摘要
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。
BS PKC3 cells, which are normal human embryonic lung fibroblast cells (2BS) overexpressing PKC βⅠ isoform, are used as the model to investigate the effect of PKC βⅠ on the growth and transformation of 2BS cells. The morphological feature is altered in BS PKC3 cells. When maintained in monolayer culture, they developed dense foci. The BS PKC3 cells overproducing PKC βⅠ lost contact inhibition and anchorage dependence, decreased colonies formed in soft agar. The partial depolymerization of microfilaments was showed in BS PKC3 cells. The experiments provide the evidence that the overexpression of PKC βⅠ may induce disturbances in growth control and the appearance of partial transforming phenotype in 2BS cells. For further study, we have observed an increased level in c Ha ras and c sis protooncogene expression and a decreased level in tumor suppressor gene Rb in BS PKC3 cells. So it seems that the activity of PKC βⅠ may be of central importance in the process of multistage carcinogenesis. The expression of increased protooncogenes and deceased antioncogene may be one of the molecular mechanism of the effect on the disordered growth in 2BS cells by PKC βⅠ.
出处
《解剖学报》
CAS
CSCD
北大核心
1997年第1期76-80,共5页
Acta Anatomica Sinica
基金
国家自然科学基金
关键词
蛋白激酶C
胚肺
成纤维细胞
原癌基因
抑癌基因
Protein Kinase C
Human Embryonic Lung Cells
Transforming Phenotype
Expression of Protooncogene and Antioncogene
