Indole-3-Carbinol Induces Apoptosis in Human Osteosarcoma MG-63 and U2OS Cells
DC Field | Value | Language |
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dc.contributor.author | Lee, Chang Min | - |
dc.contributor.author | Lee, Jongsung | - |
dc.contributor.author | Nam, Myeong Jin | - |
dc.contributor.author | Park, See-Hyoung | - |
dc.date.available | 2020-02-27T16:40:55Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2018-11 | - |
dc.identifier.issn | 2314-6133 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/5329 | - |
dc.description.abstract | This study was focused on investigating the anticancer potential of indole-3-carbinol (I3C) against osteosarcoma MG-63 and U2OS cells. A wound healing assay indicated that IC3 inhibited migration of MG-63 and U2OS cells. MTT, WST-1, and colony formation assays revealed that treatment of MG-63 and U2OS cells with I3C decreased cell viability. Fluorescence-activated cell sorting (FACS) analysis showed that I3C induced apoptosis in a dose-and time-dependent manner in MG-63 and U2OS cells. Moreover, via terminal deoxynucleotidyl transferase- (TdT-) mediated dUTP-biotin nick-end labeling (TUNEL) assay, we detected that I3C induced DNA fragmentation. Western blotting demonstrated that activated forms of caspase-3, caspase-7, and caspase-9, as well as poly (ADP-ribose) polymerase (PARP) were increased in MG-63 and U2OS cells, following treatment with I3C. Furthermore, protein expression levels of FOXO3, Bax, and Bim extra-large form were increased while those of Akt, JNK, p38, phosphorylated ERK, and Bcl-xL were decreased by I3C treatment inMG-63 and U2OS cells. Thus, the study indicates that I3C may induce apoptosis in human osteosarcoma MG-63 and U2OS cells via the activation of apoptotic signaling pathways by FOXO3. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | HINDAWI LTD | - |
dc.relation.isPartOf | BIOMED RESEARCH INTERNATIONAL | - |
dc.title | Indole-3-Carbinol Induces Apoptosis in Human Osteosarcoma MG-63 and U2OS Cells | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000452971200001 | - |
dc.identifier.doi | 10.1155/2018/7970618 | - |
dc.identifier.bibliographicCitation | BIOMED RESEARCH INTERNATIONAL, v.2018 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.scopusid | 2-s2.0-85058783225 | - |
dc.citation.title | BIOMED RESEARCH INTERNATIONAL | - |
dc.citation.volume | 2018 | - |
dc.contributor.affiliatedAuthor | Lee, Chang Min | - |
dc.contributor.affiliatedAuthor | Nam, Myeong Jin | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | PROTEIN-KINASE PATHWAYS | - |
dc.subject.keywordPlus | PROSTATE-CANCER | - |
dc.subject.keywordPlus | DNA FRAGMENTATION | - |
dc.subject.keywordPlus | EMERGING ROLES | - |
dc.subject.keywordPlus | CYCLE ARREST | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | CASPASE-3 | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordPlus | JNK | - |
dc.subject.keywordPlus | SUPPRESSION | - |
dc.relation.journalResearchArea | Biotechnology & Applied Microbiology | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalWebOfScienceCategory | Biotechnology & Applied Microbiology | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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