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ATF4:p52 Complex Activates Oncogenic Enhancers in Multiple Myeloma via p300/CBP Recruitment to Regulate BACH1

GSE292455 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 31 samples Submitted 2025/04/21 Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 31 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
Multiple myelomaThis series is part of our curated briefing on it.
Samples
31 samples: 11 conditions, mostly in triplicateGroups 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
ATF4:p52 complex activates oncogenic enhancers in multiple myeloma via p300/CBP recruitment to regulate BACH1Cancer letters · 2025
Summary (written by the submitters)
Multiple myeloma (MM) is a B-cell malignancy accounting for 20% of all blood-associated cancers. MM patients with a poorer prognosis and high-risk stratification were previously observed to be causally linked to the constitutive activation of non-canonical NF-kB (ncNF-kB) pathway. Consistent with this, the ncNF-kB p52 transcription factor was earlier found to regulate the enhancer landscape of MM to potentiate oncogenic transcription.
Read the full summary ↓
However, the mechanism by which aberrant p52 expression is involved in coordinating enhancer activity has not been well explored. In this study, we analysed H3K27ac ChIP-seq and ATAC-seq data from MM cell lines and patient samples to screen for putative transcription factors that cooperate with p52 to regulate enhancers activated in MM. We report that ATF4 interacts with p52 and together, this complex mediates the activity of a subset of MM-associated enhancers through the recruitment of histone acetyltransferases (HATs), p300 and CBP (CREB-binding protein). We also identified a novel ATF4:p52 regulated target gene BACH1 under the regulation of a proximal super-enhancer, which was found to drive oncogenesis in MM by promoting cell cycle progression and proliferation. Together, our findings provide further mechanistic insights into how aberrant enhancer activation observed in MM tumours could lead to disease progression.
Published in
ATF4:p52 complex activates oncogenic enhancers in multiple myeloma via p300/CBP recruitment to regulate BACH1
Ang DA, Harmston N, Li Y · Cancer letters 2025 · PMID 40250789 · doi:10.1016/j.canlet.2025.217727
This dataset
Open GSE292455 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Multiple myeloma 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 GSE292455_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 PRJNA1238805 and SRA study SRP571882. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40250789) ↗
Study design
11 conditions, mostly in triplicate
KMS11, endogenous, ATF4 ChIP, ×3 MM1144, endogenous, ATF4 ChIP, ×3 KMS11, endogenous, BACH1 ChIP, ×3 KMS11,LentiV2_ATF4g3, H3K27ac ChIP seq, ×3 KMS11,control, H3K27ac ChIP seq, ×3 MM1144,LentiV2_ATF4g3, H3K27ac ChIP seq, ×3 MM1144,LentiV2, H3K27ac ChIP seq, ×3 KMS11,LentiV2_BACH1g4, H3K27ac ChIP seq, ×3 +3 more

Supports a between-group comparison across 31 samples.

How we read this: 11 replicated groups read from 31 sample titles; they account for 31 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
More Multiple myeloma datasets

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