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ChIP-seq analysis for H3K4me3, H3K27ac, H3K27me3, p-STAT3, POU2AF1 and ELL2 in MM.1S cells

GSE298692 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2026/02/15 Platform GPL18573
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 14 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
14 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
IL-6-driven POU2AF1 and ELL2 are key regulators of multiple myeloma-distinct transcriptional and splicing programsBlood advances · 2026
Summary (written by the submitters)
Multiple myeloma (MM) is a plasma cell neoplasm that depends on the bone marrow (BM) microenvironment; however, the underlying mechanisms of epigenetic contribution to the pathogenesis of MM are incompletely understood. Here, we delineate the epigenetic-driven transcriptional and splicing program crucial for MM.
Read the full summary ↓
We recharacterized transcriptional program induced by IL-6/JAK/STAT3 pathway by ChIP-seq and RNA-seq analyses combined with CRIPSR knockout screening database, and identified B cell lineage factors, POU2AF1 and ELL2, as crucial IL-6/JAK/STAT3 targets that are essential for MM cell growth and survival. Genetic depletion of these factors suppressed MM cell growth in vitro and in the xenograft model of IL-6 humanized mice. Mechanistically, POU2AF1 and ELL2 govern MM-distinct transcriptional program representing immaturity, and IL-6/JAK/STAT3 pathway augments this program through upregulating and recruiting these factors to the MM-signature genes. Furthermore, we showed that IL-6 induces alternative splicing that is partly mediated by POU2AF1. Proteomic study identified novel POU2AF1-associated factors that converge in regulation of RNA, including RNA splicing. Indeed, POU2AF1 is adjacent to multiple splicing factors required for MM cell survival and is involved in the organization of nuclear speckles. Finally, we showed that gapmer antisense oligonucleotides (ASOs) targeting POU2AF1 inhibit its expression and MM cell growth in the presence of soluble BM stromal cell factors, including IL-6. Our data demonstrate that IL-6-driven B cell-lineage factors are the vulnerability of MM cells and may represent novel therapeutic targets for this incurable tumor.
Published in
IL-6-driven POU2AF1 and ELL2 are key regulators of multiple myeloma-distinct transcriptional and splicing programs
Ohguchi Y, Ajiro M, Ogiya D et al. · Blood advances 2026 · PMID 41925579 · doi:10.1182/bloodadvances.2025018710
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 GSE298692_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 PRJNA1270960 and SRA study SRP589247. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 14 more — browse all 14 samples with per-sample file links →

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