<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/SRR523/004/SRR5237284/SRR5237284.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/006/SRR5237286/SRR5237286.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/005/SRR5237285/SRR5237285.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/009/SRR5237289/SRR5237289.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/008/SRR5237288/SRR5237288.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/000/SRR5237290/SRR5237290.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/007/SRR5237287/SRR5237287.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR523/003/SRR5237283/SRR5237283.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/PRJNA371739</full_dataset_link><scientific_name>Homo sapiens</scientific_name><tag>xref:PubMed:30258097</tag><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: mRNA profiles of A549 lung cancer cells treated with control or si-ZNF322A oligo were generated by RNA-sequencing</long_description><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 [RNA-Seq]</description><dates><last_updated>2025-09-24</last_updated><first_public>2019-09-27</first_public></dates><accession>PRJNA371739</accession><cross_references><GEO>GSE94537</GEO><taxon>9606</taxon><PubMed>30258097</PubMed></cross_references></HashMap>