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H3K27ac and H3K27me3 ChIP-seq analysis for MDA-MB-468 cells treated with SAHA and sonidedgib

GSE189215 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 30 samples Submitted 2024/10/18 Platform GPL20795
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 30 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
Breast cancerThis series is part of our curated briefing on it.
Samples
30 samples: 10 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)
Epigenetic therapies that cause genome-wide epigenetic alterations, could trigger local interplay between different histone marks, leading to a switch of transcriptional outcome and cellular phenotypes. In human cancers with diverse oncogenic activation, how oncogenic pathways cooperate with epigenetic modifiers to regulate the histone mark interplay is poorly understood.
Read the full summary ↓
We herein discover that the hedgehog (Hh) pathway reprograms the histone methylation landscape in triple-negative breast cancer (TNBC), which facilitates histone acetylation caused by histone deacetylase (HDAC) inhibitors and gives rise to new therapeutic vulnerability of combination therapies. Specifically, overexpression of zinc finger protein of the cerebellum 1 (ZIC1) in TNBC promotes Hh activation, facilitating the switch of H3K27 methylation (H3K27me) to acetylation (H3K27ac). The mutually exclusive relationship of H3K27me and H3Kac allows their functional interplay at oncogenic gene locus and switches therapeutic outcomes. Using multiple in vivo TNBC models including patient-derived xenograft, we show that Hh signaling-orchestrated H3K27me and H3Kac interplay tailors combination epigenetic drugs in treating TNBC.
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 GSE189215_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 PRJNA781990 and SRA study SRP346954. Searching any of these in the dataset finder brings you back here.

Study design
10 conditions, mostly in triplicate
H3K27ac_con ×3 H3K27me3_con ×3 Input_of_H3K27ac_con ×3 Input_of_H3K27me3_con ×3 H3K27me3_sonidedgib ×3 Input_of_H3K27me3_sonidedgib ×3 H3K27ac_SAHA+sonidedgib ×3 Input_of_H3K27ac_SAHA+sonidedgib ×3 +2 more

Supports a between-group comparison across 30 samples.

How we read this: 10 replicated groups read from 30 sample titles; they account for 30 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
More Breast cancer 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.