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ZNF274 constrains lineage plasticity and drives intrinsic resistance to CDK7 inhibitors in pancreatic cancer

GSE285406 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 48 samples Submitted 2026/03/31 Platform GPL34284Platform GPL30173
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 48 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
Pancreatic cancerThis series is part of our curated briefing on it.
Samples
48 samples: 16 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
ZNF274 constrains lineage plasticity and drives intrinsic resistance to CDK7 inhibitors in pancreatic cancerNature communications · 2026
Summary (written by the submitters)
Pancreatic Ductal Adenocarcinoma (PDAC) is characterized by two distinct transcriptional subtypes: classical and basal, which may interconvert. We show the KRAB-ZNF protein, ZNF274, correlates with PDAC subtype and regulates sensitivity to CDK7 inhibition by facilitating heterochromatin maintenance and gene suppression. We find ZNF274 loss drives a classical to basal transition, induces invasive protrusions and facilitates invasion capacity.
Read the full summary ↓
We define two mechanistic arms to this regulation. ZNF274 directly suppresses ZEB1 expression. When ZNF274 is lost, ZEB1 facilitates acquisition of mesenchymal features, keratin gene expression, and susceptibility to CDK7 inhibition. Second, ZNF274 dampens expression of repetitive elements including human endogenous retroviruses (HERVs). HERV expression following ZNF274 loss induces a double stranded RNA response that reinforces the classical to basal subtype transition. Here, we show ZNF274 is an important epigenetic regulator of cellular plasticity and sensitivity to CDK7 inhibition, presenting a therapeutic liability of PDAC subtype transition that is actionable in the clinic.
Published in
ZNF274 constrains lineage plasticity and drives intrinsic resistance to CDK7 inhibitors in pancreatic cancer
Gianopulos JE, Schutter A, Dobersch S et al. · Nature communications 2026 · PMID 42177198 · doi:10.1038/s41467-026-73380-x
This dataset
Open GSE285406 in finder → Find more human RNA-seq datasets → Pancreatic cancer 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 GSE285406_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 PRJNA1203584 and SRA study SRP554058. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42177198) ↗
Study design
16 conditions, mostly in triplicate
ASPC1 AZA 5uM ×3 ASPC1 siCTRL ×3 ASPC1 DMSO ×3 ASPC1 siZNF274 ×3 CFPAC1 AZA 5uM ×3 CFPAC1 siCTRL ×3 CFPAC1 DMSO ×3 Panc3.27 CTRL ×3 +9 more

Supports a between-group comparison across 47 samples.

How we read this: 16 replicated groups read from 48 sample titles; they account for 47 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

+ 8 more — browse all 48 samples with per-sample file links →

More Pancreatic 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.