GEO series

AP-1 Mediates Oncogenic Transcription and Predicts Fatality in Lung Squamous Cell Carcinoma Patients [ChIP-seq]

GSE267597 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 36 samples Submitted 2026/05/15 Platform GPL21290

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)
Topic: Lung cancerThis series is part of our curated briefing on it.
Samples: 36 samples: 18 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: AP-1 promotes oncogenic transcription in lung cancer cells by bridging promoter-enhancer interactionsCancer gene therapy · 2026

Summary (written by the submitters)

Despite the growing volume of genomic data, there remains a gap in our understanding of the mechanisms driving oncogenic transcription during non-small cell lung cancer (NSCLC) progression. In this study, we employed a model cell line-guided, multi-omic approach including promoter-capture Hi-C, ATAC-Seq, transcriptomics, and epigenomics, to uncover the epigenomic and three-dimensional (3D) genomic alterations on oncogenes in NSCLC patients from the Cancer Genome Atlas (TCGA).

Read the full summary ↓

Our model cell lines recapitulate key aspects of the transcriptomic and chromatin-accessibility changes observed in NSCLC patients. ChIP-Seq analysis in model cell lines, revealed increased activity at promoters and enhancers, but decreased activity at insulators in NSCLC patients. We identified several increased promoter-enhancer interaction events in upregulated oncogenes. These aberrant enhancer-promoter looping events were mediated by the transcription factor AP-1. Survival analysis revealed a significant correlation between AP-1 expression levels and mortality in lung squamous carcinoma patients, but not in lung adenocarcinoma patients. Inhibition of AP-1, using AP-1 or JNK inhibitors, suggests that the abnormal activity of AP-1 is modulated by JNK kinases within the MAPK pathway, which promotes oncogenic transcription in NSCLC. These findings highlight the role of AP-1 in promoting lung squamous cell carcinoma progression and suggest that AP-1 and JNK inhibitors could be useful in treating high AP-1 lung squamous cell cancers.

Published in

AP-1 promotes oncogenic transcription in lung cancer cells by bridging promoter-enhancer interactions

Tan X, Kroneberg M, Sun F et al. · Cancer gene therapy 2026 · PMID 41339492 · doi:10.1038/s41417-025-00974-w

This dataset

Open GSE267597 in finder → Find more human ChIP / ATAC / CUT&Tag datasets → Lung 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 GSE267597_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 PRJNA1111911 and SRA study SRP507995. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41339492) ↗

Study design

18 conditions, mostly in duplicate

A549, pol II, ChIP, ×2 A549, H3K4me3, ChIP, ×2 A549, Med1, ChIP, ×2 A549, H3K27ac, ChIP, ×2 A549, JunB, ChIP, ×2 A549, Jun, ChIP, ×2 A549, JunD, ChIP, ×2 A549, Input, ×2 +10 more

Supports a between-group comparison across 36 samples.

How we read this: 18 replicated groups read from 36 sample titles; they account for 36 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

GSM8269961 A549, pol II, ChIP, rep1 A549, pol II, ChIP,
GSM8269962 A549, H3K4me3, ChIP, rep1 A549, H3K4me3, ChIP,
GSM8269963 A549, Med1, ChIP, rep1 A549, Med1, ChIP,
GSM8269964 A549, H3K27ac, ChIP, rep1 A549, H3K27ac, ChIP,
GSM8269965 A549, JunB, ChIP, rep1 A549, JunB, ChIP,
GSM8269966 A549, Jun, ChIP, rep1 A549, Jun, ChIP,
GSM8269967 A549, JunD, ChIP, rep1 A549, JunD, ChIP,
GSM8269968 A549, Input, rep1 A549, Input,
GSM8269969 B2B, pol II, ChIP, rep1 B2B, pol II, ChIP,
GSM8269970 B2B, H3K4me3, ChIP, rep1 B2B, H3K4me3, ChIP,
GSM8269971 B2B, Med1, ChIP, rep1 B2B, Med1, ChIP,
GSM8269972 B2B, H3K27ac, ChIP, rep1 B2B, H3K27ac, ChIP,
GSM8269973 B2B, Rad21, ChIP, rep1 B2B, Rad21, ChIP,
GSM8269974 B2B, CTCF, ChIP, rep1 B2B, CTCF, ChIP,
GSM8269975 B2B, JunB, ChIP, rep1 B2B, JunB, ChIP,
GSM8269976 B2B, Jun, ChIP, rep1 B2B, Jun, ChIP,
GSM8269977 B2B, JunD, ChIP, rep1 B2B, JunD, ChIP,
GSM8269978 B2B, Input, rep1 B2B, Input,
GSM8269979 A549, pol II, ChIP, rep2 A549, pol II, ChIP,
GSM8269980 A549, H3K4me3, ChIP, rep2 A549, H3K4me3, ChIP,
GSM8269981 A549, Med1, ChIP, rep2 A549, Med1, ChIP,
GSM8269982 A549, H3K27ac, ChIP, rep2 A549, H3K27ac, ChIP,
GSM8269983 A549, JunB, ChIP, rep2 A549, JunB, ChIP,
GSM8269984 A549, Jun, ChIP, rep2 A549, Jun, ChIP,
GSM8269985 A549, JunD, ChIP, rep2 A549, JunD, ChIP,
GSM8269986 A549, Input, rep2 A549, Input,
GSM8269987 B2B, pol II, ChIP, rep2 B2B, pol II, ChIP,
GSM8269988 B2B, H3K4me3, ChIP, rep2 B2B, H3K4me3, ChIP,
GSM8269989 B2B, Med1, ChIP, rep2 B2B, Med1, ChIP,
GSM8269990 B2B, H3K27ac, ChIP, rep2 B2B, H3K27ac, ChIP,
GSM8269991 B2B, Rad21, ChIP, rep2 B2B, Rad21, ChIP,
GSM8269992 B2B, CTCF, ChIP, rep2 B2B, CTCF, ChIP,
GSM8269993 B2B, JunB, ChIP, rep2 B2B, JunB, ChIP,
GSM8269994 B2B, Jun, ChIP, rep2 B2B, Jun, ChIP,
GSM8269995 B2B, JunD, ChIP, rep2 B2B, JunD, ChIP,
GSM8269996 B2B, Input, rep2 B2B, Input,

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