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Analysis of chromatin accessibility changes by ATAC-seq to determine how sustained exposure to physiologically relevant Tryptophan metabolites in HNSCC cells remodels chromatin.

GSE334545 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/06/09 Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 12 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
Head and neck cancerThis series is part of our curated briefing on it.
Samples
12 samples: 3 × OSC19 cells (oral quaous cell carcinoma cells), treated with vehicle, vs 3 × OSC19 cells (oral quaous cell carcinoma cells), treated with TCDD, vs 3 × OSC19 cells (oral quaous cell carcinoma cells), treated with Tryp metabolites, vs 3 × OSC19 cells (oral quaous cell carcinoma cells), treated with Tryp metabolites and CH223191,Groups 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)
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor implicated in inflammation, immune modulation, and tumor progression. While environmental AHR ligands have been extensively studied, the impact of sustained exposure to physiologically relevant endogenous AHR agonists on tumor-intrinsic behavior remains poorly defined.
Read the full summary ↓
Circulating tryptophan (Tryp) metabolites—including kynurenine and indole derivatives—are continuously present in human serum and collectively contribute to basal AHR activity. This study is designed to determine if prolonged exposure to these metabolites promotes aggressive tumor phenotypes in head and neck squamous cell carcinoma (HNSCC). Using a defined mixture of six serum-derived Tryp metabolites and a custom dish-in-dish culture system to model sustained exposure, we demonstrate persistent AHR activation in HN30 and OSC19 cells, evidenced by induction of canonical target genes and nuclear translocation of AHR. Transcriptomic profiling revealed upregulation of inflammatory and tumor-associated gene programs, including CSF3, MMP1, and AP-1–associated targets. ATAC-seq analysis in OSC19 cells showed ligand-dependent chromatin remodeling and enrichment of inflammatory transcription factor motifs, supporting epigenetic reprogramming under prolonged AHR signaling.
This dataset
Open GSE334545 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Head and neck cancer landscape →
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 GSE334545_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 PRJNA1475429 and SRA study SRP707209. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
3 × OSC19 cells (oral quaous cell carcinoma cells), treated with vehicle, vs 3 × OSC19 cells (oral quaous cell carcinoma cells), treated with TCDD, vs 3 × OSC19 cells (oral quaous cell carcinoma cells), treated with Tryp metabolites, vs 3 × OSC19 cells (oral quaous cell carcinoma cells), treated with Tryp metabolites and CH223191,

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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 Head and neck cancer datasets

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