PDCD5蛋白联合米非司酮对前列腺癌细胞增殖及相关基因表达的影响  

The Effects of PDCD5 Combined with Mifepristone on Proliferation in Prostate Cancer Cells

作　　者：杜彦丹[1,2] 于靖[1] 赵雪飞[1] 林平[1] 刘紫君[1] 于晓光[1] 

机构地区：[1]哈尔滨医科大学生物化学与分子生物学教研室,黑龙江哈尔滨150081 [2]内蒙古林业总医院检验科,内蒙古牙克石022150

出　　处：《肿瘤基础与临床》2009年第2期96-99,共4页journal of basic and clinical oncology

基　　金：黑龙江省教育厅科学技术研究面上项目(编号:11531084);哈尔滨市科技创新人才研究专项资金(编号:2007RFXXS039)

摘　　要：目的观察PDCD5蛋白协同米非司酮（MIF）对前列腺癌细胞增殖及相关基因表达的影响。方法MTT法分别检测10、20、50和100μmol/L MIF作用于PC-3M细胞24-96 h的吸光度（A）值。扩增包含PDCD5序列的真核表达载体PCI-neo-PDCD5，用脂质体介导的方法转染前列腺癌PC-3M细胞。在转染PDCD5的细胞中分别加入10、20μmol/L MIF，继续培养24 h，MTT比色法检测细胞增殖，RT-PCR方法检测细胞增殖相关基因CyclinD1、Ki-67的表达。结果MTT实验表明，与对照组相比，10μmol/L MIF组的A值差异无统计学意义（P〈0.05），20、50和100μmol/L MIF组的A值显著降低（P〈0.05），MIF对前列腺癌PC-3M细胞的抑制作用呈剂量依赖性；PDCD5真核表达载体成功转染PC-3M细胞并得到了瞬时表达，转染PCI-neo-PDCD5并加入MIF后，与对照组及单独应用MIF组相比，细胞增殖受到明显抑制（P〈0.05），增殖相关基因CyclinD1、Ki-67表达降低。结论PDCD5蛋白能够协同米非司酮抑制前列腺癌PC-3M细胞增殖，可能是通过调节某些增殖相关基因的表达来实现的，并有望成为前列腺癌的辅助治疗药物。Objective To investigate the effects of PDCD5 combined with mifepristone on proliferation of prostate cancer PC-3M cells. Methods The A values of the prostate cancer cells PC-3M that were treated with various concentrations （10,20,50,100 μmol/L） of MIF on time-course （24-96 h） were detected by MTT assay. The eukaryote expression vector PCI-neo-PDCD5 was amplified and transfected into PC- 3M cells,and then the PC-3M cells were treated with 10 or 20 μmol/L MIF,the proliferation of the PC-3M cells was assayed by MTT,the expression of mRNA of CyclinD1 ,Ki-67 were detected by RT-PCR. Results The A values of the cancer cells treated with 10 μmol/L of MIF were similar to those of controls（P 〈 0. 05 ） ,while those of the cells treated with 20,50 and 100 μmol/L of MIF were significantly different from those of controls （P 〈0.01 ）. MIF markedly inhibited cell proliferation of prostate cancer PC-3M cells on a dose- and time-depending manner. The eukaryote expression vector PCI-neo-PDCD5 was successfully transfected and transient expressed in PC-3M cells. Compared with the control and MIF group,the viability of PC-3M cells treated with PDCD5 and MIF was decreased obviously, the expressions of CyclinD1 ,Ki-67 were down-regulated strikingly. Conclusion The results suggest that PDCD5 may inhibit proliferation in PC-3M cells in combination with MIF. Its mechanism is maybe involved in the proliferation-related gene ,including CyclinD1 ,Ki-67.

关 键 词：前列腺癌 PC-3M细胞 PDCD5 米非司酮 细胞增殖 

分 类 号：R737.25[医药卫生—肿瘤]