转导野生型p53的K562细胞出现生长抑制和凋亡  

Presentation of growth retardation and apoptosis in the wild p53 transduced K562 cells

作　　者：陈德喜[1] 王申五[1] 曹国栋[1] 马丽萍[1] 潘秀英[1] 

机构地区：[1]北京医科大学人民医院中心实验室,北京100044

出　　处：《中国实验血液学杂志》1998年第3期224-226,共3页Journal of Experimental Hematology

基　　金：国家自然科学基金 编号39470316

摘　　要：把重组有编码野生型p53的逆转录病毒载体转导到p53蛋白缺失的K562细胞,以观察野生型p53蛋白在K562细胞表达后对K562细胞增殖和凋亡的影响。应用RT-PCR和Western印迹杂交方法检测K562细胞p53表达,应用流式细胞仪计数检测细胞的增殖,采用梯形DNA和细胞形态学方法检测细胞凋亡变化。研究结果表明:感染pLXSN-p53病毒24小时后,K562细胞p53表达阳性,K562-p53细胞的生长受到抑制,少数细胞进入凋亡状态。结论提示,野生型p53可促进p53表达阴性的K562细胞生长抑制与凋亡。The wild type p53-coding sequence recombined in retroviral vector (pLXSN) was transfered into the p53 deficient cell line (K562) in order to observe p53 gene expression, cell proliferation and apoptosis. RT-PCR and Western blot were used to detect the expression of p53 mRNA and protein respectively in the transduced K562 cells, flow cytometry was used to analyze cell proliferation, DNA 'ladder' and morphological changes were used to study apoptosis. Results showed that p53 expression in K562 cells became positive after pLXSN-p53 was transduced 96 hours. The cell growth was inhibited while some cells were getting on apoptosis. Conclusion suggested that the wild p53 could promote growth retardation and apoptosis of K562 cells.

关 键 词：K562细胞 细胞凋亡 P53基因 PLXSN 

分 类 号：R733.7[医药卫生—肿瘤] Q782[医药卫生—临床医学]