GEO series
MYOD1L122R induces cancer stem cell pathways to impart chemotherapy and radiation-resistance in aggressive rhabdomyosarcoma [ChIP-seq]
GSE274637
Homo sapiens (human)
ChIP-seq / ATAC-seq (genome binding and open chromatin)
32 samples
Submitted 2026/01/14
Platform GPL30173Platform GPL21697
At a glance
ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 32 samples
- What it is
- ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
- Organism
- Homo sapiens (human)
- Samples
- 32 samples: 16 conditions, mostly in duplicateGroups are read from the sample names, not from the paper. Check the list below.
- Data you can get
- A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
- Paper
- The PIK3CA/AKT pathway drives therapy resistance in rhabdomyosarcomaNature communications · 2025
Summary (written by the submitters)
Rhabdomyosarcoma (RMS) is a common pediatric soft tissue sarcoma of skeletal muscle. Worse outcomes are associated with specific subtypes of RMS, including the 10% of fusion-negative tumors that harbor point mutations in the DNA binding domain of MYOD1 (myogenic differentiation 1) transcription factor. Due to the rarity of these patient samples and dearth of cell lines/animal models, the molecular function of MYOD1L122R remains unknown.
Read the full summary ↓
Here, we create the first animal model of this disease showing that MYOD1L122R is not oncogenic but collaborates with RAS activation to create highly aggressive RMS in transgenic zebrafish, akin to what is reported in human disease. Limiting dilution cell transplantation revealed that MYOD1L122R also elevated the overall frequency of tumor propagating cells in the zebrafish model. We next generated isogenic knock-in MYOD1L122R human cell line models and showed that these cells were refractory to standard of care vincristine, actinomycin, and cyclophosphamide while also elevating the overall frequency of tumor propagating cells. Indeed, single-cell RNA transcriptional profiling and single-cell assay for transposase-accessible chromatin with sequencing (ATAC-Seq) of patient and patient-derived xenografts confirmed the elevation of cancer stem cell programs within MYOD1L122R tumors. Using unbiased whole-genome ChIP and RNA sequencing, we next identified the shared and differential genomic binding regions by MYOD1L122R as compared to wildtype MYOD1. Most notably, MYOD1L122R bound uniquely to and transcriptionally upregulated mesenchymal pathway enriched genes that are known to correlate with RMS cancer stemness. Finally, mechanistic studies uncovered that MYOD1L122R binds to the regulatory element of ROR2 (receptor tyrosine kinase like orphan receptor 2), upregulating its expression, which then turns on a novel WNT11-ROR2-VANGL2 axis to induce non-canonical WNT signaling and elevate cancer stemness.
Published in
Yang Q, Wang Y, Corchete Sanchez LA et al.
· Nature communications 2025
· PMID 41372143
· doi:10.1038/s41467-025-66632-9
This dataset
Download · which file do I need?
Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.
1 · Just have a look
Processed table
The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.
2 · Re-analyse it
Supplementary files
The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE274637_RAW.tar (it can run to tens of gigabytes).
3 · Start from the raw reads
Raw sequencing reads
The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.
What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.
Also filed as BioProject PRJNA1147321 and SRA study SRP525894. Searching any of these in the dataset finder brings you back here.
Study design
16 conditions, mostly in duplicate
RD, MYOD1, Input, ×2
RD, MYOD1, MYOD1, ×2
RD, MYOD1, H3K27ac, ×2
RD, MYOD1, H3K4me3, ×2
RD, L122R, Input, ×2
RD, L122R, L122R, ×2
RD, L122R, H3K27ac, ×2
RD, L122R, H3K4me3, ×2
+8 more
Supports a between-group comparison across 32 samples.
How we read this: 16 replicated groups read from 32 sample titles; they account for 32 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.
Samples in this study
- GSM8454038 RD, MYOD1, Input, R1 RD, MYOD1, Input,
- GSM8454039 RD, MYOD1, MYOD1, R1 RD, MYOD1, MYOD1,
- GSM8454040 RD, MYOD1, H3K27ac, R1 RD, MYOD1, H3K27ac,
- GSM8454041 RD, MYOD1, H3K4me3, R1 RD, MYOD1, H3K4me3,
- GSM8454042 RD, MYOD1, Input, R2 RD, MYOD1, Input,
- GSM8454043 RD, MYOD1, MYOD1, R2 RD, MYOD1, MYOD1,
- GSM8454044 RD, MYOD1, H3K27ac, R2 RD, MYOD1, H3K27ac,
- GSM8454045 RD, MYOD1, H3K4me3, R2 RD, MYOD1, H3K4me3,
- GSM8454046 RD, L122R, Input, R1 RD, L122R, Input,
- GSM8454047 RD, L122R, L122R, R1 RD, L122R, L122R,
- GSM8454048 RD, L122R, H3K27ac, R1 RD, L122R, H3K27ac,
- GSM8454049 RD, L122R, H3K4me3, R1 RD, L122R, H3K4me3,
- GSM8454050 RD, L122R, Input, R2 RD, L122R, Input,
- GSM8454051 RD, L122R, L122R, R2 RD, L122R, L122R,
- GSM8454052 RD, L122R, H3K27ac, R2 RD, L122R, H3K27ac,
- GSM8454053 RD, L122R, H3K4me3, R2 RD, L122R, H3K4me3,
- GSM8454054 Ruch2, MYOD1, Input, R1 Ruch2, MYOD1, Input,
- GSM8454055 Ruch2, MYOD1, MYOD1, R1 Ruch2, MYOD1, MYOD1,
- GSM8454056 Ruch2, MYOD1, H3K27ac, R1 Ruch2, MYOD1, H3K27ac,
- GSM8454057 Ruch2, MYOD1, H3K4me3, R1 Ruch2, MYOD1, H3K4me3,
- GSM8454058 Ruch2, MYOD1, Input, R2 Ruch2, MYOD1, Input,
- GSM8454059 Ruch2, MYOD1, MYOD1, R2 Ruch2, MYOD1, MYOD1,
- GSM8454060 Ruch2, MYOD1, H3K27ac, R2 Ruch2, MYOD1, H3K27ac,
- GSM8454061 Ruch2, MYOD1, H3K4me3, R2 Ruch2, MYOD1, H3K4me3,
- GSM8454062 Ruch2, L122R, Input, R1 Ruch2, L122R, Input,
- GSM8454063 Ruch2, L122R, L122R, R1 Ruch2, L122R, L122R,
- GSM8454064 Ruch2, L122R, H3K27ac, R1 Ruch2, L122R, H3K27ac,
- GSM8454065 Ruch2, L122R, H3K4me3, R1 Ruch2, L122R, H3K4me3,
- GSM8454066 Ruch2, L122R, Input, R2 Ruch2, L122R, Input,
- GSM8454067 Ruch2, L122R, L122R, R2 Ruch2, L122R, L122R,
- GSM8454068 Ruch2, L122R, H3K27ac, R2 Ruch2, L122R, H3K27ac,
- GSM8454069 Ruch2, L122R, H3K4me3, R2 Ruch2, L122R, H3K4me3,
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