CCL229细胞经诱导后蛋白激酶C及抑制剂活性的变化
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Study on Relationship Between Protein Kinase C, Its Inhibitor and Differentiation of Human Coloretal Cancer Cell CCL229
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    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CCL229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)2VD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.

    Abstract:

    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 ). The cytosolic 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 PKC inhibitor 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.

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王红梅,于秉治,王芸庆,宋今丹. CCL229细胞经诱导后蛋白激酶C及抑制剂活性的变化[J].生物化学与生物物理进展,1996,23(1):52-56

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  • 收稿日期:1995-01-20
  • 最后修改日期:1995-07-05
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