Induction of apoptosis in glioma cell lines by TRAIL/Apo-2l

✍ Scribed by Mian Wu; Asha Das; Yan Tan; Cong-ju Zhu; Taian Cui; Meng Cheong Wong

• Publisher: John Wiley and Sons
• Year: 2000
• Tongue: English
• Weight: 230 KB
• Volume: 61
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/1097-4547(20000815)61:4<464::aid-jnr14>3.0.co;2-g

✦ Synopsis

TRAIL/Apo-2L, a novel cytokine, is a member of the tumor necrosis factor (TNF) family and serves as an extracellular signal triggering apoptosis. TRAIL/Apo-2L is capable of killing various transformed cells but not unstimulated primary T cells. In this study, five human glioma cells (U87, U118, U178, U563, and A172) were examined for their susceptibility to the apoptotic effects of TRAIL/Apo-2L. TRAIL/Apo-2L cDNA was isolated by RT-PCR, and recombinant TRAIL/Apo-2L protein was purified by the pMAL-c2 system (New England Biolabs, Beverly, MA). Exposure of A172 cells to bacterially expressed soluble TRAIL/Apo-2L fusion protein at a concentration of 1 g/ml resulted in significant cell death over a 24-h period. Three experiments were performed to suggest that the TRAIL/Apo-2L killing was through the induction of apoptosis of A172 target cells. In addition, the expression of TRAIL/Apo-2L in different glioma cells was found to be variable, and TRAIL/Apo-2L-induced apoptosis was in a cell type-dependent manner. Some correlation between the susceptibility to TRAIL/Apo-2L and the expression level of one of its cognate receptors, DR4, was observed. In addition, cycloheximide worked synergistically with TRAIL/Apo-2L to induce apoptosis in glioma cells.