{"database":"ENA","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Fastqsanger.gz":["ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/002/SRR5237382/SRR5237382.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/003/SRR5237383/SRR5237383.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/004/SRR5237384/SRR5237384.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/005/SRR5237385/SRR5237385.fastq.gz"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Department of Pharmacology, College of Medicine, National Cheng Kung University"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA373804"],"scientific_name":["Homo sapiens"],"long_description":["ZNF322A, a C2H2 zinc finger transcription factor, is an oncoprotein in lung cancer. However, the transcription mechanisms of ZNF322A in lung cancer stemness remain elusive. By integrating our chromatin immunoprecipitation-sequencing and RNA-sequencing datasets, we identified and validated transcriptional targets of ZNF322A, which significantly enriched in developmental processes. Indeed, overexpression of ZNF322A promoted self-renewal ability and increased stemness-related gene expressions in vitro and in vivo. Importantly, ZNF322A bound directly to c-Myc promoter to transcriptionally suppress c-Myc expression, which in turn increased mitochondrial oxidative phosphorylation, promoted cell motility and thus maintained lung cancer stemness properties. Clinically, ZNF322AHigh/c-MycLow expression profile was revealed as an independent factor for poor outcome of lung cancer patients. Our study provides first evidence that ZNF322A-centered transcriptome promotes lung tumorigenesis and ZNF322A acts as a transcription suppressor of c-Myc to maintain lung cancer stemness by shifting metabolism phenotype to oxidative phosphorylation. Overall design: Genome-wide ZNF322A binding sites were identified via chromatin immunoprecipitation-sequencing analysis of vecoter control and HA-tagged ZNF322A overexpressing H460 lung cancer cells. ChIP-seq analyses were performed in duplicated samples using Applied Biosystems SOLiD system."],"tag":["xref:PubMed:30258097"],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"Homo sapiens","description":"Oncogenic zinc finger protein ZNF322A promotes lung cancer stemness through transcriptionally suppressing c-Myc expression [ChIP-Seq]","dates":{"last_updated":"2025-09-24","first_public":"2019-09-27"},"accession":"PRJNA373804","cross_references":{"GEO":["GSE94656"],"taxon":["9606"],"PubMed":["30258097"]}}