Boric Acid Suppresses Glioblastoma Cellular Survival by Regulating Ferroptosis via SOX10/GPx4/ACSL4 Signalling and Iron Metabolism

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dc.authoridHacioglu, Ceyhan/0000-0002-0993-6118
dc.authoridtuncer, cengiz/0000-0003-2400-5546
dc.contributor.authorKilic, Guven
dc.contributor.authorHacioglu, Ceyhan
dc.contributor.authorTuncer, Cengiz
dc.contributor.authorKar, Ezgi
dc.contributor.authorKar, Fatih
dc.contributor.authorTaskesen, Ahmet
dc.contributor.authorKurtulus, Adem
dc.date.accessioned2025-10-11T20:48:13Z
dc.date.available2025-10-11T20:48:13Z
dc.date.issued2025
dc.departmentDüzce Üniversitesien_US
dc.description.abstractFerroptosis, a distinct form of regulated cell death, plays a role in glioma pathogenesis. SRY-box (SOX) transcription factors are key regulators of cancer progression. In this study, we investigated the role of SOX10 in ferroptosis induction in U87 cells following boric acid treatment. First, the cytotoxic effects of boric acid on HMC3 and U87 cells were assessed using CCK8 and BrdU incorporation assays. Subsequently, SOX10, GPX4, ACSL4, GSH, MDA, total ROS, Fe2+, and TFR levels were analysed using ELISA, Western blot, and RT-PCR techniques. Additionally, DAPI staining was performed to evaluate nuclear abnormalities. According to the CCK8 analysis, the IC50 value for boric acid was determined to be 3.12 mM for HMC3 cells and 532 mu M for U87 cells, a finding further supported by BrdU incorporation analysis, which indicated that U87 cells were more sensitive to boric acid. Western blot and RT-PCR analyses revealed that SOX10 expression was significantly higher in U87 cells compared to HMC3 cells. Boric acid treatment led to a reduction in GSH, GPX4, and SOX10 levels in U87 cells, while inducing an increase in MDA, total ROS, ACSL4, Fe2+, and TFR levels. Moreover, microscopic analysis demonstrated that boric acid treatment induced both morphological and nuclear abnormalities in U87 cells. In conclusion, our findings demonstrate that SOX10 is involved in the ferroptosis signalling pathway and that boric acid effectively suppresses U87 cell viability by targeting the SOX10/GPX4/ACSL4 axis.en_US
dc.identifier.doi10.1111/jcmm.70529
dc.identifier.issn1582-1838
dc.identifier.issn1582-4934
dc.identifier.issue7en_US
dc.identifier.pmid40159622en_US
dc.identifier.scopus2-s2.0-105002036802en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.urihttps://doi.org/10.1111/jcmm.70529
dc.identifier.urihttps://hdl.handle.net/20.500.12684/21812
dc.identifier.volume29en_US
dc.identifier.wosWOS:001456256000001en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Cellularand Molecular Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmzKA_WOS_20250911
dc.subjectboric aciden_US
dc.subjectFerroptosisen_US
dc.subjectgliomaen_US
dc.subjectSOXen_US
dc.titleBoric Acid Suppresses Glioblastoma Cellular Survival by Regulating Ferroptosis via SOX10/GPx4/ACSL4 Signalling and Iron Metabolismen_US
dc.typeArticleen_US

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