EDAG在白血病细胞系K562中的细胞内自激因子作用  

Intracrine role of EDAG in leukemia cell line K562

作　　者：安莉莉[1] 吴克复[1] 马小彤[1] 林永敏[1] 郑国光[1] 

机构地区：[1]中国医学科学院中国协和医科大学血液学研究所,实验血液学国家重点实验室,天津300020

出　　处：《白血病．淋巴瘤》2005年第4期197-200,共4页Journal of Leukemia & Lymphoma

基　　金：高等学校博士学科点专项科研基金资助(20020023015)

摘　　要：目的为肿瘤细胞自律性生长的细胞内自激因子假设提供实验证据。方法将新发现的造血相关核蛋白EDAG基因转染人白血病细胞系K562,比较过表达EDAG对K562细胞的增生能力,以及对细胞的造血调控、凋亡及细胞周期相关蛋白表达的影响。结果在无血清培养条件下,过表达EDAG的K562细胞的增生能力明显高于两组对照细胞,并且有c蛳myb和bcl蛳2mRNA表达的显著上调。结论过表达的EDAG可以起细胞内自激因子作用。为核蛋白异常表达可以起细胞内自激因子作用提供了实验证据。Objective To confirm the hypothesis of intracrine for tumor growth autonomy. Methods The novel hemopoietic nuclear protein EDAG gene was transfected into leukemia cell line K562. Then we studied the biological effects of overexpression of EDAG in K562 cells such as the proliferation and the expression of of some genes related to cell cycle,apoptosis or hematopoiesis. Results As compared with the control K562 cells, under serum-free condition,＂the overexpression of EDAG resulted in the promotion of cell proliferation and increase in the expression of c-myb and＂ bcl-2 gene.Conclusion Overexpression of EDAG could accelerate the autonomous growth of K562 cells, thus providing evidence for the hypothesis that the abnormal expression of nuclear proteins could promote tumor growth autonomy by intracrion.

关 键 词：自律性生长 细胞内自激因子 核蛋白 EDAG 白血病细胞系 

分 类 号：R733.7[医药卫生—肿瘤]