蛋白激酶C对鼻咽癌细胞c－myc，c－fos表达的影响

用蛋白激酶Ｃ（ＰＫＣ）抑制剂Ｓｔａｕｒｏｓｐｏｒｉｎｅ（ＳＴ，抑制催化亚基）与Ｓｐｈｉｎｇｏｓｉｎｅ（ＳＳ，抑制调节亚基）处理人鼻咽癌细胞系ＣＮＥ－２Ｚ，经点印迹后扫描定量和免疫细胞化学检测ｃ－ｍｙｃ、ｃ－ｆｏｓ表达及其分布。结果发现：（１）ｃ－ｍｙｃ蛋白：主要分布于胞浆，４０．７％的细胞核与胞浆均为阳性；经ＳＳ或ＳＴ处理后，表达明显减弱，且核阳性率分别为１７．３％与２３．３％。扫描定量在ＳＳ组为对照组的６０％±２５．７％（Ｐ＜０．０５），ＳＴ组为对照组的５５％±２５．９％（Ｐ＜０．０５）。（２）Ｃ－ｆｏｓ蛋白：主要分布于胞浆，２９．４％的细胞核与胞浆均为阳性，经ＳＳ或ＳＴ处理后，表达明显减弱，且核阳性率分别为９％与１０．２％。扫描定量ＳＳ组为对照组的５８．６％±２５％（Ｐ＜０．０５），ＳＴ组为对照组的５９．７％±２６．２％（Ｐ＜０．０５）。结果表明：使用ＰＫＣ抑制剂后，两种核癌基因产物量均有不同程度的减少，并且存在细胞内分布的改变，特别是其发挥效应的核内表达明显减少。结合我们以前所发现的ＰＫＣ抑制剂明显抑制ＣＮＥ—２Ｚ细胞生长的结果，提示这些癌基因可能参与了ＰＫＣ对ＣＮＥ—２Ｚ细胞生长的调节。

EFFECT OF PROTEIN KINASE C ON THE EXPRESSION AND DISTRIBUTION OF c-myc and c-fos IN NASOPHARYNGEAL CARCINOMA CELL LINE

The effects of protein kinase C (PKC) on the expression, distribution of c-myc, c-fos inCNE-2Z were studied by using inhibitors of PKC. CNE-2Z cells were treated with Staurosporine (ST), a potent inhibitor acting on catalytic domain of PKC, and Sphingosine(SS), a potent inhibitor acting on modulating domain. The relative volume of these oncogene proteins was determined by scanning the result of dot-blotting and the distribution ofthe proteins was examined by immunohistochemistry. The results showed that (1) The protein of c-myc was mainly located in the plasma and the positive cell rate in both plasma andnuclear is 40.7% in total. After treated with SS or ST, the expression of the protein in thenuclear decreased respectively to 17. 3% and 23. 3% in total. By scanning quantitative analysis the volume of the protein reduced respectively to 60% (P<0. 05) and 55% (P<0. 05) ofthe control. (2) The protein of c-fos was mainly located in the plasma and positive cell ratein both plasma and nuclear is 29. 4% in total. After treated with SS or ST I the expression ofthe protein in the nuclear decreased respectively to 9% and 10. 2% in total. The volume of cfos protein decreased respectively to 58. 6% (P<0. 05) and 59. 7% (P<0. 05) of the controlby scanning quantitative analysis. The present findings indicate that inhibition of PKC cansuppress the expression of c-myc and c-fos in CNE-2Z, and change their distribution in thecell, suggesting that these oncogenes may involve in the modulation of PKC to the growth ofCNE-2Z.