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Nrf2 orchestrates epigenetic regulation and acts as the master regulator of KLF4 expression and activity during arsenic-induced cell transformation

GSE279482 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2025/11/17 Platform GPL18573
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 14 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
14 samples: 14 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
Nrf2 Drives Epigenetic Reprogramming and Acts as the Master Regulator of KLF4 Expression and Activity in Arsenic-Induced TransformationAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
Summary (written by the submitters)
Emerging evidence suggests that Nrf2 plays a pro-carcinogenic role in various cancers. Our previous study showed that arsenic-induced Nrf2 activation promotes metabolic reprogramming and cancer stem-like cell formation. Here, we identify KLF4, a key pluripotency factor, as a direct transcriptional target of Nrf2 in arsenic-exposed human bronchial epithelial cells.
Read the full summary ↓
ChIP-seq revealed multiple Nrf2 binding peaks at the KLF4 gene locus, co-localizing with the enhancer markers H3K4me1 and H3K27Ac. Nrf2 knockout reduced KLF4 expression and decreased enhancer marker enrichment, alongside a genome-wide reduction in KLF4 binding in arsenic-treated BEAS-2B cells. In BEAS-2B cells with functional Nrf2, arsenic treatment significantly increased KLF4 binding on genes involved in several oncogenic pathways, including STAT3, SOX2, Nrf2, cell growth, Hedgehog, and epithelial-to-mesenchymal transition (EMT). We also found that KLF4 participates in a self-regulating feedback loop in response to arsenic-induced Nrf2 signaling. Co-occupancy of Nrf2 and KLF4 is crucial for establishing active enhancers, suggesting that Nrf2’s oncogenic effects are, at least in part, mediated by Nrf2-dependent self-amplification of KLF4 expression and function. Thus, co-targeting Nrf2 and KLF4 may represent a promising therapeutic strategy for eliminating cancer stem-like cells.
Published in
Nrf2 Drives Epigenetic Reprogramming and Acts as the Master Regulator of KLF4 Expression and Activity in Arsenic-Induced Transformation
Wang Z, Bi Z, Bamrah J et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2025 · PMID 40755294 · doi:10.1002/advs.202500221
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 GSE279482_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 PRJNA1173122 and SRA study SRP538634. Searching any of these in the dataset finder brings you back here.

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

Supports a case/control comparison: 3 samples read as cases, 3 as controls.

How we read this: Read from 14 sample titles: 14 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
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