GEO series
AP-1 Mediates Oncogenic Transcription and Predicts Fatality in Lung Squamous Cell Carcinoma Patients [ChIP-seq]
GSE267597
Homo sapiens
Genome binding/occupancy profiling by high throughput sequencing
36 samples
Submitted 2026/05/15
Platform GPL21290
Summary
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). 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
Tan X, Kroneberg M, Sun F et al.
· Cancer gene therapy 2026
· PMID 41339492
· doi:10.1038/s41417-025-00974-w
This dataset
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Direct links to NCBI, no account and no request form: the whole study as GSE267597_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 36 samples. Raw sequencing reads are also available from ENA.
Also filed as BioProject PRJNA1111911 and SRA study SRP507995. Searching any of these in the dataset finder brings you back here.
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.
18 replicated groups read from 36 sample titles; they account for 36 of them. Check it against the sample list below before relying on it.
Samples in this study
0 selected
- GSM8269961 A549, pol II, ChIP, rep1
- GSM8269962 A549, H3K4me3, ChIP, rep1
- GSM8269963 A549, Med1, ChIP, rep1
- GSM8269964 A549, H3K27ac, ChIP, rep1
- GSM8269965 A549, JunB, ChIP, rep1
- GSM8269966 A549, Jun, ChIP, rep1
- GSM8269967 A549, JunD, ChIP, rep1
- GSM8269968 A549, Input, rep1
- GSM8269969 B2B, pol II, ChIP, rep1
- GSM8269970 B2B, H3K4me3, ChIP, rep1
- GSM8269971 B2B, Med1, ChIP, rep1
- GSM8269972 B2B, H3K27ac, ChIP, rep1
- GSM8269973 B2B, Rad21, ChIP, rep1
- GSM8269974 B2B, CTCF, ChIP, rep1
- GSM8269975 B2B, JunB, ChIP, rep1
- GSM8269976 B2B, Jun, ChIP, rep1
- GSM8269977 B2B, JunD, ChIP, rep1
- GSM8269978 B2B, Input, rep1
- GSM8269979 A549, pol II, ChIP, rep2
- GSM8269980 A549, H3K4me3, ChIP, rep2
- GSM8269981 A549, Med1, ChIP, rep2
- GSM8269982 A549, H3K27ac, ChIP, rep2
- GSM8269983 A549, JunB, ChIP, rep2
- GSM8269984 A549, Jun, ChIP, rep2
- GSM8269985 A549, JunD, ChIP, rep2
- GSM8269986 A549, Input, rep2
- GSM8269987 B2B, pol II, ChIP, rep2
- GSM8269988 B2B, H3K4me3, ChIP, rep2
- GSM8269989 B2B, Med1, ChIP, rep2
- GSM8269990 B2B, H3K27ac, ChIP, rep2
- GSM8269991 B2B, Rad21, ChIP, rep2
- GSM8269992 B2B, CTCF, ChIP, rep2
- GSM8269993 B2B, JunB, ChIP, rep2
- GSM8269994 B2B, Jun, ChIP, rep2
- GSM8269995 B2B, JunD, ChIP, rep2
- GSM8269996 B2B, Input, rep2
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