{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gou P"],"funding":["Chongqing Municipal Education Commission Foundation"],"pagination":["172"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11997184"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["Metastatic Group 3 medulloblastoma (G3 MB) have been shown in several studies to be very high risk, particularly those harboring MYC amplification. More effective therapies are especially important for these patients. CUDC-907, a novel dual inhibitor targeting the MYC upstream pathway (HDAC/PI3K), shows significant antitumor efficacy across multiple cancer types. However, the antitumor effects and underlying mechanisms of CUDC-907 in MB, particularly in very high-risk MB, remain unexplored. In this study, we showed that MYC amplified G3 MB cells, patient-derived organoids and xenograft models were sensitive to CUDC-907. CUDC-907 inhibited MYC expression through the HDAC and PI3K pathways, and then induced G0/G1 phase arrest through the MYC-P21/P27-CDKs/cyclins axis. Furthermore, when CUDC-"],"journal":["Cell death discovery"],"pubmed_title":["The dual HDAC/PI3K inhibitor CUDC-907 inhibits the growth and proliferation of MYC-driven Group 3 medulloblastoma."],"pmcid":["PMC11997184"],"funding_grant_id":["2024WSJK028","KJON202300425"],"pubmed_authors":["Gou P","Li X","Xu M","Zhang D","Luo J","Gan L","Cui H","Fang C","Zhang L","Liang P","Li M","Wu X"],"additional_accession":[]},"is_claimable":false,"name":"The dual HDAC/PI3K inhibitor CUDC-907 inhibits the growth and proliferation of MYC-driven Group 3 medulloblastoma.","description":"Metastatic Group 3 medulloblastoma (G3 MB) have been shown in several studies to be very high risk, particularly those harboring MYC amplification. More effective therapies are especially important for these patients. CUDC-907, a novel dual inhibitor targeting the MYC upstream pathway (HDAC/PI3K), shows significant antitumor efficacy across multiple cancer types. However, the antitumor effects and underlying mechanisms of CUDC-907 in MB, particularly in very high-risk MB, remain unexplored. In this study, we showed that MYC amplified G3 MB cells, patient-derived organoids and xenograft models were sensitive to CUDC-907. CUDC-907 inhibited MYC expression through the HDAC and PI3K pathways, and then induced G0/G1 phase arrest through the MYC-P21/P27-CDKs/cyclins axis. Furthermore, when CUDC-","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2026-06-02T04:31:08.905Z","creation":"2026-04-14T03:13:27.945Z"},"accession":"S-EPMC11997184","cross_references":{"pubmed":["40229260"],"doi":["10.1038/s41420-025-02470-4"]}}