摘要
检测以维甲酸（ＲＡ）、１，２５－二羟基维生素Ｄ３（１，２５（ＯＨ）２ＶＤ３）诱导２ｄ、佛波酯（ＰＭＡ）诱导６ｈ的人大肠癌细胞ＣＣＬ（２２９）的蛋白激酶Ｃ（ＰＫＣ）及其抑制剂活性．结果显示：诱导后ＰＫＣ总活性升高（Ｐ＜０．０５）；ＲＡ、１，２５（ＯＨ）２ＶＤ３诱导引起细胞质ＰＫＣ活性增加，ＰＭＡ诱导后细胞膜ＰＫＣ比率（细胞膜活性／总活性）显著升高（Ｐ＜０．０１）；诱导后ＰＫＣ抑制剂活性均降低，其中１，２５（ＯＨ）２ＶＤ３组与对照组有显著差异（Ｐ＜０．０５）；提示ＰＭＡ引起ＰＫＣ从细胞质向细胞膜转移，不同药物诱导后ＰＫＣ及其抑制剂活性出现不同的相对均衡关系．
Protein kinase C (PKC) and its inhibitor activities were measured in human coloretal cancer cell line CCL229 induced by retinoic acid (RA) and 1, 25-dihydroxyvitamin D3 (1, 25 (OH)2VD3) both for two days and phorbol 12-myristate 13-acetate (PMA ) for six hours. The results showed that total PKC activity was markedly increased after treatment with three inducers (P < 0. 05 ). Thecytosolic PKC activities were significantly increased in RA and 1, 25 (OH)2VD3 treated CCL229 cells (P< 0. 05 ). In PMA-treated cells, the membrane ratio (membrane activity/total activity) was significantly increased (P<0. 01 ). The levels of PKCinhibitor in cytosolic membrane supernatants after treatment with three inducers were all decreased. Among these three inducers, 1, 25(OH)2VD3 caused significantly difference compared with control. The results implied that PMA translocates PKC from the cytosolic to membrane fraction, PKC and its inhibitor in RA, 1, 25 (OH)2VD3 and PMA-induced cells are in different relatively parralel relationship.
出处
《生物化学与生物物理进展》
SCIE
CAS
CSCD
北大核心
1996年第1期52-56,共5页
Progress In Biochemistry and Biophysics
关键词
大肠肿瘤
癌细胞
蛋白激酶C
抑制剂
protein kinases C, inhibitor,human coloretal cancer cells, differentiation
