AMACR siRNA表达载体对前列腺癌PC-3细胞生物学特性的影响  

Effect of AMACR RNAi eukaryotic expression vectors on biological characteristics of PC-3 cell line

作　　者：袁建林[1] 于磊[1] 张更[1] 王立国[1] 武国军[1] 

机构地区：[1]第四军医大学西京医院泌尿外科,西安710032

出　　处：《山西医科大学学报》2009年第1期39-42,共4页Journal of Shanxi Medical University

基　　金：陕西省自然科学基金国际合作资助项目(2005KW-15)

摘　　要：目的观察转染α-甲酰辅酶A消旋酶(AMACR)干涉载体后对前列腺癌PC-3细胞系生长状态的影响。方法用脂质体将pSilencer/AMACR1转染前列腺癌PC-3细胞,通过细胞计数、MTT、软琼脂克隆形成实验检测细胞的增殖能力,流式细胞仪分析细胞周期,AnnexinⅤ-FITC检测细胞凋亡。结果siRNA干涉载体瞬时转染PC-3前列腺癌细胞系后,36h细胞增殖率开始明显下降,软琼脂集落形成减少,流式细胞分析示细胞周期阻滞在G0/G1期(88.6%),Annexin Ⅴ-FITC法示早期凋亡细胞率68.3%。结论利用RNA干涉技术抑制了前列腺癌PC-3细胞系的增生,可能会成为一种有效的前列腺癌基因治疗手段。Objective To investigate the influence of expression of α-methylacyl-CoA-racemase（AMACR） on growth of PC-3 cells. Methods Using LipofectAmineTM 2000 reagent, RNAi eukaryotic expression vectors pSilencer/AMACR1 and control vector pSilencerControl were transfected into the human prostate cancer cell line PC-3. The proliferative ability of the transfected cells was determined by cell counting, MTr analysis and soft agar assay. Cell cycle was analyzed with flow cytometry. Apoptotic cells were quantified by staining with FITC-conjugated Annexin V. Results After the PC-3 cells were transfected with pSilencer/AMACR1, their proliferation rate began to decrease significantly after 36 h culture. However, the cells transfected with pSilencer-Control and wild type cells showed the same proliferation rate. The average colony forming decreased compared with PC-3 cells（ P 〈 0.05 ）. Cell cycle analysis showed the number of pSilencer/AMACR1 cells in G0/G1 phase of transfected cells was 88.6%. Approximately 68.3% PC-3 cells were induced into apoptosis. Conclusion The growth of PC-3 cell could be inhibited by pSilencer/AMACR1, which provide us an effective gene therapy for the prostate carcinoma.

关 键 词：前列腺肿瘤 AMACR RNA干扰 

分 类 号：R392.11[医药卫生—免疫学]