Evidence map›Paper›PMID 20564213›Full record

ArticleJournal of cellular biochemistry2010

Transcriptional suppression of mir-29b-1/mir-29a promoter by c-Myc, hedgehog, and NF-kappaB.

Justin L Mott, Satoshi Kurita, Sophie C Cazanave, Steven F Bronk, Nathan W Werneburg, Martin E Fernandez-Zapico

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01927354 (Observational Study on the Investigation of the Molecular Mechanism and Clinical Significance of the Interplay Between Twist1 and Other EMT Regulators Through microRNA-29 Family.), which is not on this map. Cited by 165 papers.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed
10.4field-weighted citation impact, top 1% 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.

NCT01927354 unknown statusnot on this mapstarted 2012, after this paper: background citation

Observational Study on the Investigation of the Molecular Mechanism and Clinical Significance of the Interplay Between Twist1 and Other EMT Regulators Through microRNA-29 Family.

TypeobservationalSponsorNational Taiwan University HospitalRan2012 to 2014Enrolled100ConditionsHead-and-Neck Squamous Cell Carcinoma
3 · Its place in the literature

Who cites it

165 citing papers in PubMed, 277 citations in OpenAlex.

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  16. FGF-2-dependent signaling activated in aged human skeletal muscle promotes intramuscular adipogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Role of the microRNA-29 family in myocardial fibrosis.Journal of physiology and biochemistry · 2021
    Review
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105 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 2 institutions in 1 country.

Justin L MottDivision of Gastroenterology and Hepatology, College of Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA. mott.justin@mayo.edu
Satoshi Kurita
Sophie C Cazanave
Steven F Bronk
Nathan W Werneburg
Martin E Fernandez-Zapico
Mayo Clinic · USMayo Clinic in Arizona · US

Funding

Tissue CoreP50CA102701 · NCI · MAYO CLINIC ROCHESTER · PI PETERSEN, GLORIA M. · 2004 to 2018
$32.7M
PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
Mechanism of Pancreatic CarcinogenesisR01CA136526 · NCI · MAYO CLINIC ROCHESTER · PI FERNANDEZ-ZAPICO, MARTIN ERNESTO · 2009 to 2019
$3.0M
Cholangiocyte microRNAs Regulate Mcl-1 and Cell DeathK01DK079875 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MOTT, JUSTIN L. · 2007 to 2011
$731k
NCI NIH HHS CA 136526NCI NIH HHS P50 CA102701NCI NIH HHS R01 CA136526NIDDK NIH HHS DK 79875NIDDK NIH HHS DK 84567NIDDK NIH HHS K01 DK079875NIDDK NIH HHS P30 DK084567
6 · The paper itself

Abstract

MicroRNAs regulate pathways contributing to oncogenesis, and thus the mechanisms causing dysregulation of microRNA expression in cancer are of significant interest. Mature mir-29b levels are decreased in malignant cells, and this alteration promotes the malignant phenotype, including apoptosis resistance. However, the mechanism responsible for mir-29b suppression is unknown. Here, we examined mir-29 expression from chromosome 7q32 using cholangiocarcinoma cells as a model for mir-29b downregulation. Using 5' rapid amplification of cDNA ends, the transcriptional start site was identified for this microRNA locus. Computational analysis revealed the presence of two putative E-box (Myc-binding) sites, a Gli-binding site, and four NF-kappaB-binding sites in the region flanking the transcriptional start site. Promoter activity in cholangiocarcinoma cells was repressed by transfection with c-Myc, consistent with reports in other cell types. Treatment with the hedgehog inhibitor cyclopamine, which blocks smoothened signaling, increased the activity of the promoter and expression of mature mir-29b. Mutagenesis analysis and gel shift data are consistent with a direct binding of Gli to the mir-29 promoter. Finally, activation of NF-kappaB signaling, via ligation of Toll-like receptors, also repressed mir-29b expression and promoter function. Of note, activation of hedgehog, Toll-like receptor, and c-Myc signaling protected cholangiocytes from TRAIL-induced apoptosis. Thus, in addition to c-Myc, mir-29 expression can be suppressed by hedgehog signaling and inflammatory pathways, both commonly activated in the genesis of human malignancies.

Indexed as

Binding SitesCell LineCell Line, TumorGene Expression RegulationHedgehog ProteinsHumansMicroRNAsNF-kappa BPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-mycSignal TransductionTranscription FactorsTranscription, GeneticTranscription Initiation SiteVeratrum AlkaloidscyclopamineGLI1 protein, humanHedgehog ProteinsMicroRNAsMIRN29a microRNA, humanMYC protein, humanNF-kappa BProto-Oncogene Proteins c-mycTranscription FactorsVeratrum AlkaloidsZinc Finger Protein GLI1

Identifiers

PMID20564213
PMCPMC2922950
OpenAlexW1970344564

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.