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Induction of apoptosis in indole-3-carbinol-treated lung cancer H1299 cells via ROS level elevation

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dc.contributor.authorLim-
dc.contributor.authorH.M.-
dc.contributor.authorPark, See-hyoung-
dc.contributor.authorS.-H.-
dc.contributor.authorNam-
dc.contributor.authorM.J.-
dc.date.available2021-03-17T07:46:48Z-
dc.date.created2021-02-26-
dc.date.issued2021-05-
dc.identifier.issn0960-3271-
dc.identifier.urihttps://scholarworks.bwise.kr/hongik/handle/2020.sw.hongik/12452-
dc.description.abstractThis study was focused on investigating the anticancer potential of indole-3-carbinol (I3C) against lung cancer H1299 cells via an increase in ROS levels. To investigate the induction of growth arrest and/or cell death in H1299 cells, a cell cycle arrest assay, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL) assay, and reactive oxygen species (ROS) detection assay were performed. Through the TUNEL assay, we detected I3C-induced DNA fragmentation. Fluorescence-activated cell sorting (FACS) analysis showed that I3C induced an increase in ROS levels and apoptotic rate in a dose- and time-dependent manner in H1299 cells. Western blotting demonstrated that activated forms of caspase-3, caspase-7, caspase-9, and poly (ADP-ribose) polymerase (PARP) were increased in I3C-treated H1299 cells following treatment with I3C. Furthermore, protein expression levels of FOXO3, bim, bax, and phosphorylated ERK and JNK were increased, while those of pAkt, Bcl-xL, and Bcl-2 were decreased by I3C treatment of H1299 cells. To confirm the relationship between cell apoptosis and ROS generation, H1299 cells were treated with I3C simultaneously with N-acetylcysteine (NAC), and it was shown that ROS levels decreased and viability increased. Moreover, in western blot analysis, expression of anti-apoptotic proteins (thioredoxin1, peroxiredoxin-1, Bcl-2, and Bcl-xL) in I3C-treated cells was evidently downregulated and pro-apoptotic proteins (active ASK1 and cleaved PARP) were upregulated compared to cells co-treated with NAC. The study showed that I3C induced downregulation of ROS regulator proteins and elevation of ROS, thus activating apoptotic signaling cascades in human lung cancer H1299 cells. © The Author(s) 2020.-
dc.publisherSAGE Publications Ltd-
dc.titleInduction of apoptosis in indole-3-carbinol-treated lung cancer H1299 cells via ROS level elevation-
dc.typeArticle-
dc.contributor.affiliatedAuthorPark, See-hyoung-
dc.identifier.doi10.1177/0960327120969968-
dc.identifier.scopusid2-s2.0-85094645151-
dc.identifier.wosid000636025800001-
dc.identifier.bibliographicCitationHuman and Experimental Toxicology, v.40, no.5, pp.812 - 825-
dc.relation.isPartOfHuman and Experimental Toxicology-
dc.citation.titleHuman and Experimental Toxicology-
dc.citation.volume40-
dc.citation.number5-
dc.citation.startPage812-
dc.citation.endPage825-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaToxicology-
dc.relation.journalWebOfScienceCategoryToxicology-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorH1299-
dc.subject.keywordAuthorI3C-
dc.subject.keywordAuthorlung cancer-
dc.subject.keywordAuthorreactive oxygen species (ROS)-
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