{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yi W"],"funding":["NSF","NIH NIGMS","NIGMS NIH HHS","National Science Foundation"],"pagination":["9022"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11354775"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(16)"],"pubmed_abstract":["Multiple myeloma is the second most hematological cancer. RUVBL1 and RUVBL2 form a subcomplex of many chromatin remodeling complexes implicated in cancer progression. As an inhibitor specific to the RUVBL1/2 complex, CB-6644 exhibits remarkable anti-tumor activity in xenograft models of Burkitt's lymphoma and multiple myeloma (MM). In this work, we defined transcriptional signatures corresponding to CB-6644 treatment in MM cells and determined underlying epigenetic changes in terms of chromatin accessibility. CB-6644 upregulated biological processes related to interferon response and downregulated those linked to cell proliferation in MM cells. Transcriptional regulator inference identified E2Fs as regulators for downregulated genes and MED1 and MYC as regulators for upregulated genes. CB-"],"journal":["International journal of molecular sciences"],"pubmed_title":["Molecular Signatures of CB-6644 Inhibition of the RUVBL1/2 Complex in Multiple Myeloma."],"pmcid":["PMC11354775"],"funding_grant_id":["P20 GM121322","P20 GM103434","2125872","U54 GM104942"],"pubmed_authors":["Mangano RS","Frisch SM","Hu G","McBee J","Adjeroh DA","Yi W","Dziadowicz SA","Hazlehurst LA","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"Molecular Signatures of CB-6644 Inhibition of the RUVBL1/2 Complex in Multiple Myeloma.","description":"Multiple myeloma is the second most hematological cancer. RUVBL1 and RUVBL2 form a subcomplex of many chromatin remodeling complexes implicated in cancer progression. As an inhibitor specific to the RUVBL1/2 complex, CB-6644 exhibits remarkable anti-tumor activity in xenograft models of Burkitt's lymphoma and multiple myeloma (MM). In this work, we defined transcriptional signatures corresponding to CB-6644 treatment in MM cells and determined underlying epigenetic changes in terms of chromatin accessibility. CB-6644 upregulated biological processes related to interferon response and downregulated those linked to cell proliferation in MM cells. Transcriptional regulator inference identified E2Fs as regulators for downregulated genes and MED1 and MYC as regulators for upregulated genes. CB-","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-04-08T19:43:05.997Z","creation":"2025-04-06T13:47:19.811Z"},"accession":"S-EPMC11354775","cross_references":{"pubmed":["39201707"],"doi":["10.3390/ijms25169022"]}}