<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/GSE303nnn/GSE303244/</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=GSE303244</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>The PARP Inhibitor Talazoparib efficiently Suppresses Tumor Growth in Castration-Resistant Prostate Cancer</name><description>To address the limited understanding of PARP inhibitor monotherapy in castration-resistant prostate cancer (CRPC), we investigated the antitumor effects of Talazoparib in CRPC cells with homologous recombination repair (HRR) gene mutations. We treated DU 145 and PC-3 cells with Talazoparib and observed reduced proliferation, migration, and colony formation. Western blot analysis showed increased apoptosis and DNA damage. RNA sequencing revealed downregulation of key HRR genes (BRCA1/2, ATM, ATR), and gene set enrichment analysis confirmed suppression of DNA repair pathways and activation of immune-related responses. These findings suggest that Talazoparib not only exploits synthetic lethality but also impairs HRR gene expression, supporting its potential as monotherapy in HRR-deficient CRPC.</description><dates><publication>2026/07/31</publication></dates><accession>GSE303244</accession><cross_references><GSM>GSM9121683</GSM><GSM>GSM9121685</GSM><GSM>GSM9121684</GSM><GSM>GSM9121687</GSM><GSM>GSM9121686</GSM><GSM>GSM9121688</GSM><GPL>24676</GPL><GSE>303244</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>