肿瘤坏死因子突变体对胃癌细胞肿瘤坏死因子受体的调节

本文采用放射配基结合分析法和蛋白合成抑制试验研究了肿瘤坏死因子突变体（ＴＮＦ－ｍ）对ＳＧＣ７９０１细胞ＴＮＦ受体的影响。结果表明，ＴＮＦ－ｍ可显著降低ＳＧＣ７９０１细胞表面ＴＮＦ受体数目并呈剂量、时间、温度依赖关系，对受体亲和力无影响，ＴＮＦ－ｍ可使胞浆ＴＮＦ受体数目增加，去除ＴＮＦ－ｍ３ｈ后，膜ＴＮＦ受体大约可恢复６０％，显著高于胰蛋白酶处理组ＴＮＦ受体的恢复率，放线菌素Ｄ对ＴＮＦ－ｍ处理的细胞ＴＮＦ受体的抑制作用显著低于对照组，且ＴＮＦ受体的半衰期约为９０ｍｉｎ．据此认为，ＴＮＦ－ｍ通过介导ＴＮＦ受体的内化从而使膜ＴＮＦ受体数降低。

Effects of Tumor Necrosis Factor Mutant(TNF-m) on the Regulation of TNF-Receptor on Gastric Cancer Cells

In this paper, the effects of TNF-m on TNFR on SGC7901 cells were studied with radio-ligand binding assay and protein synthesis inhibition experiment.It was found that the number of TNFR on the surface of SGC7901 cells could be significantly decreased by TNF-m with dose, time and temperature dependences, but without any effect on the affinity of the receptors. TNF-m could also make the number of TNFR in cytoplasm increase. There was a restoration rate of approximately 60% of TNFR on the membrane 3 hours after the removal of TNF-m, which was markedly higher than that of TNFR in trypsin-treated group. Actinomycin D exerted less inhibition on TNFR on the surface of the cells which has been treated with TNF-m than that in the control group, with the half-life of TNFR being about 90 minutes. It appears that TNF-m makes the number of TNFR decrease by mediating the internalization of TNFR.