Bcl-2基因加强表达对SK细胞编程死亡的效应  

EFFECTS OF ENFORCED BCL-2 OVER-EXPRESSION ON THE PROGRAMMED CELL DEATH IN THE HUMAN NEUROBLASTOMA SK CELL LINE

作　　者：温龙平[1] 陈亚兵[1] 蔡毓[1] 曾桂生[1] 俞春东[1] 曾定[1] 

机构地区：[1]厦门大学肿瘤细胞工程国家专业实验室,厦门361005

出　　处：《细胞生物学杂志》1996年第2期73-78,共6页Chinese Journal of Cell Biology

基　　金：国家自然科学基金;福建省自然科学基金

摘　　要：TNF和OA诱发人神经母细胞瘤SK细胞编程死亡(PCD)。将编码Bcl-2完整蛋白质的cDNA植入pXJ 41neo载体中,由HCMV病毒启动子控制其表达。形成的正向(pBcl-2-S)及反向(pBcl-2-AS)表达质粒经转染导入SK细胞中获得稳定转染子。Western印迹表明正向转染子表达较大量的26kd Bcl-2蛋白,而反向转染子则不表达。增强表达的Bcl-2基因产物能抑制由TNF引发的PCD,但不影响由OA引发的PCD,从而证明Bcl-2基因产物抗细胞死亡效应的特异性。TNF and OA induce cell death in the human neuroblastoma SK cell line with the characteristic features of apoptosis. A 1.6kb cDNA encoding the full-length human Bcl-2 protein was inserted into mammalian expression vector pXJ 41 neo and placed under the control of HMCV promoter in either the sense (pBcl-2-s) or anti-sense (pBcl-2-AS) orientation. The above two plasmids were transfected into SK cells and stable transfectants were obtained. pBcl-2-S-transfected SK cells expressed high level of 26 Kd Bcl-2 protein, as evidenced by Western blotting, while pBcl-2-AS-transfected cells showed no detectable Bcl-2 expression. Over-expressed Bcl-2 protein effectively inhibited TNF-induced, but not OA-induced SK cell death, therefore demonstrating the specificity of Bcl-2 action.

关 键 词：神经母细胞瘤 SK细胞 细胞编程死亡 基因表达 

分 类 号：R730.264[医药卫生—肿瘤]