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Targeting Mediator MED23 inhibits HCC development by inhibiting compensatory proliferation and promoting ROS-mediated cell death [ChIP-seq]

GSE295432 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2025/08/17 Platform GPL20795
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 12 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
12 samples: 12 samples, each with a distinct title — no replicated groupsGroups 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
Targeting MED23 inhibits hepatocellular carcinoma development by suppressing compensatory proliferation and facilitating ROS-mediated cell deathCell death & disease · 2025
Summary (written by the submitters)
Hepatocellular carcinoma (HCC) is frequently linked to compensatory proliferating hepatocytes in damaged livers, yet the underlying molecular mechanisms remain elusive. The Mediator complex precisely coordinates multiple transcription factors and cofactors to regulate diverse physiological and pathological processes. Here we discovered that Mediator subunit MED23 is involved in the progression of HCC.
Read the full summary ↓
Both constitutive and inducible liver-specific ablation of Med23 effectively inhibited HCC development in diethylnitrosamine (DEN)-induced HCC mouse models. Mechanistically, MED23 deficiency significantly compromised hepatocyte cell viability by reducing the stability of the NQO1 protein, thereby leading to an increase in reactive oxygen species (ROS) production. Furthermore, MED23 collaborates with the transcription factor RFX5 to regulate a novel enhancer function for IGF2 expression, which thus influences hepatocyte viability and HCC development. Consistently, overexpression of IGF2 in MED23-deficient HCC cells stabilizes NQO1 and partially restored cell growth and reduced apoptosis. Collectively, our findings underscore the significance of the MED23-IGF2-NQO1 axis in HCC progression and propose a novel therapeutic strategy for the treatment of HCC.
Published in
Targeting MED23 inhibits hepatocellular carcinoma development by suppressing compensatory proliferation and facilitating ROS-mediated cell death
Zhao X, Wang Z, Min L et al. · Cell death & disease 2025 · PMID 41436431 · doi:10.1038/s41419-025-08348-8
This dataset
Open GSE295432 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 GSE295432_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 PRJNA1254672 and SRA study SRP580777. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41436431) ↗
Study design
12 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 12 sample titles: 12 distinct titles with little repetition. 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 Hepatocellular carcinoma datasets

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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.