Fuhrer J P, Evans C H
Cancer Lett. 1983 Jul;19(3):283-92. doi: 10.1016/0304-3835(83)90096-4.
Membrane glycoprotein synthesis was studied in non-tumorigenic and tumor cells treated with the lymphokine hormone, lymphotoxin, to define the biochemical mechanisms by which lymphotoxin prevents carcinogenesis and inhibits growth of tumor cells. Syrian hamster lymphotoxin increased the synthesis of high molecular weight (50,000-250,000) membrane glycoproteins in non-tumorigenic secondary passage NIH/N Syrian hamster embryo fibroblasts and caused a decrease in the synthesis of high molecular weight glycoproteins in benzo[a]pyrene-induced hamster tumor cells. Increased glycoprotein synthesis varied directly with lymphotoxin concentration and duration of treatment and occurred contemporaneously with lymphotoxin-initiated prevention of carcinogen-induced morphologic transformation. These lymphotoxin-stimulated fluctuations in membrane glycoprotein synthesis are evidence of specific biochemical target cell changes associated with the anticarcinogenic and tumor-inhibitory actions of this immunologic hormone.
研究了用淋巴因子激素淋巴毒素处理的非致瘤细胞和肿瘤细胞中的膜糖蛋白合成,以确定淋巴毒素预防致癌作用和抑制肿瘤细胞生长的生化机制。叙利亚仓鼠淋巴毒素增加了非致瘤传代NIH/N叙利亚仓鼠胚胎成纤维细胞中高分子量(50,000 - 250,000)膜糖蛋白的合成,并导致苯并[a]芘诱导的仓鼠肿瘤细胞中高分子量糖蛋白的合成减少。糖蛋白合成的增加与淋巴毒素浓度和处理持续时间直接相关,并与淋巴毒素引发的致癌物诱导的形态转化预防同时发生。这些淋巴毒素刺激的膜糖蛋白合成波动是与这种免疫激素的抗癌和肿瘤抑制作用相关的特定生化靶细胞变化的证据。