摘要
目的 pp3501来自19号染色体,是一个功能未知的基因。文中探讨pp3501基因对不同表型肝癌细胞生长的影响。方法将3株肝癌细胞系(HepG2、Hep3B、PLC/PRF/5)分别设空白组、对照组[转染空质粒pEGFPN1入肝细胞癌(hepatocellular carcinoma cells,HCC)细胞]、pp3501组(将pEGFPN1-pp3501转染入HCC细胞)。MTT法和克隆形成率检测肝癌细胞增殖,Western blot检测死亡相关蛋白激酶蛋白(death-associated protein kinase,DAPK)表达。结果 pp3501抑制肝癌细胞增殖,pp3501转染3株肝癌细胞(HepG2细胞、Hep3B细胞和PLC/PRF/5细胞)的克隆形成率分别为48.0%、40.3%和42.2%,均显著低于相应对照组的91.8%、80.1%、80.5%(P<0.05)。pp3501转染组DAPK磷酸化水平降低,灰度值分析均显著低于相应的对照组(P<0.05),但总的DAPK水平不变。结论 pp3501可能通过降低DAPK磷酸化水平激活DAPK抑制肝癌细胞增殖。
Objective pp3501, from chromosome 19, is a gene of unknown function. This study investigated the effect of the pp3501 gene on the growth of different phenotypes of human hepatoeellular carcinoma （HCC） cells. Methods The proliferation of HCC cells was measured by MTT and clone-formation detection. The expression of death-associated protein kinase （DAPK） was de- termined by Western blot. Results pp3501 inhibited the proliferation of HCC cells. The clone formation rates of the three strains of pp3501-transfeeted HCC cells （HepG2, Hep3B and PLC/PRF/5 cells） were 48%, 40.3% and 42.2%, respectively, significantly lower than those in the control group （ P 〈 0.05 ）. The phosphorylation levels and gray values of DAPK were significantly decreased in the pp3501 transfeetion group as compared with those in the control （ P 〈 0.05 ）, but total DAPK levels remained stable. Conclusion pp3501 can inhibit the proliferation of HCC cells by lowering the phosphorylation level of DAPK and activating DAPK.
出处
《医学研究生学报》
CAS
北大核心
2014年第3期236-239,共4页
Journal of Medical Postgraduates
基金
广东省科技计划项目(2008B030301025)
东莞市科技计划项目(200910815258)
关键词
肝癌细胞
pp3501
死亡相关蛋白激酶
Hepatocellular carcinoma cell
pp3501
Death-associated protein kinase protein
