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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
【摘要】 为了探讨干扰素-γ对胃癌细胞(SGC7901)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125I-肿瘤坏死因子突变体(123I—TNF—m)为配体,用放射配体结合分析法研究了干扰素-γ对SGC7901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SGC7901细胞TNF受体数目由0.56×10-11 nmol/细胞增加到0.94×10-11nmol/细胞(P<0.01),而对受体亲和力无影响(kd值:2.78×10-10mol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SGC7901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。
【Abstract】 To explore the effect of interferon-γ (IFN-γ) on tumor necrosis factor (TNF) receptor of human gastric cancer cells (SGC7901) 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 SGCT7901 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 SGC7901 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: 2.78×10-10mol versus 2.64×10-10mol, 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 SGC7901 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.
【Key words】 Radioligand assay · Tumor necrosis factor · Interferon; Gamma;
- 【文献出处】 中国病理生理杂志 ,Chinese Journal of Pathophysiology , 编辑部邮箱 ,1997年04期
- 【分类号】R735.2
- 【下载频次】29