<HashMap><database>ENA</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR215/009/SRR2155769/SRR2155769.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR215/002/SRR2155772/SRR2155772.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR215/001/SRR2155771/SRR2155771.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR215/000/SRR2155770/SRR2155770.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Genomics</omics_type><center_name>Medicinaren 25/Neo, Department of Biosciences and Nutrition, Karolinska Institutet</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA292652</full_dataset_link><scientific_name>Homo sapiens</scientific_name><tag>xref:PubMed:26792858</tag><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.</long_description><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Homo sapiens</name><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]</description><dates><last_updated>2025-09-24</last_updated><first_public>2016-10-10</first_public></dates><accession>PRJNA292652</accession><cross_references><GEO>GSE71976</GEO><taxon>9606</taxon><PubMed>26792858</PubMed></cross_references></HashMap>