论文部分内容阅读
近年来发现蛋白激酶不但参与细胞的代谢调节,还与细胞的增殖和分化密切相关。除酪氨酸蛋白激酶是某些癌基因的表达产物外,钙-磷脂依赖性蛋白激酶(又称蛋白激酶C,PK-C)是促癌剂TPA(12-O-tetradecanoyl-phorbol-13-aeetatc)的受体。作者在前文中曾报导:分化诱导剂视黄酸可使人肝癌细胞株SMMC-7721中蛋白激酶C的活力明显降低;而蛋白激酶A(cAMP依赖性蛋白激酶,PKA)则明显增加。本文研究化学诱发大鼠肝癌早期病变中这两种蛋白激酶的变化,观察有无和视黄酸处理时相反的改变。为了证实诱癌是否成
In recent years, protein kinase not only involved in the regulation of cell metabolism, but also with cell proliferation and differentiation are closely related. In addition to tyrosine protein kinase is the expression product of some oncogenes, calcium-phospholipid-dependent protein kinase (also known as protein kinase C, PK-C) is a promoter of TPA (12-O-tetradecanoyl-phorbol-13- aeetatc) receptors. The authors previously reported that retinoic acid, a differentiation-inducing agent, significantly reduced the activity of protein kinase C in human hepatocellular carcinoma cell line SMMC-7721, while PKA (protein kinase A, PKA) was significantly increased. In this paper, the changes of these two protein kinases in chemically induced early lesions of hepatocellular carcinoma were observed to observe the changes in the opposite direction of the retinoic acid treatment. In order to confirm whether the induced cancer