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)

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 .

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

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.