Evidence map›Paper›PMID 22710712›Full record

ArticleOncogene2013

Alveolar rhabdomyosarcoma-associated proteins PAX3/FOXO1A and PAX7/FOXO1A suppress the transcriptional activity of MyoD-target genes in muscle stem cells.

F Calhabeu, S Hayashi, J E Morgan, F Relaix, P S Zammit

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Lrrc75b is a novel negative regulator of C2C12 myogenic differentiation.International journal of molecular medicine · 2016
    Pooled it
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  14. Current Thoughts of Notch's Role in Myoblast Regulation and Muscle-Associated Disease.International journal of environmental research and public health · 2021
    Review
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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

5 authors at 3 institutions in 2 countries.

F CalhabeuKing's College London, Randall Division of Cell and Molecular Biophysics, London, UK.
S Hayashi
J E Morgan
F Relaix
P S Zammit
Inserm · FRKing's College London · GBUniversity College London · GB

Funding

Medical Research CouncilWellcome Trust 085137/Z/08/ZWorldwide Cancer Research 07-0151
6 · The paper itself

Abstract

Rhabdomyosarcoma (RMS) is the commonest soft-tissue sarcoma in childhood and is characterized by expression of myogenic proteins, including the transcription factors MyoD and myogenin. There are two main subgroups, embryonal RMS and alveolar RMS (ARMS). Most ARMS are associated with chromosomal translocations that have breakpoints in introns of either PAX3 or PAX7, and FOXO1A. These translocations create chimeric transcription factors termed PAX3/FOXO1A and PAX7/FOXO1A respectively. Upon ectopic PAX3/FOXO1A expression, together with other genetic manipulation in mice, both differentiating myoblasts and satellite cells (the resident stem cells of postnatal muscle) can give rise to tumours with ARMS characteristics. As PAX3 and PAX7 are part of transcriptional networks that regulate muscle stem cell function in utero and during early postnatal life, PAX3/FOXO1A and PAX7/FOXO1A may subvert normal PAX3 and PAX7 functions. Here we examined how PAX3/FOXO1A and PAX7/FOXO1A affect myogenesis in satellite cells. PAX3/FOXO1A or PAX7/FOXO1A inhibited myogenin expression and prevented terminal differentiation in murine satellite cells: the same effect as dominant-negative (DN) Pax3 or Pax7 constructs. The transcription of MyoD-target genes myogenin and muscle creatine kinase were suppressed by PAX3/FOXO1A or PAX7/FOXO1A in C2C12 myogenic cells again as seen with Pax3/7DN. PAX3/FOXO1A or PAX7/FOXO1A did not inhibit the transcriptional activity of MyoD by perturbing MyoD expression, localization, phosphorylation or interaction with E-proteins. Chromatin immunoprecipitation on the myogenin promoter showed that PAX3/FOXO1A or PAX7/FOXO1A did not prevent MyoD from binding. However, PAX3/FOXO1A or PAX7/FOXO1A reduced occupation of the myogenin promoter by RNA polymerase II and decreased acetylation of histone H4, but did not directly bind to the myogenin promoter. Together, these observations reveal that PAX3/FOXO1A and PAX7/FOXO1A act to prevent myogenic differentiation via suppression of the transcriptional activation of MyoD-target genes.

Indexed as

AnimalsCell DifferentiationCell LineCreatine Kinase, MM FormForkhead Box Protein O1Forkhead Transcription FactorsGene Expression RegulationMiceMyoD ProteinMyogeninOncogene Proteins, FusionPaired Box Transcription FactorsPAX3 Transcription FactorPAX7 Transcription FactorRhabdomyosarcoma, AlveolarSatellite Cells, Skeletal MuscleCreatine Kinase, MM FormForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mouseMyoD1 myogenic differentiation proteinMyoD ProteinMyogeninOncogene Proteins, FusionPaired Box Transcription FactorsPAX3-FKHR fusion protein, mousePax3 protein, mousePAX3 Transcription FactorPAX7-FOXO1A fusion protein, mousePax7 protein, mousePAX7 Transcription Factor

Identifiers

PMID22710712
OpenAlexW2019686407

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.