干扰素—γ对胃癌细胞肿瘤坏死因子受休的调控  

Regulation of tumor necrosis factor receptors on human gastric cancer cells by interferon-γ

作　　者：冉瑞琼[1] 孙建中[1] 吴裕炘[2] 付华[2] 王国平 曹世龙[1] 

机构地区：[1]上海医科大学肿瘤医院流式细胞室,上海200032 [2]上海瑞金医院消化科 [3]中科院上海原子核所

出　　处：《中国病理生理杂志》1997年第4期429-432,共4页Chinese Journal of Pathophysiology

摘　　要：为了探讨干扰素-γ对胃癌细胞(SGC_(7901))肿瘤坏死因子(TNF)受体的影响及干扰素—γ肿瘤坏死因子突变体(TNF—m)协同抗肿瘤的机制,以_(125)I-肿瘤坏死因子突变体(^(123)I—TNF—m)为配体,用放射配体结合分析法研究了干扰素-γ对SGC_(7901)细胞TNF受体表达及TNF—m内化和降解的影响。外用MTT法研究了干扰素-γ与TNF-m协同抗肿瘤作用。结果表明:干扰素-γ使SGC_(7901)细胞TNF受体数目由0.56×10^(-11) nmol/细胞增加到0.94×10^(-11)nmol/细胞(P<0.01),而对受体亲和力无影响(kd值:2.78×10^(-10)mol对2.64×10^(-10) mol.P>0.5);干扰素-γ可明显增加TNF—m内化和降解的绝对数量而对其比率无影响。干扰素-γ使TNF—m对SGC_(7901)细胞的最大杀伤率由60.48%上升到96.76%(P<0.01)。提示:干扰素-γ通过上调TNF受体而加强TNF—m的体外抗肿瘤作用。To explore the effect of interferon-γ (IFN-γ) on tumor necrosis factor (TNF) receptor of human gastric cancer cells (SGC_(7901)) and the mechanism of anti-tumor synergism of IFN-γ and tumor necrosis factor mutant (TNF-m), radio-ligand binding assay was applied to detect the effect of IFN-γ on the expressin of TNF receptor on SGCT_(7901) cell and on the internalization and degradation of TNF-m. MTT colorimetric method was used in the study of anti-tumor synergism of IFN-γ and TNF-m. Results showed: The number of TNF receptor on SGC_(7901) cell increased from 0.56×10^(-11) nmol/cell to 0.94×10^(-11) nmol/cell (P<0.01), with no effect on the affinity of the receptors. (kd value: 2.78×10^(-10)mol versus 2.64×10^(-10)mol, P>0.5). IFN-γ could promote the synthesis of TNF receptor protein; IFN-γ could markedly increase the absolute number of the internzalization and degradation of TNF-m but exerted no effect on their rate. The maximum rate of cytotoxicity of TNF-m on SGC_(7901) increased from 60.48% to 96.76%(P<0.01) owing to IFN-γ. It was indicated that IFN-γ could increase in vitro the anti-tumor effect of TNF-m by up-regulating TNF receptors.

关 键 词：放射配位体测定 肿瘤坏死因子 干扰素-Γ 胃肿瘤 

分 类 号：R735.205[医药卫生—肿瘤]