摘要
通过耗竭蛋白激酶C(PKC),用PKC抑制剂和激活剂等方法,观察PKC在鼻咽癌细胞系CNE-2Z生长中的作用。发现:随TPA浓度增大,细胞PKC含量降低,生长指数也逐渐减少;作用于PKC蛋白催化区的PKC抑制剂Staurosporine(ST)与作用于调节区的抑制剂Sphingosine(SS)均抑制CNE-2Z细胞的生长,最低有效浓度分别为2×10-7mol/L与10-5mol/L,随浓度增大而作用增强;PKC刺激剂OAG(0.1~100μg/ml)单独作用时对CNE-2Z的生长无明显影响,但4μg/ml可基本阻断ST或SS最低有效浓度的抑制效应。提示:PKC在鼻咽癌细胞CNE-2Z生长中起重要作用,阻断PKC的作用将为鼻咽癌的防治提供新的途径。
The role of protein kinase C(PKC)in the growth of nasopharyngeal carcinoma (NPC)epithelial cell line(CNE-2Z)was further studied by consuming PKC,and using inhibitors or stimulator.12-o-tetra-decanoylphorbol-13-acetate(TPA)(10-5mol/L) could partly consume PKC to 47.6%of control and cellular growth was inhibited by 40.2%of the control.Staurosporine(ST),a potent inhibitor acting on catalytic domain of PKC,and sphingosine(SS) ,a potent inhibitor acting on modulating domain,both could inhibit the growth of CNE-2Z.The lowest effective concentrations of ST and SS were 2×10-7mol/L and 10-5mo1/L respectively.Although OAG,a stimulator of PKC,could not make marked effect on cellular growth at concenttraion from 0.1μg/ml to 100μg/ml,4μg/ml basically blocked the inhibition effect of ST(2×10-7mol/L)and SS(10-5mol/L).Authors'findings give a strong suggestion that PKC plays an important role in growth of CNE-2Z cells,so blocking the action of PKC may be a new pathway to prevent and cure NPC.
出处
《广东医学院学报》
1995年第2期93-96,共4页
Journal of Guangdong Medical College
关键词
蛋白激酶C
鼻咽肿瘤
细胞株
病因
病理
protein kinase C
inhibitor
nasopharyngeal
neoplasm
Cell line
growth