<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/SRR523/002/SRR5237382/SRR5237382.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/003/SRR5237383/SRR5237383.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/004/SRR5237384/SRR5237384.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/005/SRR5237385/SRR5237385.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><center_name>Department of Pharmacology, College of Medicine, National Cheng Kung University</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA373804</full_dataset_link><scientific_name>Homo sapiens</scientific_name><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.</long_description><tag>xref:PubMed:30258097</tag><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Homo sapiens</name><description>Oncogenic zinc finger protein ZNF322A promotes lung cancer stemness through transcriptionally suppressing c-Myc expression [ChIP-Seq]</description><dates><last_updated>2025-09-24</last_updated><first_public>2019-09-27</first_public></dates><accession>PRJNA373804</accession><cross_references><GEO>GSE94656</GEO><taxon>9606</taxon><PubMed>30258097</PubMed></cross_references></HashMap>