Borax regulates iron chaperone- and autophagy-mediated ferroptosis pathway in glioblastoma cells

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dc.authoridkar, fatih/0000-0001-8356-9806en_US
dc.authoridtuncer, cengiz/0000-0003-2400-5546en_US
dc.authoridFATIH, DAVRAN/0000-0002-6086-6602en_US
dc.authoridHacioglu, Ceyhan/0000-0002-0993-6118en_US
dc.authorscopusid57208671422en_US
dc.authorscopusid57208669078en_US
dc.authorscopusid36468092600en_US
dc.authorscopusid22956370600en_US
dc.authorwosidkar, fatih/HJY-4385-2023en_US
dc.contributor.authorHacioglu, Ceyhan
dc.contributor.authorKar, Fatih
dc.contributor.authorDavran, Fatih
dc.contributor.authorTuncer, Cengiz
dc.date.accessioned2024-08-23T16:07:17Z
dc.date.available2024-08-23T16:07:17Z
dc.date.issued2023en_US
dc.departmentDüzce Üniversitesien_US
dc.description.abstractGlioblastoma (GBM) is classified as a stage-IV glioma. Unfortunately, there are currently no curative treatments for GBM. Poly(rC)-binding protein 1 (PCBP1) is a cytosolic iron chaperone with diverse functions. PCBP1 is also known to regulate autophagy, but the role of PCBP1 in ferroptosis, iron-dependent cell death pathway, remains unrevealed in GBM cells. Here, we investigated the effects of borax, a boron compound, on the ferroptosis signaling pathway mediated by PCBP1 and autophagy. The study analyzed cell viability, proliferation, and cell cycle on U87-MG and HMC3 cells to investigate the effects of borax. After determining the cytotoxic concentrations of borax, morphological analyzes and measurement of PCBP1, Beclin1, malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase 4 (GPx4) and acyl-CoA synthetase long chain family member 4 (ACSL4) levels were performed. Finally, expression levels of PCBP1, Beclin1, GPx4 and ACSL4, and caspase-3/7 activity were determined. We found that borax reduced U87-MG cell viability in a concentration- and time-dependent manner. Additionally, borax altered cell proliferation and remarkably reduced S phase in the U87-MG cells and exhibited selectivity by having an opposite effect on normal cells (HMC3). According to DAPI staining, borax caused nuclear deficits in U87-MG cells. The result showed that borax in U87-MG cells induced reduction of the PCBP1, GSH, and GPx4 and enhancement of Beclin1, MDA, and ACSL4. Furthermore, borax triggered apoptosis by activating caspase 3/7 in U87-MG cells. Our study indicated that the borax has potential as an anticancer treatment for GBM via regulating PCBP1/Beclin1/GPx4/ACSL4 signaling pathways.en_US
dc.identifier.doi10.1002/tox.23797
dc.identifier.endpage1701en_US
dc.identifier.issn1520-4081
dc.identifier.issn1522-7278
dc.identifier.issue7en_US
dc.identifier.pmid36988300en_US
dc.identifier.scopus2-s2.0-85151975397en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage1690en_US
dc.identifier.urihttps://doi.org/10.1002/tox.23797
dc.identifier.urihttps://hdl.handle.net/20.500.12684/14567
dc.identifier.volume38en_US
dc.identifier.wosWOS:000960346300001en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofEnvironmental Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectautophagyen_US
dc.subjectboraxen_US
dc.subjectferroptosisen_US
dc.subjectglioblastomasen_US
dc.subjectpoly(C)-binding protein 1en_US
dc.subjectNeutron-Capture Therapyen_US
dc.subjectCanceren_US
dc.subjectMechanismen_US
dc.subjectProteinsen_US
dc.subjectDeathen_US
dc.titleBorax regulates iron chaperone- and autophagy-mediated ferroptosis pathway in glioblastoma cellsen_US
dc.typeArticleen_US

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