硼替佐米对人胃癌SGC-7901细胞uPA、NF-κB表达的影响及与其侵袭力关系

摘要

目的 硼替佐米对人胃癌SGC-7901细胞uPA、NF-κB表达的影响及与其侵袭力关系.方法 Brdu ELISA法测细胞增殖活性;Boyden小室培养测细胞的迁移率;Western blot测细胞uPA、NF-κB的蛋白水平;细胞免疫化学测NF-κB细胞表达及细胞定位.结果 (1)与对照组(无血清培养基组)相比,10% FCS组细胞增殖活性与迁移率明显增高(P0.05);(4)细胞免疫化学结果示:硼替佐米(4 μg·L-1)抑制10%FCS诱导人胃癌SGC-7901细胞NF-κB核移位.结论① 硼替佐米抑制血清诱导胃癌SGC-7901细胞增殖迁移及uPA、NF-κB蛋白表达,② 硼替佐米降低胃癌SGC-7901细胞侵袭力可能与其抑制NF-κB活性,降低UPA水平有关.%Aim To observe the effect of bortezomib on the expression of NF-kB and UAP as well as cell invasiveness in human SGC-7901 gastric cancer cells. Methods Proliferation activity and migration level of human SGC-7901 cells were respectively determined by Bromodeoxyuridine ( BrdU ) ELISA and Boyden chamber. The expression of NF-kB and uPA in human SGC-7901 cells was determined by Western blot. The expression and localization of NF-kB in human SGC-7901 cells were further revealed by immunocytochemistry. Results Compared with the control group ( the serum-free medium group ), proliferation and migration of human SGC-7901 cells were significantly increased in 10% FCS group ( P 0. 05 ). The expression of NF-kB-p65 nuclear protein in the group of bortezomib at 4 μg · L-1 was significantly decreased when compared with 10% FCS group ( P 0. 05 ). Immunocytochemistry showed that NF-kB nuclear translocation in human SGC-7901 cells induced by 10% FCS was inhibited by bortezomib with a concentration of 4 μg · L-1. Conclusions (T) Bortezomib inhibits the expression of uPA and NF-kB as well as cell proliferation and migration in human SGC-7901 cells. (2) The inhibition of bortezomib on the invasive-ness of human SGC-7901 cells may relate to its inhibition on NF-kB activity and UPA expression.