{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ma X"],"funding":["Guizhou Institute of Technology High-level Talent Scientific Research Start-up Fund","National Outstanding Youth Science Fund Project of National Natural Science Foundation of China","Zunyi Technology and Big data Bureau Moutai institute Joint Science and Technology Research and Development Project"],"pagination":["24962"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11496540"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["To determine the synergistic effect and mechanism of AO/854, a new Bloom syndrome protein (BLM) helicase inhibitor, and cisplatin (CDDP), a DNA-crosslinking agent, cell viability assays, neutral comet assays, and Western blotting (WB) were performed on prostate cancer (PCa) cells. According to our findings, combining AO/854 and CDDP enhanced the antiproliferative capabilities of PC3 cell lines. As evidenced by the upregulation of γH2AX, cleaved caspase-3/caspase-3, and BAX/Bcl-2, AO/854 dramatically increased PC3 apoptosis and DNA damage induced by CDDP. Furthermore, combining AO/854 and CDDP synergistically inhibited PC3 cell migration and invasion. In addition, AO/854 inhibited CDDP-induced S-phase cell-cycle arrest in PC3 cells while enhancing G2/M-phase cell-cycle arrest. In vivo, the "],"journal":["Scientific reports"],"pubmed_title":["Synergistic effects of bloom helicase (BLM) inhibitor AO/854 with cisplatin in prostate cancer."],"pmcid":["PMC11496540"],"funding_grant_id":["31860242","2023GCC066","ZunaShiJiaoHe HZ zi[2020]316"],"pubmed_authors":["Tian F","Xiao Y","Ma X","Huang M","Song D","Chen X","Xu H"],"additional_accession":[]},"is_claimable":false,"name":"Synergistic effects of bloom helicase (BLM) inhibitor AO/854 with cisplatin in prostate cancer.","description":"To determine the synergistic effect and mechanism of AO/854, a new Bloom syndrome protein (BLM) helicase inhibitor, and cisplatin (CDDP), a DNA-crosslinking agent, cell viability assays, neutral comet assays, and Western blotting (WB) were performed on prostate cancer (PCa) cells. According to our findings, combining AO/854 and CDDP enhanced the antiproliferative capabilities of PC3 cell lines. As evidenced by the upregulation of γH2AX, cleaved caspase-3/caspase-3, and BAX/Bcl-2, AO/854 dramatically increased PC3 apoptosis and DNA damage induced by CDDP. Furthermore, combining AO/854 and CDDP synergistically inhibited PC3 cell migration and invasion. In addition, AO/854 inhibited CDDP-induced S-phase cell-cycle arrest in PC3 cells while enhancing G2/M-phase cell-cycle arrest. In vivo, the ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-06-02T21:56:39.32Z","creation":"2025-04-04T02:57:38.822Z"},"accession":"S-EPMC11496540","cross_references":{"pubmed":["39438537"],"doi":["10.1038/s41598-024-75938-5"]}}