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KLF5 controls subtype-independent highly interactive enhancers in pancreatic cancer to regulate cell survival [ChIP-Seq]

GSE301284 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 46 samples Submitted 2025/07/01 Platform GPL30173
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 46 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
46 samples: 18 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.
Summary (written by the submitters)
Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal cancer with a 5-year survival rate of 13%. Despite recent molecular stratification of tumors into distinct classical and basal-like cell states, most tumors are heterogeneous contain of both subtypes. Therefore, therapeutic approaches targeting one subtype may not be suitable for PDAC therapy.
Read the full summary ↓
Here, we integrated chromatin accessibility (ATAC-seq), genome-wide occupancy (ChIP-seq) for epigenetic status (H3K27ac) and H3K4me3-anchored chromatin topology (HiChIP) to uncover subtype-independent highly interactive enhancers that interact with essential genes in PDAC. Motif analysis revealed these common enhancers were bound by KLF5 with subsequent depletion leading to decreased cell viability via induction of apoptosis. To elucidate the transcriptional and epigenetic mechanisms by which KLF5 functions in PDAC, we employed rapid depletion of KLF5 with dTAG technology and profiled the effects on the open and active chromatin landscape and transcription with nascent RNA and mRNA-seq over time. Enhancer inactivation via KRAB domain Zim3-dCas9 fusion protein confirmed KLF5-bound enhancers regulate target genes, including the anti-apoptotic gene BCL2L1. Multiplex immunofluorescence confirmed co-staining of KLF5 and Bcl-xL in patient samples and overexpression of Bcl-xL rescued the induction of apoptosis after KLF5 depletion. Taken together, this study provides new insights into common mechanisms to target highly heterogeneous PDAC tumors.
This dataset
Open GSE301284 in finder → Find more human 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 GSE301284_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 PRJNA1283515 and SRA study SRP595798. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
18 conditions, mostly in triplicate
ChIPseq_AsPC1_CTCF ×3 ChIPseq_L36pl_CTCF ×3 ChIPseq_L36plClone2_dTAG_0h_H3K27ac ×3 ChIPseq_L36plClone2_dTAG_0h_H3K4me3 ×3 ChIPseq_L36plClone2_dTAG_1h_H3K27ac ×3 ChIPseq_L36plClone2_dTAG_1h_H3K4me3 ×3 ChIPseq_L36plClone2_dTAG_24h_H3K27ac ×3 ChIPseq_L36plClone2_dTAG_24h_H3K4me3 ×3 +10 more

Supports a between-group comparison across 46 samples.

How we read this: 18 replicated groups read from 46 sample titles; they account for 46 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

+ 6 more — browse all 46 samples with per-sample file links →

More Pancreatic cancer datasets

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

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