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

摘要

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,re-spectively.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.%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 －cad-herin 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。