan Wang
Kenji Kudo
Elaine J Gavin
Yaguang Xi
Jingfang Ju
USA Mitchell Cancer Institute · USWuhan University · CNStony Brook University Hospital · USUniversity of South Alabama · US

Funding

Modulation of Serotonergic TransportersR01MH075020 · NIMH · GEORGETOWN UNIVERSITY · PI SIDHU, ANITA · 2007 to 2010
$1.3M
Novel Method for Isolating Actively Translated mRNAsR21CA114043 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI JU, JINGFANG · 2006 to 2007
$259k
NCI NIH HHS CA114043NCI NIH HHS R21 CA114043NIMH NIH HHS MH075020NIMH NIH HHS R01 MH075020
6 · The paper itself

Abstract

purposeThe purpose of this study is to investigate the molecular mechanism of miR-192 in colon cancer. EXPERIMENTAL

designHuman colon cancer cell lines with different p53 status were used as our model system to study the effect of miR-192 on cell proliferation, cell cycle control, and mechanism of regulation.

resultsOur results show that one of the key miR-192 target genes is dihydrofolate reductase (DHFR). miR-192 affects cellular proliferation through the p53-miRNA circuit. Western immunoblot analyses indicated that the expression of DHFR was significantly decreased by miR-192. Further investigation revealed that such suppression was due to translational arrest rather than mRNA degradation. More profound inhibition of cellular proliferation was observed by ectopic expression of miR-192 in colon cancer cell lines containing wild-type p53 than cells containing mutant p53. Thus, the effect of miR-192 on cellular proliferation is mainly p53 dependent. Overexpression of miR-192 triggered both G1 and G2 arrest in HCT-116 (wt-p53) cells but not in HCT-116 (null-p53) cells. The cell cycle checkpoint control genes p53 and p21 were highly overexpressed in cells that overexpressed miR-192. Endogenous miR-192 expression was increased in HCT-116 (wt-p53) and RKO (wt-p53) cells treated with methotrexate, which caused an induction of p53 expression. Chromatin immunoprecipitation-quantitative reverse transcription-PCR analysis revealed that the p53 protein interacted with the miR-192 promoter sequence.

conclusionThese results indicate that miR-192 may be another miRNA candidate that is involved in the p53 tumor suppressor network with significant effect on cell cycle control and cell proliferation.

Indexed as

Gene Expression Regulation, EnzymologicCell CycleCell ProliferationHCT116 CellsHT29 CellsHumansMethotrexateMicroRNAsPromoter Regions, GeneticTetrahydrofolate DehydrogenaseTumor Suppressor Protein p53MethotrexateMicroRNAsTetrahydrofolate DehydrogenaseTumor Suppressor Protein p53

Identifiers

PMID19088023
PMCPMC2653201
OpenAlexW2076526862

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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.