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Transcriptional reprogramming by AP-1-bound cis-regulatory elements drives melanoma development

GSE326324 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 36 samples Submitted 2026/07/21 Platform GPL30173
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 36 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
MelanomaThis series is part of our curated briefing on it.
Samples
36 samples: 36 samples, each with a distinct title — no replicated groupsGroups 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)
Malignant melanoma is characterized by high metastatic potential and cellular plasticity. Its progression is driven not only by genetic alterations but also by epigenetic repro-gramming and changes in the transcriptome, mediated by transcription factors. The AP-1 family favors an invasive cell state by facilitating processes such as angiogenesis and migration.
Read the full summary ↓
However, the AP-1-driven regulatory landscape and its implications for melanoma plasticity remain poorly understood. Here, we further elucidate the role of the AP-1 members c-Jun and Fra-1 in enhancer-driven gene regulation during melanoma development. Integrative ChIP-seq and RNA-seq analyses revealed extensive enhancer reprogramming during tumor formation and significant upregulation of genes annotated to enhancers gained in melanoma cells. On average, half of these regions are directly bound by c-Jun/Fra-1, given a high AP-1 motif rate (~80%) and chromatin accessibility. Enhancer-regulated c-Jun/Fra-1 targets are functionally linked to an invasive phenotype and comprise well-known melanoma drivers involved in migration and EMT. Clinically, high c-Jun/Fra-1 and target gene expression correlate with poor survival in BRAF wild-type and NRAS mutant melanoma patients, highlighting c-Jun/Fra-1 as a potential biomarker and therapeutic target. Overall, our data identify c-Jun/Fra-1 as major drivers of melanoma development through enhancer-mediated transcriptional programs.
This dataset
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.

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 GSE326324_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1445106 and SRA study SRP687699. Searching any of these in the dataset finder brings you back here.

Study design
36 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 36 sample titles: 36 distinct titles with little repetition. 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 Melanoma 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.