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Esculetin induces cell cycle arrest and apoptosis in human colon cancer LoVo cells

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dc.contributor.authorChoi, Yong J.-
dc.contributor.authorLee, Chang M.-
dc.contributor.authorPark, See-Hyoung-
dc.contributor.authorNam, Myeong J.-
dc.date.available2020-07-10T02:38:51Z-
dc.date.created2020-07-06-
dc.date.issued2019-10-
dc.identifier.issn1520-4081-
dc.identifier.urihttps://scholarworks.bwise.kr/hongik/handle/2020.sw.hongik/1082-
dc.description.abstractWe investigated the anti-cancer effects of ESC in human colon cancer LoVo cells. Cell counting assay results showed that ESC inhibited the proliferation of LoVo cells. Cell cycle arrest results showed that cell cycle was arrested during the G0/G1 phase in the ESC-treated LoVo cells. Western blot results showed that the cell cycle inhibitory proteins p53, p27, and p21 were increased, and cyclin D1, the cell cycle progressive protein, was decreased. Sp1 is a transcription factor regulating cell proliferation, was decreased in the ESC-treated LoVo cells. Annexin V/propidium iodide staining results showed that ESC induces apoptosis in LoVo cells. Western blot results showed that Bax, cleaved caspase -3, -7, -9, and poly(ADP-ribose) polymerase, which are proapoptotic proteins, were increased and the antiapoptotic protein Bcl-2 was decreased. Taken together, ESC induced apoptosis and has an anti-cancer effect in LoVo cells.-
dc.language영어-
dc.language.isoen-
dc.publisherWILEY-
dc.subjectTRANSCRIPTION FACTOR SP1-
dc.subjectORAL SQUAMOUS CANCER-
dc.subjectCOLORECTAL-CANCER-
dc.subjectUP-REGULATION-
dc.subjectEXPRESSION-
dc.subjectINHIBITOR-
dc.subjectCOUMARIN-
dc.subjectINDUCTION-
dc.subjectANTITUMOR-
dc.subjectCURCUMIN-
dc.titleEsculetin induces cell cycle arrest and apoptosis in human colon cancer LoVo cells-
dc.typeArticle-
dc.contributor.affiliatedAuthorPark, See-Hyoung-
dc.identifier.doi10.1002/tox.22815-
dc.identifier.scopusid2-s2.0-85069717620-
dc.identifier.wosid000476065800001-
dc.identifier.bibliographicCitationENVIRONMENTAL TOXICOLOGY, v.34, no.10, pp.1129 - 1136-
dc.relation.isPartOfENVIRONMENTAL TOXICOLOGY-
dc.citation.titleENVIRONMENTAL TOXICOLOGY-
dc.citation.volume34-
dc.citation.number10-
dc.citation.startPage1129-
dc.citation.endPage1136-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaEnvironmental Sciences & Ecology-
dc.relation.journalResearchAreaToxicology-
dc.relation.journalResearchAreaWater Resources-
dc.relation.journalWebOfScienceCategoryEnvironmental Sciences-
dc.relation.journalWebOfScienceCategoryToxicology-
dc.relation.journalWebOfScienceCategoryWater Resources-
dc.subject.keywordPlusTRANSCRIPTION FACTOR SP1-
dc.subject.keywordPlusORAL SQUAMOUS CANCER-
dc.subject.keywordPlusCOLORECTAL-CANCER-
dc.subject.keywordPlusUP-REGULATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusINHIBITOR-
dc.subject.keywordPlusCOUMARIN-
dc.subject.keywordPlusINDUCTION-
dc.subject.keywordPlusANTITUMOR-
dc.subject.keywordPlusCURCUMIN-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorcell cycle-
dc.subject.keywordAuthorcolon cancer cell-
dc.subject.keywordAuthoresculetin-
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