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The lineage master transcription factor, p63 recruits a cancer-specific cofactor, FOXK1 to mediate oncogenic 3D chromatin dynamics in squamous cell carcinoma[ATAC-seq]

GSE274411 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2026/07/13 Platform GPL20301Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 16 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)
Samples
16 samples: 8 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)
Transcriptional dysregulation by a lineage master transcription factor (TF) is a critical mechanism in cancer, involving alteration of three-dimensional (3D) chromatin architecture. However, the underlying mechanisms of altered master TF-dependent chromatin interactions in cancer cells remain unclear. Here, we employ multi-omic approaches to examine chromatin interactions dependent on p63, a master TF in epidermis, in squamous cell carcinomas (SCCs) compared to normal keratinocytes (KCs), integrating chromatin looping and accessibility, transcriptome, p63 binding and proteomics.
Read the full summary ↓
p63 facilitates higher connectivity between the promoters of prognostic genes in SCCs, and distal enhancers. Many SCC-specific p63-dependent genes are connected to SCC-specific p63-dependent epigenetic signature via a cis-regulatory element (CRE) without the signature, referred to as ‘Secondary’ regulation mode. Notably, we identify FOXK1 as a cancer-specific cofactor, cooperating with p63 to shape the oncogenic chromatin landscape, inhibiting cell proliferation. Our findings suggest the p63-FOXK1 axis as a potential target for cancer therapy in SCCs.
This dataset
Open GSE274411 in finder → Find more human ChIP / ATAC / CUT&Tag datasets →
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 GSE274411_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 PRJNA1146374 and SRA study SRP525366. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
8 conditions, mostly in duplicate
CAL27,control siRNA, ×2 CAL27,p63 siRNA, ×2 SCC13,control siRNA, ×2 SCC13,p63 siRNA, ×2 Undifferentiated KC,control siRNA, ×2 Undifferentiated KC,p63 siRNA, ×2 Differentiated KC,control siRNA, ×2 Differentiated KC,p63 siRNA, ×2

Supports a between-group comparison across 16 samples.

How we read this: 8 replicated groups read from 16 sample titles; they account for 16 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
Datasets on a similar topic

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