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Effect of interferon-γ on the susceptibility to Fas (CD95/APO-1)-mediated cell death in human hepatoma cells

Authors
 Eui-Cheol Shin ; Woo-Chul Shin ; Se Jong Kim ; Jeon Han Park ; Hoguen Kim ; Youjeong Choi 
Citation
 Cancer Immunology Immunotherapy, Vol.50(1) : 23~30, 2001 
Journal Title
 Cancer Immunology Immunotherapy 
ISSN
 0340-7004 
Issue Date
2001
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.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/142136
DOI
10.1007/s002620000166
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Microbiology
1. 연구논문 > 1. College of Medicine > Dept. of Pathology
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Link
 http://link.springer.com/article/10.1007/s002620000166
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