GEO series

FOXA2/AP-1 drives prostate cancer lineage plasticity [ChIP-seq]

GSE232552 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 24 samples Submitted 2024/04/22 Platform GPL30173Platform GPL18573Platform GPL30172

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 24 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: 24 samples: 24 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.
Paper: FOXA2 rewires AP-1 for transcriptional reprogramming and lineage plasticity in prostate cancerNature communications · 2024

Summary (written by the submitters)

FOXA (Forkhead Box Protein A) family proteins function as pioneer transcription factors by loosening the compact chromatin structure and facilitating access for other transcription factors. The role of FOXA1 has been intensively studied in normal prostate epithelial cells and the adenocarcinoma subtype of prostate cancer (PCa) where it acts as a critical pioneer factor for the chromatin binding of androgen receptor (AR).

Read the full summary ↓

Recent studies have indicated the emergence of FOXA2 as an adaptive response to AR signaling inhibition, particularly in prostate tumors that have undergone lineage reprogramming to a neuroendocrine PCa subtype. However, the molecular basis for this transition from FOXA1 to FOXA2 and its role in regulating the development of PCa lineage plasticity remains unclear. In this study, we show that FOXA2 binds to distinct chromatin regions in multiple AR-null PCa models with different molecular subtypes and that its binding is dependent on an epigenetic factor, LSD1. More importantly, we demonstrate that FOXA2 can function as a major pioneer factor of JUN and govern the chromatin binding of AP-1 complex in PCa exhibiting lineage plasticity. Mechanistically, differential reprogramming of JUN activates lineage-specific super-enhancers that may promote PCa progression by enhancing cell state transitions to multiple lineages. Overall, our study reveals a pivotal function of the LSD1-FOXA2 axis in rewiring AP-1 to induce differential transcriptional reprogramming required for PCa lineage plasticity.

Published in

FOXA2 rewires AP-1 for transcriptional reprogramming and lineage plasticity in prostate cancer

Wang Z, Townley SL, Zhang S et al. · Nature communications 2024 · PMID 38851846 · doi:10.1038/s41467-024-49234-9

This dataset

Open GSE232552 in finder → Find more 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 GSE232552_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 PRJNA972717 and SRA study SRP437782. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38851846) ↗

Study design

24 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 24 sample titles: 24 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

GSM7350172 NCI-H660 cells, ORY-1001, ChIP-FOXA2
GSM7350173 NCI-H660 cells, vehicle, ChIP-FOXA2
GSM7350174 NCI-H660 cells, siFOXA2, ChIP-JUN
GSM7350175 NCI-H660 cells, siNC, ChIP-JUN
GSM7350176 NCI-H660 cells, vehicle, ChIP-H3K4me2
GSM7350177 NCI-H660 cells, vehicle, ATAC
GSM7350178 LNCaP_FOXA2OE cells, vehicle, ChIP-FOXA2
GSM7350179 LNCaP_FOXA2OE cells, vehicle, ChIP-JUN
GSM7350180 LNCaP cells, siFOXA1, ChIP-JUN
GSM7350181 LNCaP cells, siNC, ChIP-JUN
GSM7350182 PC3 cells, C12, ChIP-FOXA2
GSM7350183 PC3 cells, ORY-1001, ChIP-FOXA2
GSM7350184 PC3 cells, vehicle, ChIP-FOXA2
GSM7350185 PC3 cells, siFOXA2, ChIP-FOSL1
GSM7350186 PC3 cells, siFOXA2, ChIP-JUN
GSM7350187 PC3 cells, siNC, ChIP-FOSL1
GSM7350188 PC3 cells, siNC, ChIP-JUN
GSM7350189 PC3 cells, vehicle, ChIP-H3K27AC
GSM7350190 PC3 cells, vehicle, ATAC
GSM8015521 LNCaP_FOXA2K265R cells, vehicle, ChIP-JUN
GSM8015522 PC3 cells, vehicle,ChIP-FOXA2
GSM8015523 PC3 cells,vehicle, ChIP-FOXA2
GSM8080192 DKO cells, vehicle,ChIP-FOXA2
GSM8080193 DKO cells, ORY-1001, ChIP-FOXA2

Datasets on a similar topic

GSE232555 FOXA2/AP-1 drives prostate cancer lineage plasticity 101 samples shares foxa2, ap-1, plasticity, prostate, lineage, drives
GSE289247 Crosstalk between the polycomb repressive complex 2 and DNA methylation mediates neuroendocrine prostate cancer lineage plasticity [ChIP-Seq] 35 samples shares plasticity, prostate, chip-seq, lineage
GSE270547 Mutant CEBPA promotes tolerance to inflammatory stress through deficient AP-1 activation [ChIP-seq] 40 samples shares ap-1, chip-seq
GSE267775 KMT2C Deficiency Drives Luminal Transdifferentiation into Double-Negative Prostate Cancer and Sensitizes to Fatty Acid Synthase Inhibition [CUT&Tag] 26 samples shares prostate, drives
GSE282726 FOXA1 loss drives basal/squamous de-differentiation of prostate cancer and induces an immunosuppressive tumor microenvironment 25 samples shares prostate, drives
GSE198204 Endothelial plasticity in atrial fibrosis by integrating single-cell sequencing and genetic lineage tracing 8 samples shares plasticity, lineage
GSE237016 APOBEC3 promotes squamous differentiation and metastases via IL1A/AP-1 signaling 9 samples shares ap-1
GSE8126 Genomic profiling of microRNA and messenger RNA reveals deregulated microRNA expression in prostate cancer. 76 samples shares prostate

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

Share this dataset

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.