Borax induces ferroptosis of glioblastoma by targeting HSPA5/NRF2/GPx4/GSH pathways

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dc.authoridHacioglu, Ceyhan/0000-0002-0993-6118en_US
dc.authorscopusid22956370600en_US
dc.authorscopusid57208671422en_US
dc.contributor.authorTuncer, Cengiz
dc.contributor.authorHacioglu, Ceyhan
dc.date.accessioned2024-08-23T16:04:15Z
dc.date.available2024-08-23T16:04:15Z
dc.date.issued2024en_US
dc.departmentDüzce Üniversitesien_US
dc.description.abstractGlioblastoma multiforme (GBM) is a highly aggressive and lethal form of primary brain tumour. Borax has been demonstrated to exhibit anti-cancer activity through cell death pathways. However, the specific impact of borax on ferroptosis in GBM is not well-established, and the underlying regulatory mechanisms remain unclear. Initially, the effective concentration of borax on cell viability and proliferation in U251 and A172 cells was determined. Subsequently, the effects of borax on the wound healing were analysed. Nuclear factor erythroid 2-related factor 2 (NRF2), glutathione peroxidase 4 (GPx4), glutathione (GSH), HSP70 protein 5 (HSPA5), malondialdehyde (MDA) levels and caspase-3/7 activity were determined in borax-treated and untreated cells. Finally, the protein expression levels of HSPA5, NRF2 and GPx4 were analysed. Borax suppressed cell viability and proliferation in U251 and A172 cells in a concentration- and time-dependent manner. In addition, borax treatment decreased GPx4, GSH, HSPA5 and NRF2 levels in U251 and A172 cells while increasing MDA levels and caspase-3/7 activity. Moreover, borax reduced mRNA and protein levels of HSPA5, NRF2 and GPx4 in U251 and A172 cells. Consequently, borax may induce ferroptosis in GBM cells and regulate the associated regulatory mechanisms targeting NRF2 and HSPA5 pathways. This knowledge may contribute to the development of novel therapeutic approaches targeting ferroptosis in GBM and potentially improve patient outcomes.en_US
dc.identifier.doi10.1111/jcmm.18206
dc.identifier.issn1582-1838
dc.identifier.issn1582-4934
dc.identifier.issue7en_US
dc.identifier.pmid38494858en_US
dc.identifier.scopus2-s2.0-85188045838en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1111/jcmm.18206
dc.identifier.urihttps://hdl.handle.net/20.500.12684/14132
dc.identifier.volume28en_US
dc.identifier.wosWOS:001186191800001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Cellular And Molecular Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectboraxen_US
dc.subjectferroptosisen_US
dc.subjectglioblastoma multiformeen_US
dc.subjectHSPA5en_US
dc.subjectNRF2en_US
dc.subjectCanceren_US
dc.subjectHsp70en_US
dc.subjectCellsen_US
dc.subjectAciden_US
dc.subjectNrf2en_US
dc.titleBorax induces ferroptosis of glioblastoma by targeting HSPA5/NRF2/GPx4/GSH pathwaysen_US
dc.typeArticleen_US

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