Boric acid Increases Susceptibility to Chemotherapy by Targeting the Ferritinophagy Signaling Pathway in TMZ Resistant Glioblastoma Cells

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dc.authoridHacioglu, Ceyhan/0000-0002-0993-6118en_US
dc.authorscopusid57208671422en_US
dc.authorscopusid22956370600en_US
dc.contributor.authorHacioglu, Ceyhan
dc.contributor.authorTuncer, Cengiz
dc.date.accessioned2024-08-23T16:07:04Z
dc.date.available2024-08-23T16:07:04Z
dc.date.issued2024en_US
dc.departmentDüzce Üniversitesien_US
dc.description.abstractGlioblastoma (GBM) is a common and highly lethal form of brain cancer. Temozolomide (TMZ) is the primary chemotherapy used for GBM, but it has limited effectiveness, with about half of the patients developing resistance. Iron regulatory proteins (IRPs) modulate genes involved in iron metabolism, while the nuclear receptor coactivator 4 (NCOA4) controls iron metabolism through a process called ferritinophagy. In this study, we investigated whether boric acid increases chemosensitivity mediated by ferritinophagy via the NCOA4 and IRP2 signaling pathways in TMZ-resistant GBM cells. First, we generated TMZ-resistant GBM cells (A172-R and T98G-R cells). Next, we investigated the effects of boric acid on cell viability, proliferation, cell cycle, and cell morphology in these cells. Additionally, following boric acid treatment, we analyzed the expression and protein levels of various biochemical markers in these cells. Boric acid treatment in A172-R and T98G-R cells suppressed cell viability and proliferation, arrested these cells in the G1/G0 cell cycle, and induced morphological differences. Boric acid increased NCOA4, IRP2, iron, and malondialdehyde (MDA) levels in A172-R and T98G-R cells, while glutathione (GSH) and glutathione peroxidase 4 (GPx4) levels decreased. Moreover, boric acid treatment increased intracellular iron levels and lipid peroxidation by inducing NCOA4 and IRP2 expression levels in TMZ-resistant cells. According to our results, boric acid may regulate chemosensitivity in A172-R and T98G-R cells mediated by NCOA4 and IRP2. In conclusion, the manipulative effects of boric acid on the ferritinophagy pathway hold the potential to sensitize TMZ-resistant GBM cells to chemotherapy.en_US
dc.identifier.doi10.1007/s12011-023-03930-7
dc.identifier.endpage3587en_US
dc.identifier.issn0163-4984
dc.identifier.issn1559-0720
dc.identifier.issue8en_US
dc.identifier.pmid37906374en_US
dc.identifier.scopus2-s2.0-85175349943en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage3574en_US
dc.identifier.urihttps://doi.org/10.1007/s12011-023-03930-7
dc.identifier.urihttps://hdl.handle.net/20.500.12684/14468
dc.identifier.volume202en_US
dc.identifier.wosWOS:001091234400001en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringernatureen_US
dc.relation.ispartofBiological Trace Element Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectBoric aciden_US
dc.subjectChemosensitivityen_US
dc.subjectFerritinophagyen_US
dc.subjectGlioblastomaen_US
dc.subjectTemozolomideen_US
dc.subjectTemozolomide Resistanceen_US
dc.subjectFerroptosisen_US
dc.subjectDeathen_US
dc.subjectMetabolismen_US
dc.subjectStrategiesen_US
dc.subjectOvercomeen_US
dc.subjectCanceren_US
dc.subjectNcoa4en_US
dc.subjectFormen_US
dc.titleBoric acid Increases Susceptibility to Chemotherapy by Targeting the Ferritinophagy Signaling Pathway in TMZ Resistant Glioblastoma Cellsen_US
dc.typeArticleen_US

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