Investigation of apoptotic effects of Cucurbitacin D, I, and E mediated by Bax/Bcl-xL, caspase-3/9, and oxidative stress modulators in HepG2 cell line

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dc.authoridUremis, Muhammed Mehdi/0000-0003-2296-2422
dc.authorwosidUremis, Muhammed Mehdi/HKP-0531-2023
dc.contributor.authorUremis, Muhammed Mehdi
dc.contributor.authorTurkoz, Yusuf
dc.contributor.authorUremis, Nuray
dc.date.accessioned2024-08-04T20:55:10Z
dc.date.available2024-08-04T20:55:10Z
dc.date.issued2024
dc.departmentİnönü Üniversitesien_US
dc.description.abstractCucurbitacins, natural compounds highly abundant in the Cucurbitaceae plant family, are characterized by their anticancer, anti-inflammatory, and hepatoprotective properties. These compounds have potential as therapeutic agents in the treatment of liver cancer. This study investigated the association of cucurbitacin D, I, and E (CuD, CuI, and CuE) with the caspase cascade, Bcl-2 family, and oxidative stress modulators in the HepG2 cell line. We evaluated the antiproliferative effects of CuD, CuI, and CuE using the MTT assay. We analyzed Annexin V/PI double staining, cell cycle, mitochondrial membrane potential, and wound healing assays at different doses of the three compounds. To examine the modulation of the caspase cascade, we determined the protein and gene expression levels of Bax, Bcl-xL, caspase-3, and caspase-9. We evaluated the total antioxidant status (TAS), total oxidant status (TOS), superoxide dismutase (SOD), glutathione (GSH), Total, and Native Thiol levels to measure cellular redox status. CuD, CuI, and CuE suppressed the proliferation of HepG2 cells in a dose-dependent manner. The cucurbitacins induced apoptosis by increasing caspase-3, caspase-9, and Bax activity, inhibiting Bcl-xL activation, causing loss of Delta psi m, and suppressing cell migration. Furthermore, cucurbitacins modulated oxidative stress by increasing TOS levels and decreasing SOD, GSH, TAS, and total and native Thiol levels. Our findings suggest that CuD, CuI, and CuE exert apoptotic effects on the hepatocellular carcinoma cell line by regulating Bax/Bcl-xL, caspase-3/9 signaling, and causing intracellular ROS increase in HepG2 cells.en_US
dc.description.sponsorshipInonu University [TSA-2021-2256]; Inonu University Scientific Research Project Unitsen_US
dc.description.sponsorshipThis research was financed by Inonu University Scientific Research Project Units (Project No.: TSA-2021-2256).en_US
dc.identifier.doi10.1002/ddr.22174
dc.identifier.issn0272-4391
dc.identifier.issn1098-2299
dc.identifier.issue2en_US
dc.identifier.pmid38494997en_US
dc.identifier.scopus2-s2.0-85188243467en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1002/ddr.22174
dc.identifier.urihttps://hdl.handle.net/11616/101886
dc.identifier.volume85en_US
dc.identifier.wosWOS:001186184700001en_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.ispartofDrug Development Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectapoptosisen_US
dc.subjectBcl-2en_US
dc.subjectcaspase cascadeen_US
dc.subjectcucurbitacin D, I, Een_US
dc.subjectoxidative stressen_US
dc.subjectROSen_US
dc.titleInvestigation of apoptotic effects of Cucurbitacin D, I, and E mediated by Bax/Bcl-xL, caspase-3/9, and oxidative stress modulators in HepG2 cell lineen_US
dc.typeArticleen_US

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