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Regulation of melanoma cellular plasticity by the Mediator complex drives therapeutic resistance [ChIP-Seq]

GSE316620 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 54 samples Submitted 2026/04/29 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 54 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
54 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)
Melanoma exhibits profound cellular plasticity that enables adaptive responses to therapeutic pressure and ultimately drives treatment resistance. However, the transcriptional mechanisms governing melanoma cell-state transitions remain incompletely understood. Here, we identify the Mediator complex as a central regulator of melanoma cellular plasticity that promotes resistance to targeted therapy.
Read the full summary ↓
Using genetic and pharmacological perturbations, we show that disruption of Mediator function induces melanoma cell-state switching, promotes dedifferentiation programs, characterized by loss of lineage-specific transcriptional programs and activation of survival-associated gene expression, and enhances resistance to MAPK pathway inhibition. Mechanistically, Mediator tail depletion rewires transcriptional networks governing cell identity and adaptive signaling, enabling melanoma cells to bypass MAPK pathway blockade. Collectively, our findings identify the Mediator tail module as a key transcriptional safeguard against melanoma dedifferentiation and reveal its unexpected role in suppressing cellular plasticity–driven resistance to targeted therapy.
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 GSE316620_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 PRJNA1403485 and SRA study SRP662796. Searching any of these in the dataset finder brings you back here.

Study design
18 conditions, mostly in triplicate
A375_GFP_DMSO_H3K27ac ×3 A375_GFP_Vemu_H3K27ac ×3 A375_MED12sg_DMSO_H3K27ac ×3 A375_MED12sg_Vemu_H3K27ac ×3 A375_MED19sg_DMSO_H3K27ac ×3 A375_MED19sg_Vemu_H3K27ac ×3 A375_MED23sg_DMSO_H3K27ac ×3 A375_MED23sg_Vemu_H3K27ac ×3 +11 more

Supports a between-group comparison across 53 samples.

How we read this: 18 replicated groups read from 54 sample titles; they account for 53 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

+ 14 more — browse all 54 samples with per-sample file links →

More Melanoma datasets

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

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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.