Boric Acid Induces Oxidative Damage and Apoptosis Through SEMA3A/PLXNA1/NRP1 Signalling Pathway in U251 Glioblastoma Cell

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dc.contributor.authorKar, Ezgi
dc.contributor.authorOvenler, Zeynep
dc.contributor.authorHacioglu, Ceyhan
dc.contributor.authorKar, Fatih
dc.date.accessioned2025-10-11T20:48:13Z
dc.date.available2025-10-11T20:48:13Z
dc.date.issued2025
dc.departmentDüzce Üniversitesien_US
dc.description.abstractGlioblastoma is one of the deadliest cancers with a very low chance of survival. Glioblastomas have a poor prognosis because of their infiltrative nature, which makes them difficult to totally isolate with rigorous surgery, radiation, and chemotherapy. Our aim in this study was to investigate the efficacy of boric acid, which has anti-cancer properties, on glioblastoma, which has very limited treatment options. U251 human glioblastoma cell lines were treated with IC25 (15.62 mu g/mL), IC50 (31.25 mu g/mL) and IC75 (62.5 mu g/mL) doses of boric acid. Cell viability and proliferation levels were tested. At the same time, the activity of boric acid on cells was tested through oxidative stress, apoptosis, and semaphorin signalling pathway parameters. Our findings indicate that boric acid induced dose-dependent oxidative stress, cellular growth inhibition, apoptosis and morphological changes in U251 cells. Additionally, treatments with increasing amounts of boric acid resulted in a rise in the production of biomarkers of the semaphorin pathway, which may limit cell growth and proliferation. We found that boric acid activates apoptosis by triggering ROS formation at high doses and at the same time inhibits cell proliferation by increasing semaphorin signalling pathway expressions. Boric acid may act as an anti-cancer agent by activating different mechanisms in a dose-dependent manner.en_US
dc.description.sponsorshipTUBITAKen_US
dc.description.sponsorshipThis manuscript will be supported by TUBITAK if it is accepted as open access.en_US
dc.identifier.doi10.1111/jcmm.70578
dc.identifier.issn1582-1838
dc.identifier.issn1582-4934
dc.identifier.issue9en_US
dc.identifier.pmid40318008en_US
dc.identifier.scopus2-s2.0-105004198786en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.urihttps://doi.org/10.1111/jcmm.70578
dc.identifier.urihttps://hdl.handle.net/20.500.12684/21811
dc.identifier.volume29en_US
dc.identifier.wosWOS:001480430200001en_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.subjectapoptosisen_US
dc.subjectboric aciden_US
dc.subjectglioblastomaen_US
dc.subjectoxidative damageen_US
dc.subjectsemaphorinen_US
dc.titleBoric Acid Induces Oxidative Damage and Apoptosis Through SEMA3A/PLXNA1/NRP1 Signalling Pathway in U251 Glioblastoma Cellen_US
dc.typeArticleen_US

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