Fleer E A, Berkovic D, Eibl H, Unger C
Department of Hematology and Oncology, University Clinic of Goettingen, Germany.
Lipids. 1993 Aug;28(8):731-6. doi: 10.1007/BF02535995.
The uptake of [(9,10)-3H]hexadecylphosphocholine (HePC) in six tumor cell lines was studied. All cell lines incorporated HePC in similar amounts, with the exception of the epidermoid cancer cell line KB, which took up higher amounts of HePC. The uptake of HePC at 37 degrees C was shown to be time and concentration dependent. At 20 degrees C, uptake was drastically reduced and at 4 degrees C it was blocked completely. Binding of HePC, at 4 degrees C, was not saturable at concentrations between 5 micrograms/mL (11.8 microM) and 100 micrograms/mL (235.3 microM), indicating that cell surface binding is not receptor-mediated. Furthermore, the effects of inhibitors of endocytosis were investigated. We observed a pronounced inhibitory effect by monensin and cytochalasin B. Colchicine was somewhat less effective whereas chloroquine was almost without effect. From these data we conclude that uptake of HePC is most probably mediated via a receptor-independent endocytotic mechanism.
研究了六种肿瘤细胞系对[(9,10)-3H]十六烷基磷胆碱（HePC）的摄取情况。除表皮样癌细胞系KB摄取量较高外，所有细胞系摄取HePC的量相似。HePC在37℃时的摄取表现出时间和浓度依赖性。在20℃时，摄取量大幅降低，在4℃时则完全被阻断。在4℃时，HePC在5微克/毫升（11.8微摩尔）至100微克/毫升（235.3微摩尔）浓度范围内的结合不饱和，表明细胞表面结合不是受体介导的。此外，还研究了内吞作用抑制剂的影响。我们观察到莫能菌素和细胞松弛素B有明显的抑制作用。秋水仙碱的效果稍差，而氯喹几乎没有作用。从这些数据我们得出结论，HePC的摄取很可能是通过一种不依赖受体的内吞机制介导的。
