Fas stimulation activates NF-κB in SK-Hep1 hepatocellular carcinoma cells

被引：0

作者：

Okano, H ^{[1
]}

Shiraki, K ^{[1
]}

Inoue, H ^{[1
]}

Kawakita, T ^{[1
]}

Saitou, Y ^{[1
]}

Enokimura, N ^{[1
]}

Yamamoto, N ^{[1
]}

Sugimoto, K ^{[1
]}

Murata, K ^{[1
]}

Nakano, T ^{[1
]}

机构：

[1] Mie Univ, Sch Med, Dept Internal Med 1, Tsu, Mie 5148507, Japan

来源：

ONCOLOGY REPORTS | 2003年 / 10卷 / 05期

关键词：

Fas; NF-kappa B; hepatocellular carcinoma; TNF-receptor;

D O I：

暂无

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The TNF-receptor family has a dual signaling pathway, including induction of apoptosis and NF-kappaB activation associated with cell survival. Hepatocellular carcinoma (HCC) cells express TNF-receptor family members and the signaling from these receptors induces NF-kappaB activation. However, the role of Fas in induction of NF-kappaB activation in HCC cells is not well understood. In this study, SK-Hep1, HepG2 or HLE cells were stimulated by anti-Fas agonistic antibody. Fas stimulation induced NF-kappaB activation in a dose-dependent manner in SK-Hep1 and HepG2 cell lines, but not in HLE cells. Anti-Fas agonistic antibody or the metabolic inhibitor, cyclo-heximide (CHX), failed to kill SK-Hep1 cells, but co-incubation with anti-Fas agonistic antibody and CHX was effective for induction of apoptosis. SK-Hep1 cell lines receiving Fas stimulation had increased viability, but the extent of cell proliferation was not dose-dependent. The observation suggests that Fas stimulation may contribute to HCC cell survival or proliferation.

引用

页码：1145 / 1148

页数：4

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