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Apoptosis of human fibrosarcoma HT-1080 cells by epigallocatechin-3-O-gallate via induction of p53 and caspases as well as suppression of Bcl-2 and phosphorylated nuclear factor-κB.

DC FieldValueLanguage
dc.contributor.author박종철-
dc.contributor.author이미희-
dc.date.accessioned2014-12-20T16:25:10Z-
dc.date.available2014-12-20T16:25:10Z-
dc.date.issued2011-
dc.identifier.issn1360-8185-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/92680-
dc.description.abstractAnimal tumor bioassays and in vitro cell culture systems have demonstrated that epigallocatechin-3-O-gallate (EGCG), the predominant catechin in green tea, possesses anti-proliferative and pro-apoptotic effects on various cancer cells and tumors. In this study, we investigated the effects of EGCG on cell growth, cell cycle progression, and apoptosis in human fibrosarcoma HT-1080 cells. The involvement of p53, Bcl-2, Bax, caspases, and nuclear factor-κB (NF-κB) was examined as a mechanism for the anti-cancer activity of EGCG. Time-dependent intracellular trafficking of EGCG was also determined using fluorescein isothiocyanate (FITC)-conjugated EGCG (FITC-EGCG). Our data show that EGCG treatment caused dose-dependent cell growth inhibition, cell cycle arrest at the G(0)/G(1) phase, and DNA fragmentation suggesting the induction of apoptosis in HT-1080 cells. Immunoblot analysis revealed that the expression of p53, caspase-7 and -9 as well as the ratio of Bax/Bcl-2 protein increased significantly with higher EGCG concentrations and longer incubation times. Moreover, expression of phosphorylated NF-κB/p65 in HT-1080 cells was inhibited by EGCG treatment in a dose-dependent manner, while that of unphosphorylated NF-κB/p65 remained unaffected. Here we also reveal time-dependent internalization of FITC-EGCG into the cytosol of HT-1080 cells and its subsequent nuclear translocation. These results suggest that EGCG may interrupt exogenous signals directed towards genes involved in proliferation and cell cycle progression. Taken together, our data indicate that HT-1080 apoptosis may be mediated through the induction of p53 and caspases by the pro-oxidant activity of internalized EGCG, as well as suppression of Bcl-2 and phosphorylated NF-κB by the antioxidant activity of EGCG.-
dc.description.statementOfResponsibilityopen-
dc.format.extent75~85-
dc.relation.isPartOfApoptosis-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHActive Transport, Cell Nucleus/drug effects-
dc.subject.MESHAnticarcinogenic Agents/pharmacology*-
dc.subject.MESHAnticarcinogenic Agents/therapeutic use-
dc.subject.MESHApoptosis*/drug effects-
dc.subject.MESHCaspases/genetics-
dc.subject.MESHCaspases/metabolism*-
dc.subject.MESHCatechin/analogs & derivatives*-
dc.subject.MESHCatechin/pharmacology-
dc.subject.MESHCatechin/therapeutic use-
dc.subject.MESHCell Cycle/drug effects-
dc.subject.MESHCell Division/drug effects-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHCell Nucleus/genetics-
dc.subject.MESHCell Nucleus/metabolism-
dc.subject.MESHFibrosarcoma/drug therapy-
dc.subject.MESHFibrosarcoma/genetics-
dc.subject.MESHFibrosarcoma/metabolism-
dc.subject.MESHGene Expression/drug effects-
dc.subject.MESHHumans-
dc.subject.MESHNF-kappa B/antagonists & inhibitors*-
dc.subject.MESHNF-kappa B/genetics-
dc.subject.MESHNF-kappa B/metabolism-
dc.subject.MESHPhosphorylation/drug effects-
dc.subject.MESHProto-Oncogene Proteins c-bcl-2/antagonists & inhibitors*-
dc.subject.MESHProto-Oncogene Proteins c-bcl-2/genetics-
dc.subject.MESHProto-Oncogene Proteins c-bcl-2/metabolism-
dc.subject.MESHSignal Transduction/drug effects-
dc.subject.MESHTumor Suppressor Protein p53/genetics-
dc.subject.MESHTumor Suppressor Protein p53/metabolism*-
dc.subject.MESHbcl-2-Associated X Protein/genetics-
dc.subject.MESHbcl-2-Associated X Protein/metabolism*-
dc.titleApoptosis of human fibrosarcoma HT-1080 cells by epigallocatechin-3-O-gallate via induction of p53 and caspases as well as suppression of Bcl-2 and phosphorylated nuclear factor-κB.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Medical Engineering (의학공학)-
dc.contributor.googleauthorMi Hee Lee-
dc.contributor.googleauthorDong-Wook Han-
dc.contributor.googleauthorSuong-Hyu Hyon-
dc.contributor.googleauthorJong-Chul Park-
dc.identifier.doi10.1007/s10495-010-0548-y-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01662-
dc.contributor.localIdA02777-
dc.relation.journalcodeJ00195-
dc.identifier.pmid20963498-
dc.identifier.urlhttp://link.springer.com/article/10.1007%2Fs10495-010-0548-y-
dc.subject.keywordEpigallocatechin-3-O-gallate-
dc.subject.keyword Human fibrosarcoma cells-
dc.subject.keyword Apoptosis-
dc.subject.keyword p53 Caspases -
dc.subject.keywordNuclear factor-κB -
dc.contributor.alternativeNamePark, Jong Chul-
dc.contributor.alternativeNameLee, Mi Hee-
dc.contributor.affiliatedAuthorPark, Jong Chul-
dc.contributor.affiliatedAuthorLee, Mi Hee-
dc.rights.accessRightsnot free-
dc.citation.volume16-
dc.citation.number1-
dc.citation.startPage75-
dc.citation.endPage85-
dc.identifier.bibliographicCitationApoptosis, Vol.16(1) : 75-85, 2011-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Medical Engineering (의학공학교실) > 1. Journal Papers

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