Evidence map›Paper›PMID 19620785›Full record

ArticleThe Journal of clinical investigation2009

The muscle-specific microRNA miR-206 blocks human rhabdomyosarcoma growth in xenotransplanted mice by promoting myogenic differentiation.

Riccardo Taulli, Francesca Bersani, Valentina Foglizzo, Alessandra Linari, Elisa Vigna, Marc Ladanyi, Thomas Tuschl, Carola Ponzetto

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed
10.0field-weighted citation impact, top 2% 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

161 citing papers in PubMed, 262 citations in OpenAlex.

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  8. A dysfunctional miR-1-TRPS1-MYOG axis drives ERMS by suppressing terminal myogenic differentiation.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
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  11. Exploring circular MET RNA as a potential biomarker in tumors exhibiting high MET activity.Journal of experimental & clinical cancer research : CR · 2023
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  19. MicroRNA-1: Diverse role of a small player in multiple cancers.Seminars in cell & developmental biology · 2022
    Review
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101 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Riccardo TaulliDepartment of Anatomy, Pharmacology and Forensic Medicine, and Center for Experimental Research and Medical Studies, University of Torino, Torino, Italy.
Francesca Bersani
Valentina Foglizzo
Alessandra Linari
Elisa Vigna
Marc Ladanyi
Thomas Tuschl
Carola Ponzetto
University of Turin · ITCandiolo Cancer Institute · ITMemorial Sloan Kettering Cancer Center · USOspedale Regina Margherita · ITRockefeller University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many microRNAs (miRNAs), posttranscriptional regulators of numerous cellular processes and developmental events, are downregulated in tumors. However, their role in tumorigenesis remains largely unknown. In this work, we examined the role of the muscle-specific miRNAs miR-1 and miR-206 in human rhabdomyosarcoma (RMS), a soft tissue sarcoma thought to arise from skeletal muscle progenitors. We have shown that miR-1 was barely detectable in primary RMS of both the embryonal and alveolar subtypes and that both miR-1 and miR-206 failed to be induced in RMS cell lines upon serum deprivation. Moreover, reexpression of miR-206 in RMS cells promoted myogenic differentiation and blocked tumor growth in xenografted mice by switching the global mRNA expression profile to one that resembled mature muscle. Finally, we showed that the product of the MET proto-oncogene, the Met tyrosine-kinase receptor, which is overexpressed in RMS and has been implicated in RMS pathogenesis, was downregulated in murine satellite cells by miR-206 at the onset of normal myogenesis. Thus, failure of posttranscriptional modulation may underlie Met overexpression in RMS and other types of cancer. We propose that tissue-specific miRNAs such as miR-1 and miR-206, given their ability to modulate hundreds of transcripts and to act as nontoxic differentiating agents, may override the genomic heterogeneity of solid tumors and ultimately hold greater therapeutic potential than single gene-directed drugs.

Indexed as

AnimalsCell CycleCell DifferentiationCell Line, TumorHumansMiceMicroRNAsMuscle DevelopmentProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-metReceptors, Growth FactorRhabdomyosarcomaXenograft Model Antitumor AssaysMAS1 protein, humanMET protein, humanMicroRNAsProto-Oncogene MasProto-Oncogene ProteinsProto-Oncogene Proteins c-metReceptors, Growth Factor

Identifiers

PMID19620785
PMCPMC2719932
OpenAlexW2004775268

What OpenQuestion holds

Textmetadata
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.