目的:探讨雄激素受体（AR）对从前列腺癌LNCaP细胞中分选出的CK5n +CK8n +细胞的作用及其调控机制。n 方法:采用流式细胞术从LNCaP细胞中分选CK5n +CK8n +细胞，使用慢病毒载体携带AR基因转入CK5n +CK8n +细胞。实验分为转入AR的AR CK5n +CK8n +组和转入空载体的V CK5n +CK8n +组，在1、10 nmol／L二氢睾酮（DHT）培养条件下，采用蛋白质印迹法检测AR、p-AKT和bcl-2蛋白的表达，应用四甲基偶氮唑盐（MTT）法、细胞迁移实验和琼脂糖凝胶克隆形成实验检测AR对CK5n +CK8n +细胞生物学特性的影响。采用MTT法检测应用AKT信号通路活化抑制物LY 294002（LY）、γ-生育三烯酚（γ-TT）和（或）诱导AR表达的5-氮胞嘧啶（5-AZA）对CK5n +CK8n +细胞增殖的影响。n 结果:AR基因转入CK5n +CK8n +细胞后，AR表达增强，p-AKT和bcl-2蛋白表达水平降低。在1、10 nmol／L DHT作用2、4、6 d后，AR CK5n +CK8n +组细胞较V CK5n +CK8n +组细胞增殖受抑制程度高，差异均有统计学意义（均n P<0.05）。DHT 1、10 nmol／L作用3 d后，AR CK5n +CK8n +组细胞较V CK5n +CK8n +组细胞迁移能力下降[迁移细胞数：（54±9）个比（113±21）个，（13±3）个比（34±6）个]，差异均有统计学意义（n t＝4.450，n P<0.01；n t＝5.157，n P<0.01）。DHT 1、10 nmol／L作用3周后，AR CK5n +CK8n +组细胞较V CK5n +CK8n +组细胞成瘤能力弱[克隆数：（39±　7）个比（105±16）个，（41±6）个比（86±6）个]，差异有统计学意义（n t＝6.631，n P<0.01；n t＝8.662，n P<0.01）。5 nmol／L LY＋10 nmol／L 5-AZA、5 nmol／L LY＋5 nmol／L γ-TT、10 nmol／L 5-AZA＋5 nmol／Lγ-TT、2.5 nmol／L LY＋5 nmol／L 5-AZA＋2.5 nmol／L γ-TT联合1 nmol／L DHT或10 nmol／L DHT作用2、4、6 d均能抑制CK5n +CK8n +细胞增殖（均n P<0.05）。n 结论:AR可以抑制从LNCaP中分选出的CK5n +CK8n +细胞增殖，导致细胞迁移和成瘤能力下降；其可能通过抑制AKT-bcl-2信号通路的活化而发挥作用。n “,”Objective:To investigate the role of androgen receptor (AR) in CK5n +CK8n + cells isolated from prostate cancer LNCaP cells and its regulating mechanism.n Methods:CK5n +CK8n + cells were isolated from LNCaP cells by using flow cytometry. Lentivirus vector carrying AR gene was transferred in CK5n +CK8n + cells. The experiments were divided into AR CK5n +CK8n + group transfering AR and V CK5n +CK8n + group transfering blank load. The expressions of AR, p-AKT and bcl-2 were tested by using Western blot assay under different concentrations of androgen (1 nmol/L and 10 nmol/L dihydrotestosterone). Methyl thiazolyl tetrazolium (MTT) assay, cell migration assay and soft agarose gel clone formation assay was used to detect the effect of AR on the biological property of CK5n +CK8n + cells. The effect of activated inhibitors such as LY 294002 (LY), γ-tocotrienol (γ-TT) and/or 5-fluorocytosine inducing AR expression (5-AZA) through AKT signal pathways on CK5 n +CK8n + cells proliferation was detected by using MTT assay.n Results:After AR gene was transferred into CK5n +CK8n + cells, the expression of AR was increased, while the expression of p-AKT and bcl-2 was decreased. After the treatment of 1 nmol /L dihydrotestosterone and 10 nmol/L dihydrotestosterone for 2, 4 and 6 d, the cell proliferation inhibited degree of AR CK5n +CK8n + cells was higher compared with that of V CK5n +CK8n + cells, and the difference was statistically significant (all n P < 0.05). After the treatment of 1 nmol/L dihydrotestosterone and 10 nmol /L dihydrotestosterone for 3 d, the migration ability of AR CK5 n +CK8n + cells was decreased compared with that of V CK5n +CK8n + cells (the number of cell migration: 54±9 vs. 113±21, 13±3 vs. 34±6), and the differences were statistically significant (n t=4.450, n P<0.01;n t=5.157, n P<0.01).After the treatment of 1 nmol /L dihydrotestosterone and 10 nmol /L dihydrotestosterone for 3 weeks, the tumorigenic ability of AR CK5n +CK8n + cells was reduced compared with that of V CK5n +CK8n + cells (the number of clone: 39±7 vs. 105±16, 41±6 vs. 86±6), and the differences were statistically significant (n t=6.631, n P<0.01;n t=8.662, n P<0.01). And 5 nmol /L LY + 10 nmol/L 5-AZA, 5 nmol /L LY + 5 nmol/L γ-TT, 10 nmol/L 5-AZA + 5 nmol/L γ-TT, 2.5 nmol/L LY + 5 nmol/L 5-AZA + 2.5 nmol/L γ-TT combined with 1 nmol/L dihydrotestosterone or 10 nmol/L dihydrotestosterone after the treatment of 2, 4, 6 d inhibited the proliferation of CK5n +CK8n + cells (all n P < 0.05).n Conclusion:AR plays an inhibitory role in CK5n +CK8n + cells isolated from prostate cancer cell line LNCaP and reduces the cell migration and tumorigenic ability through inhibiting activation of AKT-bcl-2 signal pathway.n