【摘要】 以人胃癌细胞ＢＧＣ－８２３为模型，在佛波酯（ｐｈｏｒｂｏｌ１２－ｍｙｒｉｓｔａｔｅ１３－ａｃｅｔａｔｅ，ＰＭＡ）导致蛋白激酶Ｃ（ＰＫＣ）负效应条件下，探讨了ＰＫＣ活性的阻抑与细胞恶性表型变化的相关性及其可能作用机理。ＰＭＡ（１００μｇ／Ｌ）处理ＢＧＣ－８２３细胞７２ｈ，细胞质、膜和核中ＰＫＣ活性分别下降３５．６％和７２．３％。经电泳分析，观察到细胞核蛋白质磷酸化水平也明显下降。在ＰＫＣ活性被阻抑的同时，人胃癌细胞形态发生变化，细胞呈单层生长，出现接触抑制，在软琼脂中不能形成集落。表现出部分恶性表型丢失，并且与人胃癌细胞恶化密切相关的癌基因Ｈａ－ｒａｓ基因表达也明显被阻抑。这可能是ＰＫＣ活性被阻抑引起人胃癌细胞部分恶性表型丢失的分子机理之一。更多还原

【Abstract】 Using human gastric cancer cell line BGC-823 as a model ,we have studied the effect of the inhibition of PKC which is resulted from longer treatment by PMA on malignant phenotype of cells. When BGC823 cells are treated with PMA( 100μg/L ) for 72hrs ,the PKC activity of cytosol and membrane decreases 35. 6 % and the PKC activity of nucleus decreases 72. 3 %. Moreover, by using electrophoresis, the phosphorylation levels of endogenous proteins from nuclei extracts decrease. In comparison with BGC-823 cells,the cells which are treated with PMA 100μg/L) for 72hrs exhibit striking alterations in morphology. Cells display contact inhibition and become flattened. In contrast to cancer cells which form large colonies in soft agar,the treated cells display loss of anchorage-independent growth in soft agar. At the same time, the expression of oncogene c-Ha-ras, which is relating closely to malignancy of BGC-823 cells, is inhibited obviously-So it seems that there may be one of the molecular mechanism of loss partial malignant phenotype of human gastric cancer cells by inhibition of PKC activity.更多还原