DAPK对IFN-γ抑制PGCl_3细胞恶性表型的影响  

Effect on the IFN-γ Inhibit the Malignant Pheotype in PGCl_3 Cells by DAPK

作　　者：伍俊[1] 梁标[1] 郭兰萍[1] 

机构地区：[1]广东医学院附属医院呼吸疾病研究所,广东湛江524001

出　　处：《肿瘤防治研究》2006年第2期90-93,共4页Cancer Research on Prevention and Treatment

摘　　要：目的探讨肿瘤转移抑制基因DAPK对IFN-γ抑制高转移肺癌PGCl3细胞株运动、侵袭、黏附、克隆形成率的影响。方法用脂质体介导的基因转染方法,借助真核质粒表达载体pcDNA3.1,将抑癌基因DAPK转入高转移肺癌PGCl3细胞中,经G418筛选,获得稳定表达的细胞克隆。观察DAPK增强INF-γ抑制PGCl3细胞增殖、运动、侵袭、黏附、克隆形成率。结果DAPK基因转染的PGCl3细胞对INF-γ敏感。IFN-γ抑制转染DAPK基因的PGCl3细胞的增殖、侵袭能力、运动能力、黏附能力、克隆形成率,而且IFN-γ的影响呈剂量依赖性。结论肿瘤转移抑制基因DAPK增强INF-γ抑制PGCl3细胞的恶性表型。Objective To investigate the effect of metastasis suppress gene death-associated protein kinase （DAPK） on IFN-γ inhibit PGCl3 cells growth, invasive, migration and adhesion ability and the number of colony formation. Methods PGCl3 cells were transfected with pcDNA3. 1-DAPK by lipofectamine 2000 and the PGCl3 cells colon of expression DAPK were selected by G418. PGCh cells growth, invasive, migration and adhesion ability and the number of colony formation were examined. Results PGCl3 cells transfected by DAPK gene were sensitive to INF-γ. IFN-γ inhibited the growth of pcDNA3. 1-DAPK- transfected PGCl3 cells and decreased pcDNA3. 1-DAPK-transfected PGCl3 cells invasive, migration and adhesion ability and the number of colony formation in dose-depend manner. Conclusion Metastasis suppress gene DAPK could enhance INF-γ to inhibit PGCl3 cells malignant pheotype.

关 键 词：死亡相关蛋白激酶 转移 肺癌 

分 类 号：R734.2[医药卫生—肿瘤]