Equol Induces Mitochondria-mediated Apoptosis of Human Cervical Cancer Cells
DC Field | Value | Language |
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dc.contributor.author | Kim, Eun Young | - |
dc.contributor.author | Shin, Jin Young | - |
dc.contributor.author | Park, Young-Ja | - |
dc.contributor.author | Kim, An Keun | - |
dc.date.available | 2021-02-22T11:47:38Z | - |
dc.date.issued | 2014-09 | - |
dc.identifier.issn | 0250-7005 | - |
dc.identifier.issn | 1791-7530 | - |
dc.identifier.uri | https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/10812 | - |
dc.description.abstract | Background/Aim: The present study aimed to investigate anticancer properties of equol and demonstrate its underlying mechanisms of action in human cervical cancer HeLa cells. Materials and Methods: Inhibition of cell viability was examined by 3-(4,5-dimethylthiazoly-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. Apoptosis was evaluated by observation of apoptotic cell morphology, and an increase of annexin-V+ cells. Western blotting was used to examine apoptosis-related proteins. Flow cytometry was used to measure mitochondrial membrane potential (MMP) and reactive oxygen species (ROS). Results: Equol treatment inhibited HeLa cell proliferation in dose-and time-dependent manner. Equol-induced apoptotic cell death was accompanied by the activation of caspases, and alteration of MMP and mitochondrial membrane proteins; equol also rapidly triggered ROS production. Pre-treatment with N-acetylcysteine blocked loss of MMP, caused increase of Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio, caspase-8 activation, and apoptosis induced by equol. Conclusion: Equol is a potential anticancer agent against HeLa, with possible mechanisms involved in ROS generation and mitochondrial membrane alteration. | - |
dc.format.extent | 8 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | INT INST ANTICANCER RESEARCH | - |
dc.title | Equol Induces Mitochondria-mediated Apoptosis of Human Cervical Cancer Cells | - |
dc.type | Article | - |
dc.publisher.location | 그리이스 | - |
dc.identifier.scopusid | 2-s2.0-84908681867 | - |
dc.identifier.wosid | 000341860700043 | - |
dc.identifier.bibliographicCitation | ANTICANCER RESEARCH, v.34, no.9, pp 4985 - 4992 | - |
dc.citation.title | ANTICANCER RESEARCH | - |
dc.citation.volume | 34 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 4985 | - |
dc.citation.endPage | 4992 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | sci | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.subject.keywordPlus | BREAST-CANCER | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | CASPASE ACTIVATION | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordPlus | SURVIVAL | - |
dc.subject.keywordPlus | THERAPY | - |
dc.subject.keywordPlus | CONSUMPTION | - |
dc.subject.keywordPlus | GENISTEIN | - |
dc.subject.keywordPlus | GROWTH | - |
dc.subject.keywordPlus | TRAIL | - |
dc.subject.keywordAuthor | Equol | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | caspase | - |
dc.subject.keywordAuthor | mitochondria | - |
dc.subject.keywordAuthor | cervical cancer cells | - |
dc.identifier.url | http://ar.iiarjournals.org/content/34/9/4985.short | - |
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