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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE267599 | GEO | 2026/05/15

REPOSITORIES: GEO

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

Project description: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.

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