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目的观察紫杉醇(PA)协同吉西他滨(GE)对前列腺癌细胞系PC-3的体内外作用,并探讨其可能的作用机制。方法应用光镜形态学、噻唑蓝(MTT)法、流式细胞仪和免疫细胞化学法观察了10-6、10-7、10-8 mol/L浓度PA和10-7、10-8、10-9 mol/L浓度GE在体外单药或协同对前列腺癌细胞系PC-3的作用、对细胞DNA含量及cyclin D1表达的影响。观察PC-3细胞荷瘤裸鼠单独及协同使用PA和GE前后的体质量、肿瘤质量、血清PSA和肿瘤PSA免疫组化的变化。结果10-8 mol/L以上浓度GE作用48 h,可增强10-7 mol/L以上浓度PA对前列腺癌PC-3细胞系的生长抑制[抑制率≥(50.8±4.2)%,P<0.05],增强诱导凋亡作用[凋亡率≥(22.9±2.3)%,P<0.05],下调Cyclin D1的表达[表达率≤(9.6±1.6)%],与阳性对照组cyclin D1表达率(25.5±4.1)%相比差异有显著性(P<0.01)。GE使PA所致的G2/M期细胞周期阻滞比例由(70.3±9.7)%减至(38.2±4.2)%,部分地逆转了其G2/M期细胞周期阻滞(P<0.01)。协同治疗前后裸鼠体质量无明显变化,但肿瘤质量(3.2.±0.5 g)、血清PSA[(51±14) ng/ml]和肿瘤PSA免疫组化的表达率[(30±3.7)%]在协同治疗组显著低于其他组(P<0.05或0.01)。结论PA和GE可以在体内外协同增强对前列腺癌细胞系PC-3的生长抑制和诱导凋亡作用,显示了PA和GE协同用
Objective To observe the effect of paclitaxel (PA) and gemcitabine (GE) on prostate cancer cell line PC-3 in vitro and in vivo and to explore its possible mechanism. Methods The morphological, light microscopic, thiazolyl blue (MTT) method, flow cytometry and immunocytochemistry were used to observe the effects of 10-6,10-7,10-8 mol / L PA and 10-7,10-8, Effect of 10-9 mol / L GE on monolayer or synergistic effect of prostate cancer cell line PC-3 in vitro on DNA content and cyclin D1 expression. The body weight, tumor mass, serum PSA and tumor immunohistochemistry of PC-3 cells in nude mice bearing PA and GE were observed before and after treatment. Results A dose-effect of 10-8 mol / L GE for 48 h enhanced the growth inhibition of prostate cancer cell line PC-3 at a concentration of 10-7 mol / L PA [inhibition rate ≥ (50.8 ± 4.2)%, P <0.05 (22.9 ± 2.3)%, P <0.05], and downregulated the expression of Cyclin D1 [expression rate (9.6 ± 1.6)%], compared with the positive control group 25.5 ± 4.1% compared to the difference was significant (P <0.01). GE reduced the G2 / M phase arrest induced by PA from (70.3 ± 9.7)% to (38.2 ± 4.2)%, partially reversed its G2 / M cell cycle arrest (P <0.01). The tumor mass (3.2 ± 0.5 g), serum PSA [(51 ± 14) ng / ml] and the expression of PSA in the tumor group were significantly higher than those in the control group [(30 ± 3.7)% vs ] In the co-treatment group was significantly lower than the other groups (P <0.05 or 0.01). Conclusions Both PA and GE can synergistically enhance the growth inhibition and induce apoptosis of prostate cancer cell line PC-3 in vitro and in vivo, showing the synergistic effects of PA and GE