Chai X Y
Shanghai Medical University.
Zhonghua Zhong Liu Za Zhi. 1993 May;15(3):182-4.
Phorbol-12-myristate-13-acetate (PMA) induced a dose-dependent proliferation of human hepatocarcinoma cell line SMMC-7721. In the presence of 100 nmol/L PMA, the activity of alkaline phosphatase was decreased and gamma-glutamyltransferase increased in the cell, suggesting that PMA is a proliferative inducer of hepatocarcinoma cell. PMA (100 nmol/L) also lead to a cytosol to membrane translocation of protein kinase C (PKC) within 5 minutes and down regulation after 1 hour. The decline of PKC activity in cytosolic fraction was far faster than that of membranous fraction. After long-term treatment with PMA for 1-5 days, the activities of PKC in cytosolic or membranous fraction almost disappeared, but the tyrosine protein kinase in both subcellular fractions was increased, being most obviously on the third day of culture. The increase in cytosolic TPK was more than that of membranous TPK, further indicating that TPK is a marker of cell proliferation.
佛波醇-12-肉豆蔻酸酯-13-乙酸酯（PMA）诱导人肝癌细胞系SMMC-7721呈剂量依赖性增殖。在100 nmol/L PMA存在的情况下，细胞内碱性磷酸酶活性降低，γ-谷氨酰转移酶活性增加，提示PMA是肝癌细胞的增殖诱导剂。100 nmol/L的PMA还可在5分钟内导致蛋白激酶C（PKC）从胞质溶胶转位至细胞膜，并在1小时后下调。胞质部分PKC活性的下降远比膜部分快。用PMA长期处理1至5天后，胞质或膜部分的PKC活性几乎消失，但两个亚细胞部分的酪氨酸蛋白激酶均增加，在培养的第三天最为明显。胞质酪氨酸蛋白激酶（TPK）的增加幅度大于膜TPK，进一步表明TPK是细胞增殖的标志物。
