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Human hepatocellular carcinoma cells resist to TRAIL-induced apoptosis, and the resistance is abolished by cisplatin

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dc.contributor.author김건홍-
dc.contributor.author김세종-
dc.contributor.author김철훈-
dc.contributor.author김호근-
dc.contributor.author박전한-
dc.contributor.author안영수-
dc.date.accessioned2016-05-16T10:56:15Z-
dc.date.available2016-05-16T10:56:15Z-
dc.date.issued2002-
dc.identifier.issn1226-3613-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/143434-
dc.description.abstractTNF-related apoptosis-inducing ligand (TRAIL), a member of the TNF family, selectively induce apoptosis in various transformed cell lines but not in almost-normal tissues. It is regulated by 2 death receptors, TRAIL receptor 1(TRAIL-R1) and TRAIL-R2 and 2 decoy receptors, TRAIL-R3 and TRAIL-R4. However, the determining factors of the sensitivity to TRAIL-induced apoptosis are not clearly understood. Herein, we investigated the expression of TRAIL-R, c-FLIP, FADD-like interleukin-1β-converting enzyme inhibitory protein, and TRAIL-induced apoptosis in human hepatocellular carcinoma (HCC) cell lines. Seven of ten HCC cell lines showed resistance to TRAIL-induced apoptosis and five of seven TRAIL-resistant cell lines became sensitive to TRAIL by co-treatment with cycloheximide. In HCC cell lines, their TRAIL resistance did not correlate with the basal expression level of TRAIL receptors or c-FLIP, however, in human tissues, TRAIL-R1 and TRAIL-R2 expressions were notably decreased compared to normal counterpart. Cisplatin showed synergistic effect on TRAIL-induced apoptosis in most HCC cell lines regardless of their p53 status and TRAIL-R1 was induced by cisplatin treatment in certain cell lines. Inhibition of nuclear factor K B (NF-κB) by SN50, a peptide inhibitor of NF-κB activity, had no effect on TRAIL-induced apoptosis in HCC cells. These results suggest that (a) the majority of human HCC cell lines are resistant to TRAIL-induced apoptosis and cycloheximide-sensitive short-lived antiapoptotic molecule(s) is responsible for this resistance, (b) the expression of TRAIL-R1 and TRAIL-R2 is reduced in HCC tissues, and the increased expression of TRAIL-R1 may be a mechanism of cisplatininduced sensitization to TRAIL-induced apoptosis in some HCC cells, and (c) the activation of NF-κB may not be involved in the TRAIL resistance of HCC cells.-
dc.description.statementOfResponsibilityopen-
dc.format.extent114~122-
dc.relation.isPartOfEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHApoptosis*-
dc.subject.MESHApoptosisRegulatory Proteins-
dc.subject.MESHCASP8 and FADD-LikeApoptosisRegulating Protein-
dc.subject.MESHCarcinoma,Hepatocellular/pathology*-
dc.subject.MESHCarrier Proteins/genetics-
dc.subject.MESHCellLine-
dc.subject.MESHCisplatin/pharmacology*-
dc.subject.MESHCycloheximide/metabolism-
dc.subject.MESHHumans-
dc.subject.MESHIntracellular Signaling Peptides and Proteins*-
dc.subject.MESHMembrane Glycoproteins/physiology*-
dc.subject.MESHNF-kappa B/metabolism-
dc.subject.MESHPeptides/metabolism-
dc.subject.MESHReceptors, Tumor Necrosis Factor/genetics-
dc.subject.MESHTNF-RelatedApoptosis-Inducing Ligand-
dc.subject.MESHTumor Necrosis Factor-alpha/physiology*-
dc.titleHuman hepatocellular carcinoma cells resist to TRAIL-induced apoptosis, and the resistance is abolished by cisplatin-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pharmacology (약리학)-
dc.contributor.googleauthorEui Cheol Shin-
dc.contributor.googleauthorYoung Rim Seong-
dc.contributor.googleauthorChul Hoon Kim-
dc.contributor.googleauthor, Hoguen Kim-
dc.contributor.googleauthorYoung Soo Ahn-
dc.contributor.googleauthorKunhong Kim-
dc.contributor.googleauthorSe Jong Kim-
dc.contributor.googleauthorSeung Suh Hong-
dc.contributor.googleauthorJeon Han Park-
dc.identifier.doi10.1038/emm.2002.17-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00289-
dc.contributor.localIdA00603-
dc.contributor.localIdA01057-
dc.contributor.localIdA01183-
dc.contributor.localIdA01641-
dc.contributor.localIdA02246-
dc.relation.journalcodeJ00860-
dc.identifier.eissn2092-6413-
dc.identifier.pmid12085986-
dc.subject.keywordTRAIL-
dc.subject.keywordapoptosis-
dc.subject.keywordHCC-
dc.subject.keywordcisplatin-
dc.subject.keywordcycloheximide-
dc.contributor.alternativeNameKim, Kun Hong-
dc.contributor.alternativeNameKim, Se Jong-
dc.contributor.alternativeNameKim, Chul Hoon-
dc.contributor.alternativeNameKim, Ho Keun-
dc.contributor.alternativeNamePark, Jeon Han-
dc.contributor.alternativeNameAhn, Young Soo-
dc.contributor.affiliatedAuthorKim, Kun Hong-
dc.contributor.affiliatedAuthorKim, Se Jong-
dc.contributor.affiliatedAuthorKim, Chul Hoon-
dc.contributor.affiliatedAuthorKim, Ho Keun-
dc.contributor.affiliatedAuthorPark, Jeon Han-
dc.contributor.affiliatedAuthorAhn, Young Soo-
dc.rights.accessRightsfree-
dc.citation.volume34-
dc.citation.number2-
dc.citation.startPage114-
dc.citation.endPage122-
dc.identifier.bibliographicCitationEXPERIMENTAL AND MOLECULAR MEDICINE, Vol.34(2) : 114-122, 2002-
dc.identifier.rimsid53166-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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