Cited 27 times in
Effect of interferon-γ on the susceptibility to Fas (CD95/APO-1)-mediated cell death in human hepatoma cells
DC Field | Value | Language |
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dc.contributor.author | 김호근 | - |
dc.contributor.author | 박전한 | - |
dc.contributor.author | 김세종 | - |
dc.date.accessioned | 2016-02-19T10:59:10Z | - |
dc.date.available | 2016-02-19T10:59:10Z | - |
dc.date.issued | 2001 | - |
dc.identifier.issn | 0340-7004 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/142136 | - |
dc.description.abstract | Many tumors, including hepatocellular carcinomas (HCCs), resist Fas-mediated cell death, which is one of the effector mechanisms in the host's anti-tumor response; however, this resistance can be abolished by interferon-γ (IFN-γ). IFN-γ may sensitize Fas-mediated cell death in several ways, but the exact mechanism in HCCs is uncertain. In this study, we thoroughly investigated the effect of IFN-γ on the susceptibility of one human normal liver cell line and 12 HCC cell lines to Fas-mediated cell death. We also investigated the effect of IFN-γ on the expression of various apoptosis-related genes such as the Fas/TNF-related genes, the bcl-2 family, and the caspase family of genes. Although most cell lines showed considerable constitutive expression of Fas, all tested cell lines resisted Fas-mediated cell death without IFN-γ. When cells were pretreated with IFN-γ, only three cell lines were made significantly susceptible to Fas-mediated cell death (SNU-354, SNU-387 and SNU-423); the other 10 cell lines were not affected. IFN-γ increased the mRNA expression of Fas, TRAIL and caspase-1, and surface Fas was also increased. The strongly sensitized cell lines (SNU-354, SNU-387 and SNU-423) showed a particularly potent increment in surface Fas after IFN-γ treatment (increase in surface Fas >1.7-fold). This result enabled us to conclude that a potent increment of surface Fas expression is a major sensitizing mechanism of IFN-γ. We conclude that IFN-γ cannot play a sensitizing role in most HCC cell lines and that IFN-γ makes HCC cells susceptible to Fas-mediated cell death through a marked up-regulation of surface Fas in some HCC cells. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 23~30 | - |
dc.relation.isPartOf | CANCER IMMUNOLOGY IMMUNOTHERAPY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Apoptosis/drug effects* | - |
dc.subject.MESH | Carcinoma, Hepatocellular/pathology* | - |
dc.subject.MESH | Caspase 1/genetics | - |
dc.subject.MESH | Genes, bcl-2 | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Interferon-gamma/pharmacology* | - |
dc.subject.MESH | Liver Neoplasms/pathology* | - |
dc.subject.MESH | RNA, Messenger/analysis | - |
dc.subject.MESH | Tumor Cells, Cultured | - |
dc.subject.MESH | fas Receptor/genetics | - |
dc.subject.MESH | fas Receptor/physiology* | - |
dc.title | Effect of interferon-γ on the susceptibility to Fas (CD95/APO-1)-mediated cell death in human hepatoma cells | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Microbiology (미생물학) | - |
dc.contributor.googleauthor | Eui-Cheol Shin | - |
dc.contributor.googleauthor | Woo-Chul Shin | - |
dc.contributor.googleauthor | Youjeong Choi | - |
dc.contributor.googleauthor | Hoguen Kim | - |
dc.contributor.googleauthor | Jeon Han Park | - |
dc.contributor.googleauthor | Se Jong Kim | - |
dc.identifier.doi | 10.1007/s002620000166 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01183 | - |
dc.contributor.localId | A01641 | - |
dc.contributor.localId | A00603 | - |
dc.relation.journalcode | J00445 | - |
dc.identifier.eissn | 1432-0851 | - |
dc.identifier.pmid | 11315506 | - |
dc.identifier.url | http://link.springer.com/article/10.1007/s002620000166 | - |
dc.subject.keyword | IFN-γ | - |
dc.subject.keyword | Fas | - |
dc.subject.keyword | Cell death | - |
dc.subject.keyword | Hepatoma | - |
dc.contributor.alternativeName | Kim, Ho Keun | - |
dc.contributor.alternativeName | Park, Jeon Han | - |
dc.contributor.alternativeName | Kim, Se Jong | - |
dc.contributor.affiliatedAuthor | Kim, Ho Keun | - |
dc.contributor.affiliatedAuthor | Park, Jeon Han | - |
dc.contributor.affiliatedAuthor | Kim, Se Jong | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 50 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 23 | - |
dc.citation.endPage | 30 | - |
dc.identifier.bibliographicCitation | CANCER IMMUNOLOGY IMMUNOTHERAPY, Vol.50(1) : 23-30, 2001 | - |
dc.identifier.rimsid | 31632 | - |
dc.type.rims | ART | - |
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