摘要
目的抗血管形成治疗已被证实可延长恶性肿瘤患者的生存期。文中探讨重组人血管内皮抑制素注射液(rh-Endostatin,rh-ES)联合紫杉醇对胃癌MGC803细胞株生物学功能的影响。方法 MGC803细胞株培养于含10%胎牛血清的RPMI 1640培养基中,加入与实验组等体积的RPMI 1640培养液设为对照组;加入浓度为0.0001μg/mL紫杉醇溶液设为紫杉醇组;分别加入50、100、200μg/mL的rh-ES注射液为rh-ES50组、rh-ES100组、rh-ES200组;加入0.0001μg/mL紫杉醇和50μg/mL rh-ES设为联合50组,0.0001μg/mL紫杉醇+100μg/mL rh-ES为联合100组,0.0001μg/mL紫杉醇+200μg/mL rh-ES设为联合200组。各组分别作用于胃癌MGC803细胞,MMT法和Transwell小室法检测细胞的增殖、侵袭能力;蛋白质印迹法检测细胞VEGF、MMP-2以及MMP-9蛋白表达情况。结果 rh-ES注射液、紫杉醇及联合用药均降低MGC803细胞的增殖能力,减弱细胞侵袭能力,呈剂量依赖性,联合用药组作用最强,呈相加效应,差异有统计学意义(P<0.05)。与对照组相比,各组VEGF、MMP-2以及MMP-9蛋白表达明显下调,且随着rh-ES用药浓度的增加,各蛋白表达量下降更为明显(P<0.05)。联合50组、联合100组、联合200组VEGF相对表达量(0.420±0.374、0.364±0.020、0.306±0.033)较紫杉醇组(0.528±0.018)明显降低(P<0.05),MMP-9相对表达量(0.368±0.023、0.297±0.015、0.241±0.032)较紫杉醇组(0.457±0.037)明显降低(P<0.05),MMP-2相对表达量(0.379±0.027、0.364±0.116、0.285±0.016)较紫杉醇组(0.543±0.021)明显降低(P<0.05)。结论rh-ES联合紫杉醇能够有效抑制胃癌细胞增殖和侵袭能力,其机制可能与下调VEGF、MMP-2以及MMP-9蛋白表达有关。
Objective Antiangiogenesis therapy has been shown to prolong survival for patients with malignant tumor.However the present study has not been observed the clinical benefit of antiangiogenesis therapy combination with chemotherapy treated with gastric cancer.Human recombinant vascular endothelial inhibition（ endostar） as a multi-targeted anti-angiogenesis drug,the mechanism is different from other Antiangiogenesis drugs.It can block different pathways of signal transduction to inhibit angiogenesis.This study aimed to observe the effect of combined application of endostar and paclitaxel on biological behavior of gastric cancer cell lines.Methods MMT assay and Transwell invasion assay were respectively used to examine the inhibition rate of cell growth and invasion ability when cells were treated with various concentrations of endostar and paclitaxel alone or in combination.The protein expressions of VEGF,MMP-2 and MMP-9 were examined by Western blot.Results Endostar or paclitaxel effectively inhibited the growth of MGC803 cells and the in vitro invasion of MGC803 cells in a concentration-dependent manner.The proliferation and invasion ability of combined treatment with endostar and paclitaxel was significantly lower than that of endostar or paclitaxel alone（ P ＆lt;0.05）.Compared with control group,the VEGF,MMP-2 and MMP-9 protein expressions were decreased in experimental groups（ P ＆lt; 0.05）.Compared with paclitaxel group,the VEGF,MMP-2 and MMP-9 protein expressions were relatively reduced in combination groups（ P ＆lt; 0.05）.Conclusion Endostar combined with paclitaxel can suppress the growth and invasion of MGC803 cells,and the decreasing VEGF,MMP-2 and MMP-9 expressions may be involved in the mechanism.
出处
《医学研究生学报》
CAS
北大核心
2014年第6期587-591,共5页
Journal of Medical Postgraduates
基金
南京军区医学科技创新资助项目(联卫[2007]534)
