视黄酸对人肝癌细胞蛋白激酶的影响

Effect of Retinoic Acid on Protein Kinase Activies in Human Hepatocarcinoma Cells

视黄酸(RA)处理SMMC-7721人肝癌细胞株72小时后,胞浆、膜性组分的蛋白激酶C(PK-C)的活力及比活力均下降,活力分别下降44.9％和48.8％,比活力下降42.7％和35.0％。然而,胞浆与膜性组分的活力,比活力比值在RA处理前后并无十分明显的变化,这提示在RA作用过程中,未发生PK-C的膜-浆转位。蛋白激酶A(PK-A)的变化则相反,RA处理72小时,活力、比活力上升了295％,258％。PK-A/PK-C的活力比值则从0.342增加到1.849,比活力比值从0.210增加到0.897。因PKC和PKA分别和细胞的去分化性增殖和分化有关,故上述结果和我们已报道的RA可抑制SMMC-7721细胞株的增殖和促进其分化相一致。

After 3 days retinoic acid (RA) treatment, the protein kinase C (PK-C) activities were inhibited both in cytosol and particulate fractions of SMMC-7721 human hapatocarcinoma cells, being 44.9% and 48.8% (calculated as activity) or 42.7% and 35.0% (calculated as specific activity) of the control values. However, the ratios of the cytosol and particulate fraction were not significantly different in RA treated and control cells, inidcating that the translocatron of PK-C from cytosol to particulate had not occured during the RA treatment. In contrast, the activity and specific activity of protein kinase A (PK-A) in RA treated cells were increased to 295% and 258% of the control valuse. The ratio of PK-A/PK-C was increased from 0.342 to 1.849 (calculated as activity) or from 0.210 to 0.897 (calculated as specific activity).It was reported that PK-C was increased during cell de-differenti-ative proliferation and PK-A increased during differentiation. Therefore, the above mentioned results are consistant with the results reported by us that RA inhibits the proliferation and stimulate the differentiation of SMMC-7721 cells.