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