ArticleMolecular and cellular biology2013
Comparison of genome-wide binding of MyoD in normal human myogenic cells and rhabdomyosarcomas identifies regional and local suppression of promyogenic transcription factors.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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.
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Who cites it
51 citing papers in PubMed, 75 citations in OpenAlex.
- MyoD is essential in rhabdomyosarcoma by promoting survival through differentiation and CYLD.iScience · 2025Article
- The multifaceted roles of BAF60 subunits in muscle: regulation of differentiation, reprogramming, and metabolic homeostasis.Frontiers in cell and developmental biology · 2025Review
- Review
- Article
- Myogenesis gone awry: the role of developmental pathways in rhabdomyosarcoma.Frontiers in cell and developmental biology · 2024Review
- MYOD-SKP2 axis boosts tumorigenesis in fusion negative rhabdomyosarcoma by preventing differentiation through p57Nature communications · 2023Article
- Discovery of a non-canonical GRHL1 binding site using deep convolutional and recurrent neural networks.BMC genomics · 2023Article
- 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 · 2023Article
- Differentiation-dependent chromosomal organization changes in normal myogenic cells are absent in rhabdomyosarcoma cells.bioRxiv : the preprint server for biology · 2023Article
- TWIST2-mediated chromatin remodeling promotes fusion-negative rhabdomyosarcoma.Science advances · 2023Article
- Heat Shock Proteins: Important Helpers for the Development, Maintenance and Regeneration of Skeletal Muscles.Muscles (Basel, Switzerland) · 2023Review
- Nucleoli and the nucleoli-centromere association are dynamic during normal development and in cancer.Molecular biology of the cell · 2023Article
- Biological Role and Clinical Implications ofCancers · 2023Review
- Differentiation-dependent chromosomal organization changes in normal myogenic cells are absent in rhabdomyosarcoma cells.Frontiers in cell and developmental biology · 2023Article
- Pax3 loss of function delays tumour progression in kRAS-induced zebrafish rhabdomyosarcoma models.Scientific reports · 2022Article
- SIX1 reprograms myogenic transcription factors to maintain the rhabdomyosarcoma undifferentiated state.Cell reports · 2022Article
- SNAI2-Mediated Repression ofCancer research · 2021Article
- Mechanisms of Binding Specificity among bHLH Transcription Factors.International journal of molecular sciences · 2021Review
- Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy.Clinical epigenetics · 2021Review
- Interaction between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion Negative Rhabdomyosarcoma.Nature communications · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Rhabdomyosarcoma is a pediatric tumor of skeletal muscle that expresses the myogenic basic helix-loop-helix protein MyoD but fails to undergo terminal differentiation. Prior work has determined that DNA binding by MyoD occurs in the tumor cells, but myogenic targets fail to activate. Using MyoD chromatin immunoprecipitation coupled to high-throughput sequencing and gene expression analysis in both primary human muscle cells and RD rhabdomyosarcoma cells, we demonstrate that MyoD binds in a similar genome-wide pattern in both tumor and normal cells but binds poorly at a subset of myogenic genes that fail to activate in the tumor cells. Binding differences are found both across genomic regions and locally at specific sites that are associated with binding motifs for RUNX1, MEF2C, JDP2, and NFIC. These factors are expressed at lower levels in RD cells than muscle cells and rescue myogenesis when expressed in RD cells. MEF2C is located in a genomic region that exhibits poor MyoD binding in RD cells, whereas JDP2 exhibits local DNA hypermethylation in its promoter in both RD cells and primary tumor samples. These results demonstrate that regional and local silencing of differentiation factors contributes to the differentiation defect in rhabdomyosarcomas.
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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.