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Sulforaphane enhances caspase-dependent apoptosis through inhibition of cyclooxygenase-2 expression in human oral squamous carcinoma cells and nude mouse xenograft model

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dc.contributor.authorCho, Nam-Pyo-
dc.contributor.authorHan, Hye-Suk-
dc.contributor.authorLeem, Dae-Ho-
dc.contributor.authorChoi, In-Sun-
dc.contributor.authorJung, Ji-Youn-
dc.contributor.authorKim, Hyeong-Jin-
dc.contributor.authorMoon, Kyung-Suk-
dc.contributor.authorChoi, Kyeong-Hee-
dc.contributor.authorSoh, Yunjo-
dc.contributor.authorKong, Gu-
dc.contributor.authorCho, Sung-Dae-
dc.contributor.authorChoi, Seoung Hwan-
dc.date.accessioned2022-12-20T21:23:55Z-
dc.date.available2022-12-20T21:23:55Z-
dc.date.created2022-08-26-
dc.date.issued2009-08-
dc.identifier.issn1368-8375-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/176391-
dc.description.abstractIn this study, we found that oral squamous cell carcinomas (OSCCs) in Korean patients have a high level of COX-2 expression when compared with normal mucosa. Sulforaphane (SFN), rich in cruciferous vegetables, has been reported to display anti-cancer activity against many cancers. However, the effect and molecular mechanism of SFN in the proliferation of OSCC still remains unclear. To elucidate this mechanism, we investigated the anti-proliferative effect of SFN on KB and YD-10B cells and demonstrated that SFN significantly induced caspase-dependent apoptosis. Also, we observed that SFN inhibited COX-2 but not COX-1. In addition, bcl-2 protein, one of downstream targets of COX-2, was down-regulated by SFN. Furthermore, SFN also inhibited tumor growth in KB cell xenografts. These results show that SFN can act as a potent anti-oral cancer compound by inhibiting COX-2 activity.-
dc.language영어-
dc.language.isoen-
dc.publisherELSEVIER-
dc.titleSulforaphane enhances caspase-dependent apoptosis through inhibition of cyclooxygenase-2 expression in human oral squamous carcinoma cells and nude mouse xenograft model-
dc.typeArticle-
dc.contributor.affiliatedAuthorKong, Gu-
dc.identifier.doi10.1016/j.oraloncology.2008.07.003-
dc.identifier.scopusid2-s2.0-67650401078-
dc.identifier.wosid000268112800002-
dc.identifier.bibliographicCitationORAL ONCOLOGY, v.45, no.8, pp.654 - 660-
dc.relation.isPartOfORAL ONCOLOGY-
dc.citation.titleORAL ONCOLOGY-
dc.citation.volume45-
dc.citation.number8-
dc.citation.startPage654-
dc.citation.endPage660-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalResearchAreaDentistry, Oral Surgery & Medicine-
dc.relation.journalWebOfScienceCategoryOncology-
dc.relation.journalWebOfScienceCategoryDentistry, Oral Surgery & Medicine-
dc.subject.keywordPlusNONSTEROIDAL ANTIINFLAMMATORY DRUGS-
dc.subject.keywordPlusPROSTATE-CANCER CELLS-
dc.subject.keywordPlusMEDIATED APOPTOSIS-
dc.subject.keywordPlusTUMOR-GROWTH-
dc.subject.keywordPlusCYCLE ARREST-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusNECK-CANCER-
dc.subject.keywordPlusIN-VIVO-
dc.subject.keywordPlusHEAD-
dc.subject.keywordPlusISOTHIOCYANATE-
dc.subject.keywordAuthorHuman oral squamous cell carcinoma-
dc.subject.keywordAuthorSulforaphane-
dc.subject.keywordAuthorApoptosis-
dc.subject.keywordAuthorCOX-2-
dc.subject.keywordAuthorbcl-2-
dc.subject.keywordAuthorXenograft-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S1368837508002157?via%3Dihub-
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