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作 者:黄涛[1] 冯延平[1] 高军[1] 常青[1] 秦仁义[1] 裘法祖[1]
机构地区:[1]华中科技大学同济医学院附属同济医院外科,武汉430030
出 处:《郑州大学学报(医学版)》2006年第5期892-894,共3页Journal of Zhengzhou University(Medical Sciences)
摘 要:目的:观察蛋白激酶Cα(PKCα)反义寡核苷酸(ASODN)对人胰腺癌BXPC-3细胞体外侵袭力的影响。方法:将BXPC-3细胞分为7组:对照组,64mg/L随机寡核苷酸序列(RODN)转染组,4mg/L、8mg/L、16mg/L、32mg/L和64mg/LASODN转染组,RT-PCR方法检测PKCαmRNA表达情况;以有效转染浓度的ASODN转染BXPC-3细胞,并设对照和RODN组,Transwell侵袭小室方法检测BXPC-3细胞体外侵袭能力。结果:16mg/L、32mg/L和64mg/LASODN转染组PKCα/GADPHmRNA灰度值(0.6371±0.0360,0.5632±0.0080,0.2389±0.0200)均低于对照组(0.9121±0.0250)(P<0.05),RODN组(0.9147±0.0170)、4mg/LASODN组(0.9123±0.0180)和8mg/LASODN组(0.9116±0.0290)与对照组比较差异均无统计学意义(P>0.05)。与对照组穿膜细胞数(286±10)和RODN组(268±3)比较,转染16mg/LPKCαASODN(119±9)可降低胰腺癌BXPC-3细胞的体外侵袭力(P<0.05)。结论:靶向PKCα的ASODN可有效阻断其在人胰腺癌BXPC-3细胞中的表达,并降低癌细胞体外侵袭力。Aim :To investigate the effect of protein kinase C-α (PKCct) antisense oligodeoxynucleotides (ASODN) on invasive ability of pancreatic carcinoma BXPC-3 cells in vitro. Methods:The cultured BXPC-3 cells were divided into 7 groups: control group, 64 mg/L random oligodeoxynucleotides (RODN) group, 4 mg/L ASODN group, 8 mg/L ASODN group, 16 mg/L ASODN group, 32 mg/L ASODN group, and 64 mg/L ASODN group. The expression of PKCα mRNA was determined by RT-PCR. The invasive ability was measured by the number of cells that penetrated polycarbonates membrane. Results: PKCα/GADPH mRNA relative quantitative ratios of 16 mg/L ASODN group (0. 637 1 ±0. 036 0) , 32 mg/L ASODN group (0. 563 2 ± 0. 008 0) , 64 mg/L ASODN group(0. 238 9±0. 020 0)were significantly lower than that of control group(0. 912 1±0. 0250) ( P 〈0.05 ). There was no significant difference in the expression of PKCα mRNA among RODN group(0.914 7 ±0.017 0) , 4 mg/L ASODN group(0.912 3 ±0.018 0) , 8 mg/L ASODN group(0.911 6 ±0. 029 0), and control group (P 〉 0. 05 ). There were significant differences among 16 mg/L ASODN group (119 ± 9 ), ROD N group (268 ± 3 ) , and control group (286 ± 10)in the cell number that infiltrated the polycarbonates membrane (P 〈 0.05). Conclusion : PKCα ASODN can effectively inhibit the expression of PKCα gene, and decrease the invasion ability of BXPC-3 cells in vitro.
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