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目的:探讨肿瘤抑制因子第10号染色体上缺失与张力蛋白同源的磷酸酯酶基因(PTEN)对前列腺癌细胞增殖和耐药的作用及其作用机制。方法:收集2017年4月～2019年2月武汉市中心医院手术切除的前列腺癌组织和正常前列腺组织各32例，实时定量聚合酶链反应(Real-time PCR)实验检测前列腺癌组织和细胞以及正常前列腺组织和细胞中PTEN的表达量；细胞增殖与毒性检测(CCK-8)测定PTEN对前列腺癌细胞PC3增殖的影响；蛋白质印迹法(Western blot)检测耐药相关蛋白P-糖蛋白(P-gp)和多药耐药相关蛋白1(MRP-1)的蛋白表达水平，采用t检验进行两组间差异显著分析。结果:PTEN在肿瘤组织中mRNA和蛋白表达量均显著低于正常前列腺组织中mRNA[(0.246±0.075)比(0.827±0.076)，n t＝30.781，n P<0.05]和蛋白[(0.148±0.053)比(0.598±0.065)，n t＝30.352，n P<0.05]的表达量；PTEN在PC3细胞中表达量最低，选择PC3作为后续研究；当细胞转染pcDNA3.1-PTEN和对照空载pcDNA3.1时，细胞克隆数量差异显著[(1.26±0.26)×10n 5比(3.50±0.25)×10n 5，n t＝10.757，n P<0.05]；pcDNA3.1-PTEN组P-gp和MRP-1的蛋白表达量与pcDNA3.1组P-gp[(0.256±0.032)比(0.854±0.053)，n t＝16.730，n P<0.05]和MRP-1[(0.252±0.036)比(0.789±0.063)，n t＝12.819，n P<0.05]蛋白表达量差异显著；pcDNA3.1-PTEN组细胞外信号调节激酶(ERK)和p3蛋白表达均显著低于pcDNA3.1组ERK[(0.442±0.038)比(0.844±0.068)，n t＝8.939，n P<0.05]和p38[(0.325±0.045)比(0.932±0.075)，n t＝12.020，n P<0.05]的蛋白表达；pcDNA3.1-ERK组[(3.18±0.43)×10n 5比(1.12±0.21)×10n 5，n t＝7.456，n P<0.05]和pcDNA3.1-p38组[(4.16±0.29)×10n 5比(1.12±0.21)×10n 5，n t＝14.706，n P<0.05]细胞克隆数量均显著高于对照pcDNA3.1组。n 结论:PTEN能够抑制前列腺癌细胞PC3的增殖和耐药，其作用机制是通过调控活性氧(ROS)/p38丝裂原活化蛋白激酶(p38 MAPK)信号通路来实现的。“,”Objective:To explore the effect of tumor suppressor phosphatase and tensin homologue deleted on chromosome ten (PTEN) on proliferation and drug-resistance of prostate cancer cells and the underlying mechanism.Methods:The expression of PTEN in prostate cancer tissue and normal prostate tissue was detected by reverse transcriptase-polymerase chain reaction (RT-PCR). The effect of PTEN on the proliferation of PC3 cells was examined by cell counting kit-8 (CCK-8) assay, and the expression of P-gp and MRP-1 was detected by Western blotting.Results:The results showed that PTEN mRNA (0.246±0.075) and protein (0.148±0.053) expression in tumor tissue was significantly lower than that in normal prostate tissue (n P<0.05). The PTEN expression in PC3 cells was the lowest, and PC3 cells were selected as the following study. When PCDNA3.1-PTEN and pcDNA3.1 were transfected, the number of cell clones was (1.26±0.26)×10n 5 and (3.50±0.25)×10n 5, respectively, with significant difference (n P<0.05). The expression of P-gp (0.256±0.032) and MRP-1 (0.252±0.036) protein in PCDNA3.1-PTEN group was significantly lower than that in PCDNA3.1 group (n P<0.05), and that of ERK (0.442±0.038) and p38 (0.325±0.045) protein in PCDNA3.1-PTEN group was significantly lower than that in PCDNA3.1 group (n P<0.05). The number of cell clones in PCDNA3.1-ERK group [(3.18±0.43)×10n 5] and PCDNA3.1-p38 group [(4.16±0.29)×10n 5] was significantly higher greater that in the pcDNA3.1 group (1.12×10n 5±0.21, n P<0.05).n Conclusion:PTEN inhibits the proliferation and drug-resistance of PC3 cells by regulating ROS/p38 mitogen-activated protein kinase signal pathway, which may provide molecular basis for clinical treatment and diagnosis of prostate cancer.