| Fas stimulation activates NF-κB in SK-Hep1 hepatocellular carcinoma cells |
Authors: Hiroshi Okano, Katsuya Shiraki, Hidekazu Inoue, Tomoyuki Kawakita, Yukiko Saitou, Naoyuki Enokimura, Norihiko Yamamoto, Kazushi Sugimoto, Kazumoto Murata, Takeshi Nakano |
Affiliations:
First Department of Internal Medicine, Mie University School of Medicine, Mie 514-8507, Japan
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Pages: 1145-1148 |
Abstract:
The TNF-receptor family has a dual signaling pathway, including induction of apoptosis and NF-κB activation associated with cell survival. Hepatocellular carcinoma (HCC) cells express TNF-receptor family members and the signaling from these receptors induces NF-κB activation. However, the role of Fas in induction of NF-κB 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-κB 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.
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