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ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer (ChIP-Seq)

GSE259248 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 36 samples Submitted 2024/10/14 Platform GPL24676
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)
Samples
36 samples: 17 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.
Paper
ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancerCell reports · 2024
Summary (written by the submitters)
We previously identified KDM5B, encoding a histone H3 lysine 4 (H3K4) demethylase, as an oncogene in estrogen receptor positive (ER+) breast cancer driving endocrine resistance. Here we describe that KDM5A is frequently amplified and overexpressed in basal breast tumors and is associated with chemotherapy resistance. Using CRISPR knockout viability screens -/+ KDM5 inhibition (KDM5i), we found that deletion of the transcription factor ZBTB7A and core SAGA complex increased sensitivity to KDM5i, whereas knockout of RHO-GTPases led to resistance.
Read the full summary ↓
Integrated ChIP-seq and RNA-seq analyses revealed colocalization of ZBTB7A and KDM5s at promoters with high H3K4me3 signal and dependence of KDM5A binding on ZBTB7A. ZBTB7A knockout had a pleiotropic effect on transcriptional responses to KDM5i, in which it modulates the KDM5i-induced innate immune signaling and NF-kB-regulated genes. ZBTB7A knockout and KDM5i cooperate to alter cell states with KDM5i decreasing basal-like and ZBTB7A knockout inducing mesenchymal-like gene expression patterns. Our work furthers our understanding of KDM5-mediated gene regulation in breast cancer and identifies key pathways that mediate sensitivity to KDM5 inhibition
Published in
ZBTB7A is a modulator of KDM5-driven transcriptional networks in basal breast cancer
DiCiaccio B, Seehawer M, Li Z et al. · Cell reports 2024 · PMID 39570746 · doi:10.1016/j.celrep.2024.114991
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 GSE259248_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 PRJNA1080532 and SRA study SRP491748. Searching any of these in the dataset finder brings you back here.

Study design
17 conditions, mostly in duplicate
SUM149, ROSA26KO, DMSO, KDM5A_IP, ×2 SUM149, ROSA26KO, DMSO, KDM5B_IP, ×2 SUM149, ROSA26KO, DMSO, H3K4me3_IP, ×2 SUM149, ROSA26KO, DMSO, ZBTB7A _IP, ×2 SUM149, ROSA26KO, 10 µM C70, KDM5A_IP, ×2 SUM149, ROSA26KO, 10 µM C70, KDM5B_IP, ×2 SUM149, ROSA26KO, 10 µM C70, H3K4me3_IP, ×2 SUM149, ROSA26KO, 10 µM C70, ZBTB7A _IP, ×2 +11 more

Supports a between-group comparison across 34 samples.

How we read this: 17 replicated groups read from 36 sample titles; they account for 34 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
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