c-Jun involvement in vitamin E succinate induced apoptosis of reticuloendotheliosis virus transformed avian lymphoid cells
c-Jun involvement in vitamin E succinate induced apoptosis of reticuloendotheliosis virus transformed avian lymphoid cells
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DOI：
10.1038/sj.onc.1201181
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发表时间：
1997-07-10
期刊：
影响因子：
8
通讯作者：
Kline, K
中科院分区：
文献类型：
--
作者：
Qian, M;Kralova, J;Kline, K
先前的研究已经表明，用10 μ g/ml的抗禽网状内皮组织增生病病毒转化的RECC-UTC 4 -1（C4-1）类淋巴母细胞处理（18.8 μ M）RRR-alpha-生育酚琥珀酸酯维生素E琥珀酸酯（vitamin E succinate，VES）处理3天诱导约50%的细胞发生凋亡。c-jun mRNA和蛋白质的表达升高和延长与VES诱导的细胞死亡在时间上相关，这篇论文中提供的数据表明，c-jun信息和蛋白质的升高和延长的表达不是由增强的稳定性引起的，并且表明c-Jun参与VES诱导的这种淋巴母细胞样细胞类型的细胞凋亡，用携带c-Jun的显性负作用突变形式supjun-1的病毒感染的C4-1细胞表现出：（i）VES诱导的细胞凋亡减少71%，（ii）野生型内源性c-Jun表达减少2.0-2.5倍，和（iii）AP-1结合活性减少2.4-2.6倍。此外，用VES加RRR-a-生育酚共处理的细胞显示细胞凋亡减少70%，c-Jun表达显著降低，AP-1结合活性降低1.6倍。这些研究表明，c-Jun在VES诱导的C4-1细胞凋亡中起关键作用，并增加了对VES介导的肿瘤细胞生长抑制作用机制的理解。
Previous studies have shown that treatment of avian reticuloendotheliosis virus-transformed RECC-UTC4-1 (C4-1) lymphoblastoid cells with 10 mu g/ml (18.8 mu M) of RRR-alpha-tocopheryl succinate (vitamin E succinate, VES) for 3 days induced approximately 50% of the cells to undergo apoptosis, Elevated and prolonged expression of c-jun mRNA and protein was temporally correlated with VES-induced cell death, Data presented in this paper show that the elevated and prolonged expression of c-jun message and protein are not accounted for by enhanced stability, and show the involvement of c-Jun in VES-induced apoptosis in this lymphoblastoid cell type, C4-1 cells infected with a virus carrying a dominant, negatively acting mutant form of c-Jun, supjun-1, exhibited: (i) 71% reduction in VES-induced apoptosis, (ii) a 2.0-2.5-fold decrease in wildtype, endogenous c-Jun expression, and (iii) a 2.4-2.6-fold reduction in AP-1 binding activity, Additionally, cells co-treated with VES plus RRR-alpha-tocopherol, exhibited a 70% reduction in apoptosis, a marked reduction in c-Jun expression and a 1.6-fold reduction in AP-1 binding activity, These studies suggest that c-Jun plays a crucial role in VES-induced apoptosis in C4-1 cells, and add to understanding of mechanisms of action involved VES-mediated tumor cell growth inhibition.