保罗样激酶基因沉默体外抑制胶质瘤细胞侵袭与生长  

Invasion and Growth inhibition by plkl silencing in glioma cells in vitro

作　　者：张健[1] 石松生[2] 兰斌[3] 刘楠[1] 郑安[1] 杨卫忠[2] 

机构地区：[1]福建医科大学附属协和医院神经内科,福州350001 [2]福建医科大学附属协和医院神经外科,福州350001 [3]福建医科大学附属第一医院肿瘤外科

出　　处：《中华神经外科杂志》2007年第6期473-475,共3页Chinese Journal of Neurosurgery

摘　　要：目的观察保罗样激酶1基因(plk1)沉默对胶质瘤细胞株-H4体外生长的抑制作用,探讨plk1基因作为胶质瘤治疗靶点的可行性。方法化学合成小片断干扰RNA(siRNA)抑制plk1基因的表达,Western blot检测plk1蛋白质的表达变化,流式细胞仪检测H4细胞周期分布及凋亡程度的变化,体外侵袭实验检测H4细胞侵袭能力的变化,MTT法检测H4细胞增殖速度的变化。结果经siRNA作用48h后,plk1蛋白质水平明显降低;较多的H4细胞聚集于G2/M期附近(P<0.05);细胞凋亡明显上升(P<0.05);细胞体外侵袭能力下降(P<0.05);增殖速度明显缓于对照组(P< 0.05)。结论靶向plk1的siRNA可在体外抑制胶质瘤细胞H4的侵袭与增殖,plk1有可能成为新的潜在胶质瘤治疗靶点。Objective To observe the effect of plkl gene silencing on the growth of glioma cell line- H4 in vitro and discuss the possibility of arranging plkl as therapeutic target for glioma. Methods The plkl expression was inhibited by chemically synthesized siRNA, the plkl protein level were detected by Western blot, the change of cell cycle distribution and apoptosis was measured by flow-cytometry, the H4 cell proliferation was measured by MTY assay, lastly, the ability of H4 cell invasion in vitro was measured by cell migration and invasion assay. Results After treatment with plkl siRNA, plkl protein level decreased obviously, more H4 cells accumulated at G2/M phase and showed a higher degree of apoptosis（ P 〈 0.05 ） , H4 cells treated by plkl siRNA showed lower invasion ability in vitro（ P 〈 0.05 ）, and proliferated slowerly than control group（ P 〈 0.05 ） , Conclusions siRNA targeting plkl could inhibit invasion and proliferation of H4 cells in vitro, plkl may become another novel and potential therapeutic target for glioma.

关 键 词：脑胶质瘤 小片断干扰RNA 保罗样激酶1 有丝分裂 

分 类 号：R739.4[医药卫生—肿瘤]