biostudies-literatureAfonso JFoundation for Science and Technology (FCT)National funds from the FCT in the scope of the UCIBIOAssociate Laboratory i4HBNorte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF)ERDF under the scope of NORTE 20201418https://www.ebi.ac.uk/biostudies/studies/S-EPMC11010907biostudies-literatureUnknown16(7)Advanced urothelial bladder cancer (UBC) patients are tagged by a dismal prognosis and high mortality rates, mostly due to their poor response to standard-of-care platinum-based therapy. Mediators of chemoresistance are not fully elucidated. This work aimed to study the metabolic profile of advanced UBC, in the context of cisplatin resistance. Three isogenic pairs of parental cell lines (T24, HT1376 and KU1919) and the matching cisplatin-resistant (R) sublines were used. A set of functional assays was used to perform a metabolic screening on the cells. In comparison to the parental sublines, a tendency was observed towards an exacerbated glycolytic metabolism in the cisplatin-resistant T24 and HT1376 cells; this glycolytic phenotype was particularly evident for the HT1376/HT1376R pair, forCancersCisplatin-Resistant Urothelial Bladder Cancer Cells Undergo Metabolic Reprogramming beyond the Warburg Effect.PMC11010907projects UIDB/50026/2020 and UIDP/50026/2020UID/BIO/04469/2020, UID/QUI/0686/2020 and BioTecNorte operation (NORTE-01-0145-FEDER-000004)Fellowships SFRH/BPD/116784/2016 and SFRH/BD/145955/2019, and contract 2020.00185.CEECINDNORTE-01-0145-FEDER-000055projects UIDP/04378/2020 and UIDB/04378/2020project LA/P/0140/2020Parpot PMendes-Alves CCarapito ASantos LBaltazar FGuedes de Pinho PSilvestre RBarbosa-Matos CPereira-Vieira JGoncalves SMPinto JLongatto-Filho AAfonso JfalseCisplatin-Resistant Urothelial Bladder Cancer Cells Undergo Metabolic Reprogramming beyond the Warburg Effect.Advanced urothelial bladder cancer (UBC) patients are tagged by a dismal prognosis and high mortality rates, mostly due to their poor response to standard-of-care platinum-based therapy. Mediators of chemoresistance are not fully elucidated. This work aimed to study the metabolic profile of advanced UBC, in the context of cisplatin resistance. Three isogenic pairs of parental cell lines (T24, HT1376 and KU1919) and the matching cisplatin-resistant (R) sublines were used. A set of functional assays was used to perform a metabolic screening on the cells. In comparison to the parental sublines, a tendency was observed towards an exacerbated glycolytic metabolism in the cisplatin-resistant T24 and HT1376 cells; this glycolytic phenotype was particularly evident for the HT1376/HT1376R pair, for2024-01-01T00:00:00Z2024 Apr2025-04-26T20:11:46.43Z2025-04-06T16:20:31.43ZS-EPMC110109073861109610.3390/cancers16071418