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Spatiotemporal control of SMARCA5 by a MAPK-RUNX1 axis distinguishes mutant KRAS-driven pancreatic malignancy from tissue regeneration (ATAC-Seq)

GSE248942 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 123 samples Submitted 2025/07/01 Platform GPL28330Platform GPL24247Platform GPL29480
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 123 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
123 samples: 45 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)
De-differentiation or trans-differentiation is a common response to injury in many tissues, and the processes predispose cells to cancer. Acute pancreatitis-induced acinar-to-ductal metaplasia (ADM) is similar to pancreatic ductal adenocarcinoma (PDAC) at both the chromatin level and gene expression level. Mutant KRAS induces chromatin remodeling activities required for both regeneration and tumorigenesis at the peak of ADM, and it blocks regeneration.
Read the full summary ↓
We show that chromatin remodeler SMARCA5 (SNF2H) can promotes the regeneration defects caused by mutant KRAS by maintaining chromatin accessibility at regions specifically required for malignancy. Mechanistically, regeneration-related chromatin remodeling activities are shared between wild-type and mutant KRAS and they occur very early upon pancreatitis, while the malignancy-related chromatin regions become accessible much later. The activity of SMARCA5 is controlled spatiotemporally by transcription factor RUNX1, which is only accumulated at sufficient levels at late ADM lock-in stage. Finally, we show that the malignancy regulation activity of SMARCA5 is different from its general function in CTCF recruitment. In summary, we have identified a specific function of a general chromatin remodeler that is precisely controlled during acinar cell trans-differentiation to separate malignancy from tissue regeneration.
This dataset
Open GSE248942 in finder → Find more ChIP / ATAC / CUT&Tag 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 GSE248942_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 PRJNA1046488 and SRA study SRP475027. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
45 conditions, mostly in duplicate
ATAC_KCa_24h_Rosa ×5 ATAC_KCa_D2_Rosa ×5 ATAC_KCa_D2_Smarca5 ×5 ATAC_KCa_24h_Smarca5 ×4 ATAC_KCa_D7_Rosa ×4 ATAC_KCa_D7_Smarca5 ×4 ATAC_KCa_tumor_Rosa ×4 ATAC_Ca_8h_Rosa ×3 +47 more

Supports a case/control comparison: 7 samples read as cases, 10 as controls.

How we read this: 45 replicated groups read from 123 sample titles; they account for 113 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

+ 83 more — browse all 123 samples with per-sample file links →

More Pancreatic cancer datasets

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

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