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The Lysine Demethylase Kdm4C is an Oncogenic Driver and Regulates ERK Activity in KRAS Mutant Pancreatic Ductal Adenocarcinoma [ChIP-seq]

GSE300199 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2025/12/16 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 14 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
14 samples: 3 × AsPC1, KDM4C WT, H3K27Ac, vs 3 × AsPC1, KDM4C WT, H3K36me3, vs 3 × AsPC1, KDM4C KO1, H3K27Ac, vs 3 × AsPC1, KDM4C KO1, H3K36me3,Groups 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
The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal AdenocarcinomaCancer research communications · 2026
Summary (written by the submitters)
Deregulation of proteins involved in chromatin regulation is common in pancreatic ductal adenocarcinoma (PDAC). Lysine demethylase 4C (Kdm4C) is one of the chromatin-modifying proteins frequently overexpressed across multiple solid cancers and is linked to chromatin instability, increased cell proliferation, and enhanced stem cell-like behavior.
Read the full summary ↓
We observed upregulation of Kdm4C protein in a panel of human PDAC cell lines and patient samples compared to non-neoplastic controls. CRISPR/Cas9-mediated deletion of KDM4C in human and murine PDAC cells reduced proliferation, clonogenicity and increased survival of orthotopically implanted murine PDAC allografts. Transcriptomic and proteomics analyses revealed that loss of Kdm4C in both human and murine PDAC cell lines was associated with reduction of activated phospho-Erk, a pivotal effector downstream of mutant Ras. Using proximity labeling, we identified the histone deacetylase SIRT1 as a novel interacting protein with Kdm4C via the latter’s Tudor reader domain. SIRT1-mediated deacetylation leads to repression of downstream targets, including the dual specificity phosphatase DUSP2, which is known to inactivate Erk via dephosphorylation. In vitro propagation of KDM4C-null PDAC lines eventually led to adaptation and restitution of Erk signaling via compensatory upregulation of other KDM4 family members. To bypass this genetic compensation, we tested a preclinical pan-KDM4 inhibitor TACH107 and confirmed its efficacy in in vitro and in vivo PDAC models including those resistant to the covalent KRASG12D inhibitor MTRX1133. Our studies identify Kdm4C as an oncogenic molecule that sustains Erk signaling in KRAS-mutant PDAC and can be broadly targeted via small molecule inhibitors.
Published in
The Lysine Demethylase KDM4C Is an Oncogenic Driver and Regulates ERK Activity in KRAS-Mutant Pancreatic Ductal Adenocarcinoma
Shaheen MT, Dhebat S, Rajapakshe KI et al. · Cancer research communications 2026 · PMID 41490602 · doi:10.1158/2767-9764.CRC-25-0278
This dataset
Open GSE300199 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 GSE300199_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 PRJNA1279223 and SRA study SRP593001. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41490602) ↗
Study design
3 × AsPC1, KDM4C WT, H3K27Ac, vs 3 × AsPC1, KDM4C WT, H3K36me3, vs 3 × AsPC1, KDM4C KO1, H3K27Ac, vs 3 × AsPC1, KDM4C KO1, H3K36me3,

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 14 sample titles; they account for 12 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
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.