恩度联合草酸铂对人结肠癌细胞抑制作用研究

Inhibitory effects of Endostar combined with Oxaliplatin on human colon cancer cells

目的:体外观察恩度联合草酸铂对人结肠癌细胞增殖、迁移和黏附能力的影响。方法:采用细胞增殖试验观察恩度和草酸铂联合应用对结肠癌细胞HCT116和SW480生长的抑制作用;应用细胞迁移试验及黏附试验检测上述联合用药对HCT116和SW480细胞迁移和黏附能力的影响。结果:细胞增殖试验显示,恩度单药(18μg/mL)、草酸铂(0.25μg/mL)单药、恩度和草酸铂联合用药与对照组相比均能抑制结肠癌细胞生长,对HCT116细胞抑制率分别为24%、32%和45%;对SW480细胞抑制率分别为20%、31%和41%。联合用药组相比单药组有更强的抑制肿瘤细胞生长的作用,差异有统计学意义,在HCT116和SW480细胞中,联合用药对比恩度,P值分别为0.041和0.022;对比草酸铂,P值分别为0.033和0.029。联合用药抑制细胞增殖作用具有时间依赖性,细胞培养120h后,相比对照组,联合用药组对HCT116细胞抑制率达55%,差异有统计学意义,t=12.57,P=0.024;对SW480细胞抑制率达56%,差异有统计学意义,t=9.798,P=0.031。恩度联合草酸铂可明显抑制HCT116细胞迁移和细胞黏附,与对照组相比,联合用药对细胞迁移抑制率为86.1%,t=2.054,P=0.000 7;对细胞黏附抑制率为55.6%,t=25.74,P=0.029。联合用药不影响SW480细胞迁移能力,但抑制该细胞系的黏附能力,抑制率为66.4%,t=12.47,P=0.012。联合用药抑制HCT116细胞迁移和黏附的效果优于SW480细胞。结论:恩度与化疗药物联合应用具有协同效应。恩度联合草酸铂可以抑制结肠癌细胞的增殖、迁移和黏附等多方面功能,将为结肠癌的治疗提供新的思路。

OBJECTIVE： To explore the effects of combination of Endostar and Oxaliplatin on colon cancer cell growth, adhesion and migration in vitro. METHODS： Cell counting method was conducted for the effects of Endostar combined with Oxaliplatin on the growth of HCT116 and SW480 cells. Tumor cell migration and adhesion were tested using Boyden Chamber and crystal violet staining. RESULTS： Cell proliferation assay showed individual Endostar （18 μg/mL）, Oxaliplatin （0.25 μg/mL） or the combination of Endostar ＆ Oxaliplatin inhibited tumor cell growth compared with the control, with inhibitory rate at 24%, 32% and 45% in HCTll 6 cells and 20%, 31 % and 41 % in SW480 cells respectively. In addition, Endostar plus Oxaliplatin had stronger inhibitory effects on cell growth than single drug did,and the difference was statistically significant （P：0. 041 in HCT116 cells and P=0. 022 in SW480 cells for Endostar,P：0. 033 in HCT116 cells and P：0. 029 in SW480 cells for Oxaliplatin）. The inhibitory effects were time-dependent,in which the inhibitory rate reached 55% in HCTll6 （t：12.57,P%0. 024） and 56% in SW480 （t=9. 798,P=0. 031） after 120-hour cell culture. Endostar combined with Oxaliplatin inhibited both cell migration and adhesion in HCT116 cells. Compared with control group, combination group inhibited HCT116 cell migration by 86.1% （t =2. 054, P =0. 000 7）, and cell adhesion by 55.6 % （t= 25.74, P： 0. 029） respectively. However the combined drugs did not affect SW480 cell migration, but inhibited cell adhesion by 66.4 %（t = 12.47, P ： 0.012）. Thus, the inhibitory effects of the combined drugs on HCT116 were superior to those in SW480 with respect to cell migration and cell adhesion. CONCLUSIONS： Endostar combined with Oxali- platin showed synergistic activity on inhibiting colon cancer cell development. It shows therapeutic function for treatment of colon cancer through various steps including inhibiting cell proliferation, migration and adhesion. Our in vitro results provide theoretical rationale for colon cancer treatment using Endostar plus Oxaliplatin regimen in the future.