Galeotti T, Boscoboinik D, Azzi A
Institut für Biochemie und Molekularbiologie, Universität Bern, Switzerland.
Arch Biochem Biophys. 1993 Jan;300(1):287-92. doi: 10.1006/abbi.1993.1040.
The effect of the tumor promoter 4 beta-phorbol 12-myristate 13-acetate and of the phosphatases inhibitor okadaic acid on the binding of tumor necrosis factor-alpha (TNF-alpha) to a human osteogenic sarcoma cell line (Saos-2) was investigated. Both substances prevented almost completely TNF binding to its receptors. The effect of 4 beta-phorbol 12-myristate 13-acetate was reversed by the protein kinase C inhibitors staurosporine and calphostin C or by protein kinase C depletion. Vinblastine, under conditions causing full microtubule disassembly, produced only a 50% decrease of TNF binding. Vinblastine plus PMA was additive in fully preventing TNF binding. It is suggested that the degree of binding of TNF-alpha to its receptors in Saos-2 cells is under the control of a microtubule-dependent and of a microtubule-independent regulatory pathway.
研究了肿瘤启动子4β-佛波醇12-肉豆蔻酸酯13-乙酸酯和磷酸酶抑制剂冈田酸对肿瘤坏死因子-α（TNF-α）与人骨肉瘤细胞系（Saos-2）结合的影响。这两种物质几乎完全阻止了TNF与其受体的结合。蛋白激酶C抑制剂星形孢菌素和钙磷蛋白C或蛋白激酶C耗竭可逆转4β-佛波醇12-肉豆蔻酸酯13-乙酸酯的作用。在导致微管完全解体的条件下，长春碱仅使TNF结合减少50%。长春碱加佛波醇肉豆蔻酸酯乙酸酯在完全阻止TNF结合方面具有累加作用。提示TNF-α与Saos-2细胞中其受体的结合程度受微管依赖性和微管非依赖性调节途径的控制。
