<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/GSE330nnn/GSE330672/</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=GSE330672</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Catechol-O-methyltransferase attenuates invasive potential by upregulating desmogleins and is associated with better prognosis in ovarian cancer</name><description>Catechol-O-methyltransferase (COMT) is a key enzyme in estrogen catabolism, but its estrogen-independent roles in ovarian cancer remain largely unknown. This study aims to elucidate the molecular mechanisms by which COMT suppresses cell invasion and to evaluate its significance as a prognostic marker. We performed transcriptome analysis (RNA-seq) on ovarian cancer cells to identify downstream targets of COMT. Our results show that COMT overexpression significantly inhibits cell invasion in an estrogen-independent manner. Integrative analysis of RNA-seq and CE-MS metabolome data revealed that COMT upregulates desmoglein genes (DSG1-3), thereby strengthening cell-to-cell contact, and induces metabolic remodeling. These findings suggest that COMT suppresses metastasis by regulating cell adhesion and metabolism, serving as a potential prognostic marker and therapeutic target in ovarian cancer.</description><dates><publication>2026/05/26</publication></dates><accession>GSE330672</accession><cross_references><GSM>GSM9730114</GSM><GSM>GSM9730113</GSM><GSM>GSM9730112</GSM><GSM>GSM9730111</GSM><GPL>23227</GPL><GSE>330672</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>