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Status |
Public on Apr 01, 2018 |
Title |
MEK inhibition profoundly reprograms myogenic super enhancers in mutant-RAS driven Rhabdomyosarcoma |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
Trametinib-treated rhabdomyosarcoma cells undergo transcriptional reprogramming akin to myogenic differentiation. This reprogramming is induced by loss of ERK-mediated inhibition of MYOG expression. Restoration of MYOG allows establishment of super-enhancers at genes expressed by terminally differentiated myotubes. Our findings demonstrate that aberrant MAP kinase activity blocks differentiation in rhabdomyosarcoma and highlight trametinib as a potential therapeutic for RAS-mutated rhabdomyosarcoma.
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Overall design |
Genome-wide profiles for histone marks, DNase hypersensitivity, transcription factors in mutant-RAS driven, Fusion-Negative Rhabdomyosarcoma (FN-RMS) cell lines and tissues
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Contributor(s) |
Gryder BE, Yohe ME, Wen X |
Citation(s) |
29973406 |
Submission date |
Aug 03, 2016 |
Last update date |
May 15, 2019 |
Contact name |
Nitin Roper |
E-mail(s) |
nitin.roper@nih.gov
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Phone |
2408583571
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Organization name |
NCI, NIH
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Department |
Developmental Therapeutics Branch
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Street address |
37 Convent Dr.
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City |
Bethesda |
State/province |
MD |
ZIP/Postal code |
20892 |
Country |
USA |
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Platforms (2) |
GPL11154 |
Illumina HiSeq 2000 (Homo sapiens) |
GPL18573 |
Illumina NextSeq 500 (Homo sapiens) |
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Samples (38)
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This SubSeries is part of SuperSeries: |
GSE85171 |
Epigenetic Reprogramming of mutant RAS-driven Rhabdomyosarcoma via MEK Inhibition |
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Relations |
BioProject |
PRJNA336374 |
SRA |
SRP080881 |