{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE267nnn/GSE267597/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE267597"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"AP-1 Mediates Oncogenic Transcription and Predicts Fatality in Lung Squamous Cell Carcinoma Patients [ChIP-seq]","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.","dates":{"publication":"2026/05/15"},"accession":"GSE267597","cross_references":{"GSM":["GSM8269966","GSM8269988","GSM8269987","GSM8269965","GSM8269986","GSM8269964","GSM8269963","GSM8269985","GSM8269969","GSM8269968","GSM8269989","GSM8269967","GSM8269980","GSM8269984","GSM8269962","GSM8269983","GSM8269961","GSM8269982","GSM8269981","GSM8269977","GSM8269976","GSM8269975","GSM8269996","GSM8269974","GSM8269979","GSM8269978","GSM8269991","GSM8269990","GSM8269995","GSM8269973","GSM8269972","GSM8269994","GSM8269993","GSM8269971","GSM8269992","GSM8269970"],"GPL":["21290"],"GSE":["267597"],"taxon":["Homo sapiens"],"PMID":["[41339492]"]}}