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目的:探讨B细胞特异性莫洛尼氏白血病毒插入位点1(Bmi-1)沉默对前列腺癌PC-3细胞增殖迁移的影响及对同源性磷酸酶和张力蛋白基因(PTEN)/磷酸化蛋白激酶B(pAkt)通路的作用。方法:将Bmi-1小干扰RNA(siRNA)序列及阴性对照序列转入PC-3细胞，设为Si-Bmi-1组和Si-NC组，稳定转染Bmi-1 siRNA序列的细胞用PTEN抑制剂胰岛素模拟物Bpv干预，设为Si-Bmi-1-Bpv组。采用噻唑蓝(MTT)法和划痕实验检测各组细胞增殖和迁移能力，采用腋窝皮下接种法测细胞成瘤能力，采用蛋白质印迹法(Western blot)检测各组PTEN、pAkt蛋白表达。采用单因素方差分析多样本计量资料，采用n t检验分析两两样本的差异。n 结果:Si-Bmi-1组(0.315±0.030、0.480±0.050、0.659±0.085)和Si-Bmi-1-Bpv组(0.364±0.025、0.702±0.063、0.986±0.091) MTT实验24、48、72 h的吸光度值均低于对照组的(0.401±0.035、0.871±0.071、1.135±0.097)和Si-NC组的(0.398±0.031、0.859±0.067、1.107±0.092，n t＝24.196，n P<0.01；n t＝95.326，n P<0.01；n t＝72.103，n P<0.01)，差异均有统计学意义。Si-Bmi-1组和Si-Bmi-1-Bpv组细胞迁移率分别为(32.37±4.25)%、(55.84±5.27)%，均低于对照组和Si-NC组[(64.08±4.91)%、(63.75±5.12)%，对照组：n t＝10.919，n P<0.01；n t＝2.558，n P<0.05，Si-NC组：n t＝10.545，n P<0.01；n t＝2.407，n P<0.05]，差异均有统计学意义。Si-Bmi-1组和Si-Bmi-1-Bpv组裸鼠腋窝皮下瘤块重量分别为(0.70±0.17)、(1.45±0.18) g，均低于对照组和Si-NC组[(2.35±0.28)、(2.16±0.22) g，对照组：n t＝15.929，n P<0.01；n t＝8.550，n P<0.01，Si-NC组：n t＝16.606，n P<0.01；n t＝7.899，n P<0.01]。Si-Bmi-1组和Si-Bmi-1-Bpv组PTEN蛋白相对表达量(1.84±0.09、1.06±0.08)高于对照组和Si-NC组(0.16±0.04、0.14±0.04，对照组：n t＝22.103，n P<0.01；n t＝17.254，n P<0.01，Si-NC组：n t＝22.356，n P<0.01；n t＝6.980，n P<0.01)，pAKT蛋白相对表达量(0.18±0.04、0.35±0.05)]低于对照组和Si-NC组(1.25±0.08、1.20±0.08，对照组：n t＝20.532，n P<0.01；n t＝15.380，n P<0.01，Si-NC组：n t＝17.192，n P<0.01；n t＝9.025，n P<0.01)；Si-Bmi-1组PTEN蛋白相对表达量高于Si-Bmi-1-Bpv组(n t＝11.370，n P<0.01)，pAKT蛋白相对表达量低于Si-Bmi-1-Bpv组(n t＝8.211，n P<0.01)，差异均有统计学意义。n 结论:沉默Bmi-1可抑制前列腺癌PC-3细胞增殖和迁移能力，可能通过上调PTEN，下调pAkt水平发挥调控作用。“,”Objective:To investigate the effect of B-cell specific Moloney leukemia virus integration site 1 (Bmi-1) silencing on the proliferation and migration of prostate cancer PC-3 cells and on the phosphatase and tensin homology deleted gene/phosphorylated protein kinase B (pAkt) pathway.Methods:The Bmi-1 small interfering RNA (siRNA) sequence and negative control sequence were transfected into PC-3 cells respectively and Si-Bmi-1 group and Si-NC group were set up. The cells stably transfected with Bmi-1 siRNA sequence were treated with the phosphatase and tensin homolog deleted on chromosome ten (PTEN) inhibitor Bpv and Si-Bmi-1-Bpv group was built. The cell proliferation and migration ability of each group was tested by methyl thiazolyl tetrazolium (MTT) method and scratch test. The tumor-forming ability of each group was detected by subcutaneous inoculation method in the armpit. The expression of PTEN and pAkt protein in each group was detected by Western blotting. One-way analysis of variance was used to analyze multi-sample measurement data, and t-test was used to analyze the difference between two samples.Results:The absorbance values at 24, 48, and 72 h in Si-Bmi-1 group (0.315±0.030, 0.480±0.050, 0.659±0.085) and Si-Bmi-1-Bpv group (0.364±0.025, 0.702±0.063, 0.986±0.091) were lower than those in the control group (0.401±0.035, 0.871±0.071, 1.135±0.097) and Si-NC group (0.398±0.031, 0.859±0.067, 1.107±0.092, n t=24.196, n P<0.01;n t=95.326, n P<0.01;n t=72.103, n P<0.01). The cell migration rate in Si-Bmi-1 group and Si-Bmi-1-Bpv group was (32.37±4.25)% and (55.84±5.27)% respectively, which was lower than that in the control group and Si-NC group [(64.08±4.91)%, (63.75±5.12)%. for control group,n t=10.919, n P<0.01;n t=2.558, n P<0.05. for Si-NC group,n t=10.545, n P<0.01;n t=2.407, n P<0.05]. The weights of subcutaneous tumor masses in the axillary of nude mice in the Si-Bmi-1 group and Si-Bmi-1-Bpv group were (0.70±0.17) g and (1.45±0.18) g respectively, which were lower than those of the control group and Si-NC group [(2.35±0.28) and (2.16±0.22) g. for control group,n t=15.929, n P<0.01;n t=8.550, n P<0.01. for Si-NC group,n t=16.606, n P<0.01;n t=7.899, n P<0.01]. The relative expression of PTEN protein in the Si-Bmi-1 group and Si-Bmi-1-Bpv group (1.84±0.09, 1.06±0.08) was higher than that of the control group and Si-NC group (0.16±0.04, 0.14±0.04. for control group,n t=22.103, n P<0.01;n t=17.254, n P<0.01. for Si-NC group,n t=22.356, n P<0.01;n t=6.980, n P<0.01), and the relative expression of pAKT protein (0.18±0.04, 0.35±0.05) was lower than that of the control group and Si-NC group (1.25±0.08, 1.20±0.08. for control group,n t=20.532, n P<0.01;n t=15.380, n P<0.01. for Si-NC group,n t=17.192, n P<0.01;n t=9.025, n P<0.01). The relative expression of PTEN protein in Si-Bmi-1 group was higher than that in Si-Bmi-1-Bpv group (n t=11.370, n P<0.01), and that of pAKT protein was lower than that in Si-Bmi-1-Bpv group (n t=8.211, n P<0.01).n Conclusion:Silencing Bmi-1 can inhibit the proliferation and migration of prostate cancer PC-3 cells, which may play a regulatory role by up-regulating PTEN and down-regulating pAkt levels.