蛋白激酶C活性下降对Ha-ras基因表达及其调控序列结合蛋白的影响

THE EFFECT OF INHIBITION OF PROTEIN KINASE C ACTIVITY ON THE Ha-ras ONCOGENE EXPRESSION AND ITS BINDING PROTEIN

愈益增多的研究表明,蛋白激酶C(PKC)在细胞增殖和转化调控中占有重要位置,一些癌基因产物影响细胞增殖和转化与肌醇脂代谢信号通路,特别是与PKC活性密切有关;ras癌基因就是其中之一。在ras抗性细胞株内只有当PKC活性超过某一阈值时,ras基因产物才能表现出其转化细胞的能力,并且这种转化能力需要PKC的激活;Hsiao等发现稳定表达PKC的细胞系更易被活化的Ha-ras基因转化。上述实验表明PKC和ras癌基因在转化细胞的过程中表现出最佳的协同效应。

Transcription of Ha-ras oncogene is inhibited obviously when human gastric cancer cell line BGC-823 is treated With protein kinase C inhibitor H_7 and with PMA to deplete protein kinase C activity. Southwestern blot is used to detect DNA binding protein in Ha-ras oncogene transcriptional regulation region. Two protein bands 53 and 31K, extracted from nuclei of BGC-823 cells, can bind to 2.5kb fragment of Ha-ras oncogene regulation region, but they disappear in nuclear extract of BGC-823 cells treated with PMA to deplete protein kinase C activity. These results suggest that the two proteins may be regulated by protein kinase C. This regulation may affect the expression of Ha-ras oncogene.