{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lopez J"],"funding":["Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III)","Generalitat de Catalunya (Government of Catalonia)"],"pagination":["91"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11889205"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["A one-two punch sequential regimen of senescence-inducing agents followed by senolytic drugs has emerged as a novel therapeutic strategy in cancer. Unfortunately, cancer cells undergoing therapy-induced senescence (TIS) vary widely in their sensitivity to senotherapeutics, and companion diagnostics to predict the response of TIS cancer cells to a specific senolytic drug are lacking. Here, we hypothesized that the ability of the BH3 profiling assay to functionally measure the mitochondrial priming state-the proximity to the apoptotic threshold-and the dependencies on pro-survival BCL-2 family proteins can be exploited to inform the sensitivity of TIS cancer cells to BH3-mimetics. Replicative, mitotic, oxidative, and genotoxic forms of TIS were induced in p16-null/p53-proficient, BAX-deficie"],"journal":["Cell death discovery"],"pubmed_title":["Mitochondrial priming and response to BH3 mimetics in \"one-two punch\" senogenic-senolytic strategies."],"pmcid":["PMC11889205"],"funding_grant_id":["CP20/00003","PI22/00297","CM22/00276","2022 INV-1 00001"],"pubmed_authors":["Teixidor E","Cuyas E","Lopez-Bonet E","Menendez JA","Martin-Castillo B","Lopez J","Alarcon T","Verdura S","Lupu R","Llop-Hernandez A","Sardanyes J","Bosch-Barrera J","Martinez-Balibrea E","Serrano-Hervas E"],"additional_accession":[]},"is_claimable":false,"name":"Mitochondrial priming and response to BH3 mimetics in \"one-two punch\" senogenic-senolytic strategies.","description":"A one-two punch sequential regimen of senescence-inducing agents followed by senolytic drugs has emerged as a novel therapeutic strategy in cancer. Unfortunately, cancer cells undergoing therapy-induced senescence (TIS) vary widely in their sensitivity to senotherapeutics, and companion diagnostics to predict the response of TIS cancer cells to a specific senolytic drug are lacking. Here, we hypothesized that the ability of the BH3 profiling assay to functionally measure the mitochondrial priming state-the proximity to the apoptotic threshold-and the dependencies on pro-survival BCL-2 family proteins can be exploited to inform the sensitivity of TIS cancer cells to BH3-mimetics. Replicative, mitotic, oxidative, and genotoxic forms of TIS were induced in p16-null/p53-proficient, BAX-deficie","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-04-18T17:28:19.737Z","creation":"2025-04-07T04:58:42.991Z"},"accession":"S-EPMC11889205","cross_references":{"pubmed":["40055336"],"doi":["10.1038/s41420-025-02379-y"]}}