Dickkopf1(DKK1)逆转白血病细胞K562/NDR恶性表型及其机制  

Dickkopf1( DKK1) reverses the malignant phenotype of leukemia cell K562/NDR and its mechanism

作　　者：张嵘[1] 苗苗[1] 王洪涛[1] 李佳[1] 杨莹[1] 刘卓刚[1] 

机构地区：[1]中国医科大学附属盛京医院血液内科,辽宁沈阳110004

出　　处：《现代肿瘤医学》2016年第9期1361-1363,共3页Journal of Modern Oncology

摘　　要：目的:研究DKK1对白血病细胞K562/NDR恶性表型的影响及其机制。方法:分别利用MTT实验、PI染色、Annexin V-FITC/PI双染和Transwell实验检测DKK1蛋白处理后K562/NDR细胞的增殖、周期、凋亡和运动性。Western blot技术检测DKK1抗肿瘤机制。结果:DKK1可以明显抑制K562/NDR细胞增殖和运动,导致其凋亡和细胞周期阻滞。DKK1处理后K562/DNR细胞Cyclin D和Cyclin E蛋白表达下降,E-cadherin表达水平升高,N-cadherin表达下降。结论:DKK1可以通过抑制Cyclin D、Cyclin E和N-cadherin蛋白表达逆转K562/NDR细胞恶性表型。Objective：To detect the effects and mechanisms of DKK1 on the malignant phenotype of leukemia cell K562/NDR. Methods ： The proliferative ratio, cell cycle, apoptotic ratio, and mobility of K562/NDR cells after treated with DKK1 was detected by MTT assay, PI staining, Annexin V -FITC/PI double staining, and Transwell assay, respectively. The mechanisms were analyzed by Western blot. Results：DKK1 could inhibit proliferation and mobility, and induce cell cycle arrest and apoptosis in K562/NDR cells. The levels of Cyclin D, Cyclin E, and N - cadherin were downregulated, while E - cadherin was upregulated in treated cells than untreated ones. Conclusion： DKK1 could reverse the malignant phenotype of leukemia cell K562/NDR by suppressing Cyclin D, Cyclin E, and N - cadherin ex- pression.

关 键 词：K562/NDR细胞 DKK1 凋亡 增殖 运动 

分 类 号：R730.54[医药卫生—肿瘤] R733.7[医药卫生—临床医学]