<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE232nnn/GSE232772/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE232772</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>OTUB2 silencing promotes ovarian cancer via mitochondrial metabolic reprogramming and can be synthetically targeted by CA9 inhibition</name><description>These findings delineate the mechanism of OTUB2 epigenetic silencing in ovarian cancer, demonstrate the critical roles of OTUB2/SNX29P2 in inhibiting glycolysis and eliciting cuproptosis in cancer cells and suggest that CA9 inhibitor treatment is a promising therapeutic option for OTUB2-silenced tumors. To investigate the downstream pathway regulated by OTUB2/SNX29P2, we performed RNA sequencing (RNA-seq) in ES-2 cells expressing EV, OTUB2 or SNX29P2.</description><dates><publication>2024/04/19</publication></dates><accession>GSE232772</accession><cross_references><GSM>GSM7382868</GSM><GSM>GSM7382867</GSM><GSM>GSM7382866</GSM><GSM>GSM7382865</GSM><GSM>GSM7382869</GSM><GSM>GSM7382871</GSM><GSM>GSM7382870</GSM><GSM>GSM7382873</GSM><GSM>GSM7382872</GSM><GPL>24676</GPL><GSE>232772</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>