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Linker histone variant H1-10 promotes prostate cancer proliferation [ChIP-seq]

GSE270157 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 22 samples Submitted 2026/05/06 Platform GPL24676Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 22 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
Prostate cancerThis series is part of our curated briefing on it.
Samples
22 samples: 22 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.
Summary (written by the submitters)
While the linker histone H1 is recognized for its role in stabilizing higher-order chromatin structures, the distinct functions of its variants remain underexplored. In this study, we uncover that the H1-10 is markedly overexpressed in prostate cancer and associates with a poor prognosis. H1-10 is mainly localized to the nucleolus, where it facilitates nucleolar assembly through liquid condensation.
Read the full summary ↓
H1-10 amplifies ribosomal RNA (rRNA) transcription by directly associating with RNA polymerase I (Pol I), thereby enhancing Pol I binding affinity for ribosomal DNA (rDNA). This results in expanded production of rRNA and elevated global protein translation. By further investigation, we found that H1-10 boosts the protein translation of transcription factor E2F3, which in turn induces the transcription of cell growth genes by increasing the level of CTD serine 5 phosphorylated RNA polymerase II at gene promoters. Critically, through high-throughput virtual screening, we identified specific small molecules that inhibit H1-10 by targeting its DNA binding domain. On-target validations showed these molecules blocked H1-10-mediated Pol I rDNA occupancy, global protein translation and prostate tumor growth in vitro and in vivo. In summary, our study reveals the critical role of H1-10 in ribosome biogenesis and prostate cancer progression, and pioneers the pharmacological targeting of an H1 variant, highlighting the therapeutic promise of targeting histone variants.
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 GSE270157_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 PRJNA1125357 and SRA study SRP514797. Searching any of these in the dataset finder brings you back here.

Study design
22 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 22 sample titles: 22 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 Prostate cancer 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.