SMMC7721肝癌细胞蛋白激酶B活性增高可驱动有功能的上皮钙粘着蛋白到细胞表面(英文)  

Driving Functional E-Cadherin onto Cell Surface by Elevation of PKB Activity in SMMC 7721 Hepato-carcinoma Cells

作　　者：陈舌[1] 殷祥雷[1] 宗鸿亮[1] 范凯谊[1] 黄传新[1] 顾建新[1] 申宗侯[1] 

机构地区：[1]复旦大学上海医学院生物化学系,上海200032

出　　处：《生物化学与生物物理进展》2003年第5期715-720,共6页Progress In Biochemistry and Biophysics

基　　金：国家自然科学基金 ( 3 963 0 0 80 ,3 9870 619,3 9970 3 3 8);上海市教委重点项目基金 (B990 80 6)资助项目~~

摘　　要：为了研究蛋白激酶B (PKB)对上皮钙粘着蛋白 (E cadherin)的调节 ,使用了用胰岛素处理的野生型SMMC 772 1细胞及稳定表达持续激活PKB的SMMC 772 1细胞株 (Gag PKB/SMMC 772 1) .用RNA印迹法和蛋白质印迹法检测细胞E cadherin表达 ,发现通过胰岛素刺激或在细胞中表达持续激活PKB从而增加PKB活性 ,不影响E cadherin的转录和蛋白质合成 ,但用流式细胞术和免疫荧光定位E cadherin ,则发现PKB活性增加能明显驱动E cadherin到细胞表面 ,从而导致部分通过E cadherin途径的细胞粘聚增加和细胞调亡的抑制 .因此 ,我们提供新的证据表明 ,增加PKB活性可驱动有功能的E cadherin分子到细胞表面 .In order to study the regulation of E-cadherin by protein kinase B (PKB), wild type SMMC 7721 hepato-carcinoma cells and a Gag-PKB/SMMC 7721 cell line where PKB activity is markedly increased compared with control cells were used. Interestingly, increasing PKB activity via insulin stimulation or Gag-PKB transfection does not enhance the E-cadherin in the level of mRNA and that of protein by using Northern blot and Western blot analysis, but markedly drives E-cadherin protein to cell surface by using flow cytometry analysis and immunofluorescence analysis localization of E-cadherin, which resulted in the increase of cell aggregation and the inhibition of cell apoptosis mostly via E-cadherin. Therefore, new evidences that elevation of PKB activity could drive functional E-cadherin molecule to cell surface are provided.

关 键 词：肝癌细胞 蛋白激酶B 活性增高 上皮钙粘着蛋白 细胞表面 细胞粘聚 失巢凋亡 

分 类 号：R735.7[医药卫生—肿瘤] Q255[医药卫生—临床医学]