Different effects of p58PITSLRE on the apoptosis induced by etoposide, cycloheximide and serum-withdrawal in human hepatocarcinoma cells

被引:7
作者
Cai, MM [1 ]
Zhang, SW [1 ]
Zhang, S [1 ]
Chen, S [1 ]
Yan, J [1 ]
Zhu, XY [1 ]
Hu, Y [1 ]
Chen, C [1 ]
Gu, JX [1 ]
机构
[1] Fudan Univ, Med Ctr, Ctr Gene Res, Shanghai 20032, Peoples R China
关键词
p58(PITSLRE); apoptosis; etoposide; cycloheximide;
D O I
10.1023/A:1019950819784
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Minimal overexpression of the p58(PITSLRE) protein kinase in Chinese hamster ovary cells induces telephase delay, abnormal cytokinesis, retarded cell growth and apoptosis. Fas mediated T cell death is correlated with p58(PITSLRE) proteolysis and an increase in its histone H1 kinase activity. In this study, it was found that p58(PITSLRE) had different effects on the apoptosis induced by etoposide, cycloheximide and serum-withdrawal in human hepatocarcinoma cells. The ectopic expression of p58(PITSLRE) in human hepatocarcinoma cells suppressed apoptosis induced by etoposide, while enhancing the apoptosis induced by cycloheximide and serum-withdrawal respectively. Elevated expression of p58(PITSLRE) was found during the apoptosis induced by etoposide, whereas most of p58(PITSLRE) was proteolytically processed during apoptosis induced by cycloheximide and serum-withdrawal. Furthermore, transient transfection of p50(PITSLRE) resembling the proteolytic form of p58(PITSLRE) enhanced the 7721 cells susceptibility to apoptosis induced by all the three stimuli. These findings suggest that the full-length p58(PITSLRE) might protect the cells from the apoptosis induced by etoposide and its proteolysis might contribute to and enhance the apoptosis induced by cycloheximide and serum-withdrawal respectively.
引用
收藏
页码:49 / 55
页数:7
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