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Menin-MLL complex cooperates with NF-Y to promote HCC survival [CUT&RUN]

GSE293692 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 72 samples Submitted 2025/04/07 Platform GPL34281Platform GPL30882
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 72 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
Hepatocellular carcinomaThis series is part of our curated briefing on it.
Samples
72 samples: 16 conditions, mostly with about 4 replicates eachGroups 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
Menin-MLL1 complex cooperates with NF-Y to promote hepatocellular carcinoma survivalCell reports · 2025
Summary (written by the submitters)
Identification of new therapeutic targets in hepatocellular carcinoma (HCC) remains critical. Chromatin regulating complexes are frequently mutated or aberrantly expressed in HCC, suggesting dysregulation of chromatin environments is a key feature driving liver cancer. To investigate whether the altered chromatin state in HCC cells could be targeted, we designed and utilized an epigenome-focused CRISPR library that targets all genes involved in chromatin regulation.
Read the full summary ↓
This focused approach allowed us to test multiple cell lines in both 2D and 3D growth conditions, which revealed striking differences in the essentiality of genes involved in ubiquitination and uncovered multiple chromatin regulators vital for HCC cell survival in 2D but whose loss promoted growth in 3D. We found the core subunits of the menin-MLL1 complex among the strongest essential genes for HCC survival in all screens and thoroughly characterized the mechanism through which menin-MLL1 complex promote HCC cell growth. Inhibition of the menin-MLL1 interaction led to global changes in occupancy of the complex and concomitant decreases in H3K4me3 and gene expression. We observed that increased chromatin accessibility at sites not bound by menin-MLL1 was associated with the recruitment of the pioneer transcription factor complex NF-Y. A CRISPR/Cas9 screen of chromatin regulators in the presence of the menin-MLL1 inhibitor SNDX-5613 revealed a synergistic effect on cell death when combining NF-YB loss and menin-MLL1 interaction inhibition. Together, these data show that menin-MLL1 is necessary for HCC cell survival and cooperates with NF-Y to regulate oncogenic gene transcription.
Published in
Menin-MLL1 complex cooperates with NF-Y to promote hepatocellular carcinoma survival
Dzama-Karels M, Sokolowski M, Kuhlers P et al. · Cell reports 2025 · PMID 41296561 · doi:10.1016/j.celrep.2025.116619
This dataset
Open GSE293692 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Hepatocellular carcinoma 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 GSE293692_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 PRJNA1245698 and SRA study SRP576214. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41296561) ↗
Study design
16 conditions, mostly with about 4 replicates each
HLF treated with DMSO IP for IgG ×10 HLF treated with SNDX IP for IgG ×9 HLF treated with SNDX IP for H3K4me3 ×8 HLF treated with DMSO IP for H3K4me3 ×7 HLF treated with DMSO IP for H3K27me3 ×4 HLF treated with SNDX IP for H3K27me3 ×4 HLF treated with DMSO IP for TEAD4 ×4 HLF treated with SNDX IP for TEAD4 ×4 +10 more

Supports a between-group comparison across 70 samples.

How we read this: 16 replicated groups read from 72 sample titles; they account for 70 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

+ 32 more — browse all 72 samples with per-sample file links →

More Hepatocellular carcinoma datasets

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

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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.