Lee Y S, Sayeed M M, Wurster R D
Department of Neurological Surgery, Loyola University Medical Center, Maywood, IL 60153.
Cell Signal. 1993 Nov;5(6):803-9. doi: 10.1016/0898-6568(93)90041-j.
The effects of K+ channel modulators, tetraethylammonium, 4-aminopyridine and diazoxide, and high extracellular K+ on cell growth and agonist-induced intracellular Ca2+ mobilization were investigated. Two human brain tumour cell lines, U-373 MG astrocytoma and SK-N-MC neuroblastoma, were used as model cellular systems. K+ channel modulators and increased extracellular K+ concentration inhibited tumour cell growth in a dose-related fashion in both cell lines. In addition, agonist (carbachol or serum)-induced intracellular Ca2+ mobilization was also blocked by the pretreatment of growth-inhibitory concentrations of K+ channel modulators and high extracellular K+. Thus, these results suggest that K+ channel modulators are effective inhibitors of brain tumour cell growth and that their growth regulation may be due to the interference with the intracellular Ca2+ signalling mechanisms.
研究了钾离子通道调节剂(四乙铵、4-氨基吡啶和二氮嗪)以及高细胞外钾离子对细胞生长和激动剂诱导的细胞内钙离子动员的影响。使用两种人脑肿瘤细胞系,U-373 MG星形细胞瘤和SK-N-MC神经母细胞瘤作为模型细胞系统。钾离子通道调节剂和细胞外钾离子浓度升高以剂量相关的方式抑制了两种细胞系中的肿瘤细胞生长。此外,激动剂(卡巴胆碱或血清)诱导的细胞内钙离子动员也被生长抑制浓度的钾离子通道调节剂预处理和高细胞外钾离子所阻断。因此,这些结果表明钾离子通道调节剂是脑肿瘤细胞生长的有效抑制剂,并且它们的生长调节可能是由于干扰了细胞内钙离子信号传导机制。