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dc.contributor.authorPark, So Young-
dc.contributor.authorNho, Chu Won-
dc.contributor.authorKwon, Dae Young-
dc.contributor.authorKang, Young-Hee-
dc.contributor.authorLee, Ki Won-
dc.contributor.authorPark, Jung Han Yoon-
dc.date.accessioned2024-01-20T13:03:16Z-
dc.date.available2024-01-20T13:03:16Z-
dc.date.created2021-09-01-
dc.date.issued2013-01-28-
dc.identifier.issn0007-1145-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/128433-
dc.description.abstractMaslinic acid is found in various natural sources, most notably in pomace olive oil, and exerts pro-apoptotic activities in various cancer cells in vitro. In the present study, DU145 human prostate cancer cells were cultured with 0-25 mM-maslinic acid to examine the effects of maslinic acid on the metastatic capacity of prostate cancer cells. Maslinic acid significantly (P < 0.05) inhibited the basal and epidermal growth factor (EGF)-induced migration (27-64 %), invasion (23-60%) and adhesion (8-40%) of DU145 cells. Maslinic acid significantly (P < 0.05) down-regulated both basal and EGF-stimulated secretion of matrix metalloproteinase (MMP)-9 (25-67 %), MMP-2 (50-86 %), urokinase-type plasminogen activator (uPA, about 100 %), vascular endothelial growth factor (VEGF, 98-100 %) and tissue inhibitors of metalloproteinases (TIMP)-1, as well as expression of uPA receptor (uPAR), intercellular adhesion molecules (22-33 %), vascular cell adhesion molecules (23-46%) and E-cadherin, whereas it increased TIMP-2 secretion. Maslinic acid dramatically reduced the levels of hypoxia-inducible factor-1 alpha (HIF-1 alpha) protein and mRNA; the reduction was accompanied by reduced stability, nuclear levels and transcriptional activity of HIF-1 alpha. The levels of phospho-Akt and phospho-extracellular signal-related kinase (ERK) were reduced in cells treated with maslinic acid, and the phosphoinositide 3-kinase inhibitor LY294002 and the mitogen-activated protein kinase kinase inhibitor PD98059 reduced HIF-1 alpha levels and VEGF secretion. The results show that maslinic acid markedly inhibited the migration, invasion and adhesion of DU145 prostate cancer cells. Suppressing HIF-1 alpha activation by inhibiting Akt and ERK activation may be part of the mechanism by which maslinic acid inhibited uPAR, E-cadherin, VEGF and MMP expression in DU145 cells.-
dc.languageEnglish-
dc.publisherCAMBRIDGE UNIV PRESS-
dc.subjectMATRIX METALLOPROTEINASES-
dc.subjectNATURAL TRITERPENE-
dc.subjectFACTOR 1-ALPHA-
dc.subjectTUMOR-GROWTH-
dc.subjectEXPRESSION-
dc.subjectPROLIFERATION-
dc.subjectANGIOGENESIS-
dc.subjectPATHWAY-
dc.subjectHYPOXIA-INDUCIBLE-FACTOR-1-ALPHA-
dc.subjectHIF-1-ALPHA-
dc.titleMaslinic acid inhibits the metastatic capacity of DU145 human prostate cancer cells: possible mediation via hypoxia-inducible factor-1 alpha signalling-
dc.typeArticle-
dc.identifier.doi10.1017/S0007114512000967-
dc.description.journalClass1-
dc.identifier.bibliographicCitationBRITISH JOURNAL OF NUTRITION, v.109, no.2, pp.210 - 222-
dc.citation.titleBRITISH JOURNAL OF NUTRITION-
dc.citation.volume109-
dc.citation.number2-
dc.citation.startPage210-
dc.citation.endPage222-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000313975800003-
dc.identifier.scopusid2-s2.0-84873045777-
dc.relation.journalWebOfScienceCategoryNutrition & Dietetics-
dc.relation.journalResearchAreaNutrition & Dietetics-
dc.type.docTypeArticle-
dc.subject.keywordPlusMATRIX METALLOPROTEINASES-
dc.subject.keywordPlusNATURAL TRITERPENE-
dc.subject.keywordPlusFACTOR 1-ALPHA-
dc.subject.keywordPlusTUMOR-GROWTH-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusANGIOGENESIS-
dc.subject.keywordPlusPATHWAY-
dc.subject.keywordPlusHYPOXIA-INDUCIBLE-FACTOR-1-ALPHA-
dc.subject.keywordPlusHIF-1-ALPHA-
dc.subject.keywordAuthorMetastasis-
dc.subject.keywordAuthorProstate cancer cells-
dc.subject.keywordAuthorHypoxia-inducible factor-1 alpha-
dc.subject.keywordAuthorVascular endothelial growth factor-
dc.subject.keywordAuthorMatrix metalloproteinase-
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