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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 investigate the effect of interferon-γ on gastric cancer cell (SGC_(7901)) tumor necrosis factor (TNF) receptor and the synergistic anti-tumor mechanism of interferon-γ tumour necrosis factor mutant (TNF-m), to ) I-tumor necrosis factor mutant (~(123)I-TNF-m) was used as a ligand to study the expression of TNF receptor and TNF-m in interferon-gamma on SGC_(7901) cells by radioligand binding assay. Internalization and degradation effects. The synergistic antitumor effect of interferon-gamma and TNF-m was studied by external MTT assay. The results showed that IFN-γ increased the number of TNF receptors in SGC_(7901) cells from 0.56×10~(-11) nmol/cell to 0.94×10~(-11) nmol/cell (P<0.01). The receptor affinity has no effect (kd value: 2.78×10 -10 mol vs. 2.64×10 -10 mol.P>0.5); interferon-γ can significantly increase the internalization and degradation of TNF-m. Quantity has no effect on its ratio. Interferon-γ increased the maximum killing rate of TNF-m against SGC_(7901) cells from 60.48% to 96.76% (P<0.01). Tip: Interferon-gamma enhances the anti-tumor effect of TNF-m in vitro by upregulating TNF receptors.