{"database":"ENA","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Fastqsanger.gz":["ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR215/009/SRR2155769/SRR2155769.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR215/002/SRR2155772/SRR2155772.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR215/001/SRR2155771/SRR2155771.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR215/000/SRR2155770/SRR2155770.fastq.gz"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Medicinaren 25/Neo, Department of Biosciences and Nutrition, Karolinska Institutet"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA292652"],"scientific_name":["Homo sapiens"],"tag":["xref:PubMed:26792858"],"long_description":["Triple-negative breast cancer (TNBC) represents a highly aggressive form of breast cancer with limited treatment options. Proinflammatory cytokines such as TNF can facilitate tumor progression and metastasis. However, our knowledge of the molecular mechanisms underlying TNBC progression mediated by inflammation is still limited. Here, we define the AP-1 transcription factor c-Jun cistrome, which is comprised of 13800 binding sites responsive to TNFalpha-induced signaling in TNBC cells. In addition, we show that c-Jun regulates nearly a third of the TNFalpha-elicited transcriptome. Expression of the c-Jun-regulated pro-invasion gene program is strongly associated with clinical outcomes in TNBCs. Mechanistically we demonstrate that c-Jun drives TNFalpha-mediated TNBC tumorigenicity by transcriptional regulation of Ninj1. As exemplified by the c-Jun bound CXC chemokine genes clustered on chromosome 4, we demonstrate that NF-kB might be a pioneer factor and is required for the regulation of TNFalpha-inducible inflammatory genes, whereas c-Jun has little effect. Together, our results uncover AP-1 as an important determinant for inflammation-induced cancer progression, rather than inflammatory response. Overall design: BT549 cells were serum-starved overnight and then treated with or without TNFalpha for 3 hours."],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"Homo sapiens","description":"Genome-wide profiling of inflammatory cistrome reveals AP-1/c-Jun as a key regulator of TNFalpha-mediated triple-negative breast cancer progression [ChIP-seq]","dates":{"last_updated":"2025-09-24","first_public":"2016-10-10"},"accession":"PRJNA292652","cross_references":{"GEO":["GSE71976"],"taxon":["9606"],"PubMed":["26792858"]}}