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
Published online on: Monday, September 1, 2003
- Pages: 1145-1148
- DOI: 10.3892/or.10.5.1145
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.