Kamata T, Sullivan N F, Wooten M W
Cold Spring Harbor Laboratory, New York 11724.
Oncogene. 1987 Mar;1(1):37-46.
We have examined phosphatidylinositol turnover and C-kinase distribution in a flat cellular ras-resistant cell line (C11) derived from Kirsten murine sarcoma virus (Ki-MSV) transformed NIH/3T3 cells (DT). This cell type has been shown to express high levels of the p21 Ki-ras gene product yet is resistant to the transforming effects of this protein. Our data indicate that C11 cells have reduced levels of total C-kinase activity when compared to NIH/3T3 cells and do not retain the ability to phosphorylate the growth associated 80-kDa C-kinase substrate either in vivo or in vitro. Furthermore, whilst the steady state levels of diacylglycerol and the sum of inositol phosphates are elevated in DT cells, in C11 cells these levels are reduced to an amount equivalent to that seen in NIH/3T3 cells. These data indicate a correlation between a protein kinase C dependent pathway and resistance to transformation by ras.
我们检测了源自 Kirsten 小鼠肉瘤病毒（Ki-MSV）转化的 NIH/3T3 细胞（DT）的扁平细胞 ras 抗性细胞系（C11）中的磷脂酰肌醇周转率和 C 激酶分布。已证明这种细胞类型表达高水平的 p21 Ki-ras 基因产物，但对该蛋白的转化作用具有抗性。我们的数据表明，与 NIH/3T3 细胞相比，C11 细胞的总 C 激酶活性水平降低，并且在体内或体外均不保留磷酸化与生长相关的 80 kDa C 激酶底物的能力。此外，虽然 DT 细胞中二酰基甘油的稳态水平和肌醇磷酸的总和升高，但在 C11 细胞中这些水平降低至与 NIH/3T3 细胞中所见相当的量。这些数据表明蛋白激酶 C 依赖性途径与对 ras 转化的抗性之间存在相关性。
