论文部分内容阅读
为探讨ＰＫＣ亚类在细胞增殖与转化中的可能作用，用稳定的过表达蛋白激酶Ｃ（ｐｒｏｔｅｉｎｋｉ－ｎａｓｅＣ，ＰＫＣ）βⅠ亚类的人胚肺成纤维细胞２ＢＳ（ＢＳ－ＰＫＣ３）为模型，研究了ＰＫＣβⅠ亚类对２ＢＳ细胞生长与转化的影响。结果表明，过表达βⅠ的２ＢＳ细胞形态发生变化，单层培养时出现堆积生长，表明丧失接触抑制。进一步观察到实验组细胞中血清生长依赖性下降，贴壁依赖性降低，在软琼脂中可形成集落，同时细胞中微丝发生部分解聚。某些原癌基因如ｃ－ｓｉｓ、ｃ－Ｈａ－ｒａｓ的表达加强，而抑癌基因Ｒｂ的表达则下降。实验表明，过量表达ＰＫＣβⅠ可导致正常２ＢＳ细胞生长调节紊乱，诱导２ＢＳ细胞出现部分转化表型。因此可能在致癌多阶段过程中ＰＫＣβⅠ的活化发挥着重要作用，一些原癌基因表达的增强和抑癌基因表达之阻抑可能是ＰＫＣβⅠ作用于２ＢＳ细胞生长调节失控的分子机理之一。
In order to investigate the possible role of PKC subclass in cell proliferation and transformation, we used a model of human embryonic lung fibroblast 2BS (BS-PKC3) that was overexpressed in protein kinase C (PKC) Effect of PKCβI subclass on the growth and transformation of 2BS cells. The results showed that the morphology of 2BS cells overexpressing βⅠ changed, and the accumulation growth appeared in monolayer culture, indicating the loss of contact inhibition. Further observation showed that the experimental group of cells in serum-dependent decline in anchorage-dependent reduction in soft agar colonies can be formed at the same time, cells in the microfibril partial depolymerization. Some proto-oncogenes such as c-sis, c-Ha-ras expression increased, while the expression of tumor suppressor gene Rb decreased. Experiments show that overexpression of PKCβ Ⅰ can lead to normal 2BS cell growth disorders, inducing 2BS cells partially transformed phenotype. Therefore, it is possible that PKCβⅠactivation plays an important role in multi-stage carcinogenesis. The enhancement of some oncogenes and the suppression of tumor suppressor gene may be one of the molecular mechanisms of PKCβⅠregulating the regulation of cell growth in 2BS.