奥曲肽对前列腺癌细胞株PC-3的抑制作用及对VEGF表达的影响

目的：探讨奥曲肽（生长抑素类似物）对雄激素非依赖性前列腺癌细胞株PC-3的抑制作用及对其血管内皮生长因子（VEGF）表达的影响.方法：分别用浓度为0.1、0.3、1.0、3.0 mg/L奥曲肽对体外培养的人前列腺癌PC-3细胞进行处理,24 h、48 h、72 h后采用MTT法检测细胞生长活性,行Hoechst33258染色,用荧光显微镜观察细胞凋亡的形态学改变;用RT-PCR法测定细胞半胱氨酸天门冬氨酸蛋白酶-3（Caspase-3）及VEGF的表达.结果：奥曲肽能以剂量与时间依赖性的方式抑制PC-3细胞的生长,促进其凋亡;0.1、0.3、1.0、3.0 mg/L奥曲肽作用PC-3细胞24 h后的存活率分别为（0.971±0.016）%、（0.853±0.015）%、（0.717±0.031）%、（0.743±0.029）%,作用48 h后的存活率分别为（0.918±0.015）%、（0.835±0.015）%、（0.682±0.018）%、（0.727±0.014）%,作用72 h后的存活率分别为（0.922±0.017）%、（0.841±0.013）%、（0.717±0.017）%、（0.739±0.003）%,差别有统计学意义（P〈0.01）;Caspase-3表达较对照组明显升高;而VEGF则明显降低.结论：奥曲肽能显著抑制PC-3细胞的体外生长,促进其凋亡;VEGF可能是其中的一条途径.

Inhibitory Effects of Octreotide on Prostate Cancer PC-3 Cell Line and Expression of VEGF

Objective：To investigate the inhibitory effects of octreotide （somatostatin analogs） on androgen independent prostate cancer PC-3 cell line and the expression of vascular endothelial growth factor（VEGF）. Methods：After PC-3 cells were induced by 0.1,0.3,1.0,3.0 mg/L octreotide respectively, the cell acitvity was assayed by MTT at 24,48 and 72 hours, the morphology of apoptosis was observed by Hoechst 33258 staining under fluo rescence microscope. The level of caspase-3 and VEGF were detected by reverse transeription-polymerase chain reaction （RT PCR）. Results：Octreotide could suppress the growth and promote the apoptosis of PC-3 cells in dosedependent and time-dependent manners, and the morphology of apoptosis could be examined in the study. When cells were treated with different concentrations of oetreotide （0. 1, 0.3, 1.0 and 3.0 rag/L）, the cell surviving rate was （0. 971 ± 0.016）%,（0.853 ± 0.015）%, （0. 717 ±0.031）%,（0.743 ±0.029）% respectively at 24hours,（0.918 ± 0.015）%,（0.835 ± 0.015）%,（0.682± 0.018）%,（0.727 ± 0.014）% respectively at 48 hours and （0.922± 0. 017）%,（0. 841 ± 0.013）%,（0.717± 0.017）%,（0.739 2± 0.003）% respectively at 72 hours,the difference was obviously significant among them. The expression of Caspase-3 was upregulated while VEGF downregulated. Conclusions：Octreotide can suppress the growth and promote the apoptosis of PC 3 cells, and VEGF may involve in it.