{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Vora S"],"funding":["AstraZeneca","Department of Health | National Health and Medical Research Council (NHMRC)","Department of Health | National Health and Medical Research Council"],"pagination":["810"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11550316"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(11)"],"pubmed_abstract":["Aurora B kinase (AURKB) inhibitors have been trialled in a range of different tumour types but are not approved for any indication. Expression of the human papilloma virus (HPV) oncogenes and loss of retinoblastoma (RB) protein function has been reported to increase sensitivity to AURKB inhibitors but the mechanism of their contribution to sensitivity is poorly understood. Two commonly reported outcomes of AURKB inhibition are polyploidy and senescence, although their relationship is unclear. Here we have investigated the major cellular targets of the HPV E6 and E7, p53 and RB, to determine their contribution to AURKB inhibitor induced polyploidy and senescence. We demonstrate that polyploidy is a universal feature of AURKB inhibitor treatment in all cell types including normal primary cel"],"journal":["Cell death & disease"],"pubmed_title":["Aurora B inhibitors promote RB hypophosphorylation and senescence independent of p53-dependent CDK2/4 inhibition."],"pmcid":["PMC11550316"],"funding_grant_id":["APP1104186"],"pubmed_authors":["Urosevic J","McMillan NA","Gabrielli B","Jones MJ","Bonfim-Melo A","Vora S","Lim Y","Travers J","Fernando M","Nazareth D","Kumar S","Hooper JD","Saeh J","He Y","Ong XY","Kumar RP","Andrew A"],"additional_accession":[]},"is_claimable":false,"name":"Aurora B inhibitors promote RB hypophosphorylation and senescence independent of p53-dependent CDK2/4 inhibition.","description":"Aurora B kinase (AURKB) inhibitors have been trialled in a range of different tumour types but are not approved for any indication. Expression of the human papilloma virus (HPV) oncogenes and loss of retinoblastoma (RB) protein function has been reported to increase sensitivity to AURKB inhibitors but the mechanism of their contribution to sensitivity is poorly understood. Two commonly reported outcomes of AURKB inhibition are polyploidy and senescence, although their relationship is unclear. Here we have investigated the major cellular targets of the HPV E6 and E7, p53 and RB, to determine their contribution to AURKB inhibitor induced polyploidy and senescence. We demonstrate that polyploidy is a universal feature of AURKB inhibitor treatment in all cell types including normal primary cel","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-07-16T21:23:12.515Z","creation":"2025-04-04T14:42:52.635Z"},"accession":"S-EPMC11550316","cross_references":{"pubmed":["39521795"],"doi":["10.1038/s41419-024-07204-5"]}}