目的:研究抑癌基因KLF6对人前列腺癌细胞系PC-3细胞的生长增殖、细胞周期和对Bc l-2和Cyc lin D1蛋白表达的影响及其可能的作用机制。方法:利用RT-PCR法克隆目的基因KLF6,采用阳离子脂质体介导将含或不含KLF6的pEGFP-C1质粒转染入PC-3细...目的:研究抑癌基因KLF6对人前列腺癌细胞系PC-3细胞的生长增殖、细胞周期和对Bc l-2和Cyc lin D1蛋白表达的影响及其可能的作用机制。方法:利用RT-PCR法克隆目的基因KLF6,采用阳离子脂质体介导将含或不含KLF6的pEGFP-C1质粒转染入PC-3细胞,分别作为转染组和对照组。分别进行噻唑蓝(MTT)法观察PC-3细胞的生长抑制率,流式细胞仪检测细胞周期比例变化和凋亡率,免疫组化法观察PC-3细胞Bc l-2和Cyc lin D1的表达水平变化。结果:转染了抑癌基因KLF6的前列腺癌PC-3细胞生长抑制率为(30.0±5.4)%(对照组为0%,P<0.01);细胞周期比例表现为G2/M期减少为(11.2±0.9)%[对照组为(25.2±2.8)%,P<0.05],G0/G1期比例增加为(80.0±9.8)%[对照组为(58.6±7.3)%,P<0.05];细胞凋亡峰为(24.3±2.3)%[对照组为(5.2±0.7)%,P<0.01];Bc l-2的表达率为(18.7±3.2)%[对照组为(41.8±5.9)%,P<0.01];Cyc lin D1的表达率为(25.3±3.7)%[对照组为(38.5±4.6)%,P<0.05]。结论:抑癌基因KLF6的转染可以明显抑制前列腺癌PC-3细胞的生长增殖,并诱导其凋亡,其作用机制可能与下调Bc l-2和Cyc lin D1的表达有关。展开更多
Objective To investigate the effect of IL-6 on prostatic carcinoma cell lines, and differential effects on androgen-dependent and androgen-independent prostatic carcinoma cells. Methods The IL-6 producing capacities o...Objective To investigate the effect of IL-6 on prostatic carcinoma cell lines, and differential effects on androgen-dependent and androgen-independent prostatic carcinoma cells. Methods The IL-6 producing capacities of LNCaP and PC-3 cells were determined, and effects of exogenous IL-6 and anti-IL - 6 antibodies on LNCaP and PC - 3 cells were examined. Results LNCaP produced a very small amount of IL-6, but PC-3 produced more, the concentraion of IL-6 being 190 pg/48 h per ml(1 × 106). The exogenous IL-6 inhibited LNCaP growth significantly,but had no obvious effect on PC -3 cells. Anti-IL-6 antibodies lowered PC-3 cells growth rate but had neutral effect on LNCaP. Conclusion PC-3 cells produces IL-6 massively in autocrine manner. IL-6 could be antagonized by anti-IL-6 antibodies,resulting in slowing PC-3 cells growth, and LNCaP cells growth could be inhibited by exogenous IL-6.7 refs,2 tabs.展开更多
文摘目的:研究抑癌基因KLF6对人前列腺癌细胞系PC-3细胞的生长增殖、细胞周期和对Bc l-2和Cyc lin D1蛋白表达的影响及其可能的作用机制。方法:利用RT-PCR法克隆目的基因KLF6,采用阳离子脂质体介导将含或不含KLF6的pEGFP-C1质粒转染入PC-3细胞,分别作为转染组和对照组。分别进行噻唑蓝(MTT)法观察PC-3细胞的生长抑制率,流式细胞仪检测细胞周期比例变化和凋亡率,免疫组化法观察PC-3细胞Bc l-2和Cyc lin D1的表达水平变化。结果:转染了抑癌基因KLF6的前列腺癌PC-3细胞生长抑制率为(30.0±5.4)%(对照组为0%,P<0.01);细胞周期比例表现为G2/M期减少为(11.2±0.9)%[对照组为(25.2±2.8)%,P<0.05],G0/G1期比例增加为(80.0±9.8)%[对照组为(58.6±7.3)%,P<0.05];细胞凋亡峰为(24.3±2.3)%[对照组为(5.2±0.7)%,P<0.01];Bc l-2的表达率为(18.7±3.2)%[对照组为(41.8±5.9)%,P<0.01];Cyc lin D1的表达率为(25.3±3.7)%[对照组为(38.5±4.6)%,P<0.05]。结论:抑癌基因KLF6的转染可以明显抑制前列腺癌PC-3细胞的生长增殖,并诱导其凋亡,其作用机制可能与下调Bc l-2和Cyc lin D1的表达有关。
文摘Objective To investigate the effect of IL-6 on prostatic carcinoma cell lines, and differential effects on androgen-dependent and androgen-independent prostatic carcinoma cells. Methods The IL-6 producing capacities of LNCaP and PC-3 cells were determined, and effects of exogenous IL-6 and anti-IL - 6 antibodies on LNCaP and PC - 3 cells were examined. Results LNCaP produced a very small amount of IL-6, but PC-3 produced more, the concentraion of IL-6 being 190 pg/48 h per ml(1 × 106). The exogenous IL-6 inhibited LNCaP growth significantly,but had no obvious effect on PC -3 cells. Anti-IL-6 antibodies lowered PC-3 cells growth rate but had neutral effect on LNCaP. Conclusion PC-3 cells produces IL-6 massively in autocrine manner. IL-6 could be antagonized by anti-IL-6 antibodies,resulting in slowing PC-3 cells growth, and LNCaP cells growth could be inhibited by exogenous IL-6.7 refs,2 tabs.