GEO series

KDM6A and B-mediated transcriptional activation of EWSR1-FLI1 targets coordinates demethylase dependent and independent mechanisms in Ewing sarcoma

GSE211743 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 99 samples Submitted 2025/08/18 Platform GPL16791

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 99 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)
Topic: Ewing sarcomaThis series is part of our curated briefing on it.
Samples: 99 samples
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: KDM6 Demethylases Contribute to EWSR1::FLI1-Driven Oncogenic Reprogramming in Ewing SarcomaCancer research · 2025

Summary (written by the submitters)

Ewing Sarcoma (EwS) is a highly aggressive tumor arising in bones and soft tissues driven by the fusion oncoprotein EWSR1::FLI1. This aberrant transcription factor binds to GGAA microsatellites, causing epigenetic reprogramming through the formation of active neo-enhancers in a permissive cellular context. Inhibition of the oncogene remains challenging, and current efforts seek to exploit emergent epigenetic treatments targeting EWSR1::FLI1 cofactors.

Read the full summary ↓

In EwS, neo-enhancers are characterized by strong enrichment of the active H3K27ac mark and concomitant lack of the repressive H3K27me3 mark. These regions are typically decorated with high levels of H3K27me3 prior to EWSR1::FLI1-activation. Here, upon expression of EWSR1::FLI1 in human pediatric mesenchymal stem cells, considered the putative cell of origin of EwS, we unraveled the genome-wide redistribution of H3K27me3. Stemming from these results, we elucidated the contribution of the H3K27me3 demethylases KDM6A/UTX and KDM6B/JMJD3 in the transcriptional activity of EWSR1::FLI1 induced enhancers. KDM6A had a demethylase-independent role in recruiting BRG1 at EWSR1::FLI1-primed enhancers containing single GGAA motifs, which was critical for EwS tumor growth. Conversely, KDM6B demethylated H3K27me3 at specific EWSR1::FLI1-active enhancers, co-localizing with BRG1 at GGAA repeats. Loss of KDM6B impaired the growth of EwS tumor xenografts. These results highlight KDM6 demethylases as EWSR1::FLI1 functional partners with potential as targets for treating EwS.

Published in

KDM6 Demethylases Contribute to EWSR1::FLI1-Driven Oncogenic Reprogramming in Ewing Sarcoma

Figuerola-Bou E, Ríos-Astorch C, Blanco E et al. · Cancer research 2025 · PMID 41085408 · doi:10.1158/0008-5472.CAN-24-3452

This dataset

Open GSE211743 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Ewing sarcoma landscape →

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.

Series matrix ↓

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 GSE211743_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

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.

Raw reads on ENA ↗

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 PRJNA871927 and SRA study SRP393270. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41085408) ↗

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 99 more — browse all 99 samples with per-sample file links →

More Ewing sarcoma datasets

GSE311851 LSD1 Performs Demethylase-Independent and Context-Specific Roles in Ewing Sarcoma 114 samples same disease briefing · shares demethylase, independent, dependent
GSE267223 STAG2 loss in Ewing sarcoma alters enhancer-promoter contacts dependent and independent of EWS::FLI1 52 samples same disease briefing · shares independent, dependent
GSE267222 STAG2 loss in Ewing sarcoma alters enhancer-promoter contacts dependent and independent of EWS::FLI1 32 samples same disease briefing · shares independent, dependent
GSE286100 N'-(1-phenylethylidene)-benzohydrazide cytotoxicity is LSD1 independent and linked to Fe-S cluster disruption in Ewing sarcoma 15 samples same disease briefing · shares independent, dependent
GSE267220 STAG2 loss in Ewing sarcoma alters enhancer-promoter contacts dependent and independent of EWS::FLI1 4 samples same disease briefing · shares independent, dependent
GSE270570 Endogenous degron alleles enable tunable control of EWSR1-FLI1 oncoprotein expression 7 samples same disease briefing · shares ewsr1-fli1
GSE332586 Mevalonate pathway activation in Ewing sarcoma reveals a 3D-specific synergy between statins and BCL-xL inhibition 36 samples same disease briefing · shares activation
GSE263651 Cadherin-11 contributes to the heterogenous and dynamic Wnt-Wnt-β-catenin pathway activation in Ewing sarcoma 1 samples same disease briefing · shares activation

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.