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Small interfering RNA-mediated silencing of mutant NPM1 suppresses acute myeloid leukemia via reversing KAT7 and p300-mediated histone acetylation [CUT&Tag]

GSE307716 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 52 samples Submitted 2026/06/19 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 52 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
Acute myeloid leukemiaThis series is part of our curated briefing on it.
Samples
52 samples: 26 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.
Summary (written by the submitters)
NPM1 mutation (NPM1c)-driven acute myeloid leukemia (AML) is characterized by the sequestration of nuclear proteins and chromatin hijacking. Current treatment strategies targeting NPM1c AML are often indirect, which might lead to toxicity and resistance. In this study, we developed an allele-specific siRNA that selectively silences NPM1c while preserving the function of wild-type NPM1.
Read the full summary ↓
This approach inhibited proliferation and promoted myeloid differentiation in NPM1-mutated AML cells in vitro. Notably, the systemic delivery of chemically optimized siNPM1c via lipid nanoparticles (LNPs) significantly reduced leukemogenesis, and enhanced the therapeutic efficacy of the menin inhibitor revumenib and overcame its resistance in vivo. Mechanistically, NPM1c recruits KAT7 and p300, driving leukemogenic transcription and establishing a pathogenic acetylome and open chromatin state. KAT7 recruitment is crucial for the retention of this complex on chromatin. Targeting NPM1c with siRNA disrupts this interaction, reverses the oncogenic epigenetic landscape, and suppresses transcription. Our findings demonstrate that silencing NPM1c effectively suppresses AML by dismantling a pathogenic KAT7/p300-dependent acetylome, highlighting the potential of LNP‑delivered siNPM1c as a promising therapeutic strategy, either as a monotherapy or in combination with menin inhibition.
This dataset
Open GSE307716 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Acute myeloid leukemia 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 GSE307716_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 PRJNA1327136 and SRA study SRP619038. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
26 conditions, mostly in duplicate
NPM1c CUT&Tag, OCI-AML3 cells, siControl, Day… ×2 NPM1c CUT&Tag, OCI-AML3 cells, siNPM1c, Day3, ×2 H3K14ac CUT&Tag, OCI-AML3 cells, siControl, D… ×2 H3K14ac CUT&Tag, OCI-AML3 cells, siNPM1c, Day… ×2 H3K27ac CUT&Tag, OCI-AML3 cells, siControl, D… ×2 H3K27ac CUT&Tag, OCI-AML3 cells, siNPM1c, Day… ×2 KAT7 CUT&Tag, OCI-AML3 cells, siControl, Day3, ×2 KAT7 CUT&Tag, OCI-AML3 cells, siNPM1c, Day3, ×2 +18 more

Supports a between-group comparison across 52 samples.

How we read this: 26 replicated groups read from 52 sample titles; they account for 52 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

+ 12 more — browse all 52 samples with per-sample file links →

More Acute myeloid leukemia datasets

Search all human ChIP / ATAC / CUT&Tag datasets in GEO →

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