Kataoka Takao, Ito Mika, Budd Ralph C, Tschopp Jürg, Nagai Kazuo
Department of Bioengineering, Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan.
Exp Cell Res. 2002 Feb 15;273(2):256-64. doi: 10.1006/excr.2001.5438.
The caspase-8 inhibitor c-FLIP blocks death receptor-mediated cell death and plays an essential role in the regulation of lymphocyte homeostasis and the immune escape of tumors. The murine thymoma cell line EL-4 was resistant to Fas ligand (FasL)-induced apoptosis by constitutive expression of FLIP (L). Cycloheximide downregulated the expression of FLIP (L) and markedly sensitized EL-4 cells to FasL-induced apoptosis. In contrast, DNA-damaging agents sensitized EL-4 cells to FasL-induced cell death via an increase of cell-surface Fas without any influence on FLIP (L) expression. Enforced expression of transfected Fas rendered EL-4 cells highly susceptible to FasL-induced cell death. These findings demonstrate that susceptibility to FasL-induced cell death mainly depends on the expression level of c-FLIP versus cell-surface Fas.
半胱天冬酶-8抑制剂c-FLIP可阻断死亡受体介导的细胞死亡,并在淋巴细胞稳态调节和肿瘤免疫逃逸中发挥重要作用。鼠胸腺瘤细胞系EL-4通过组成性表达FLIP(L)对Fas配体(FasL)诱导的凋亡具有抗性。放线菌酮下调FLIP(L)的表达,并显著使EL-4细胞对FasL诱导的凋亡敏感。相反,DNA损伤剂通过增加细胞表面Fas使EL-4细胞对FasL诱导的细胞死亡敏感,而对FLIP(L)的表达没有任何影响。转染的Fas的强制表达使EL-4细胞对FasL诱导的细胞死亡高度敏感。这些发现表明,对FasL诱导的细胞死亡的敏感性主要取决于c-FLIP与细胞表面Fas的表达水平。