Borax affects cellular viability by inducing ER stress in hepatocellular carcinoma cells by targeting SLC12A5

dc.authoridHacioglu, Ceyhan/0000-0002-0993-6118en_US
dc.authorscopusid57208671422en_US
dc.authorscopusid57188932723en_US
dc.contributor.authorHacioglu, Ceyhan
dc.contributor.authorOral, Didem
dc.date.accessioned2024-08-23T16:04:15Z
dc.date.available2024-08-23T16:04:15Z
dc.date.issued2024en_US
dc.departmentDüzce Üniversitesien_US
dc.description.abstractHepatocellular carcinoma (HCC) presents a persistent challenge to conventional therapeutic approaches. SLC12A5 is implicated in an oncogenic capacity and facilitates the progression of cancer. The objective of this investigation is to scrutinize the inhibitory effects of borax on endoplasmic reticulum (ER)-stress and apoptosis mediated by SLC12A5 in HepG2 cells. Initially, we evaluated the cytotoxic impact of borax on both HL-7702 and HepG2 cell lines. Subsequently, the effects of borax on cellular morphology and the cell cycle of these lines were examined. Following this, we explored the impact of borax treatment on the mRNA and protein expression levels of SLC12A5, C/EBP homologous protein (CHOP), glucose-regulated protein-78 (GRP78), activating transcription factor-6 (ATF6), caspase-3 (CASP3), and cytochrome c (CYC) in these cellular populations. The determined IC50 value of borax for HL-7702 cells was 40.8 mM, whereas for HepG2 cells, this value was 22.6 mM. The concentrations of IC50 (22.6 mM) and IC75 (45.7 mM) of borax in HepG2 cells did not manifest morphological aberrations in HL-7702 cells. Conversely, these concentrations in HepG2 cells induced observable morphological and nuclear abnormalities, resulting in cell cycle arrest in the G1/G0 phase. Additionally, the levels of SLC12A5, ATF6, CHOP, GRP78, CASP3, and CYC were elevated in HepG2 cells in comparison to HL-7702 cells. Moreover, SLC12A5 levels decreased following borax treatment in HepG2 cells, whereas ATF6, CHOP, GRP78, CASP3, and CYC levels exhibited a significant increase. In conclusion, our data highlight the potential therapeutic effects of borax through the regulation of ER stress in HCC by targeting SLC12A5.en_US
dc.identifier.doi10.1111/jcmm.18380
dc.identifier.issn1582-1838
dc.identifier.issn1582-4934
dc.identifier.issue10en_US
dc.identifier.pmid38780503en_US
dc.identifier.scopus2-s2.0-85193968372en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1111/jcmm.18380
dc.identifier.urihttps://hdl.handle.net/20.500.12684/14130
dc.identifier.volume28en_US
dc.identifier.wosWOS:001229622900001en_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.subjectendoplasmic reticulum stressen_US
dc.subjecthepatocellular carcinomaen_US
dc.subjectTumor Progressionen_US
dc.subjectPoor Survivalen_US
dc.subjectBoric-Aciden_US
dc.subjectBoronen_US
dc.subjectRolesen_US
dc.titleBorax affects cellular viability by inducing ER stress in hepatocellular carcinoma cells by targeting SLC12A5en_US
dc.typeArticleen_US

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