CDK4在去甲二氢愈创木酸抑制恶性胶质瘤细胞增殖中的作用

目的：探讨细胞周期蛋白依赖性蛋白激酶4（CDK4）在去甲二氢愈创木酸（NDGA）抑制人恶性胶质瘤细胞系SHG－44细胞增殖中的作用。方法：采用细胞培养、细胞计数、流式细胞仪检测、免疫沉淀、免疫组化及图像分析等技术方法。结果：①在10－200μmol/L浓度范围内，NDGA可使SHG－44细胞增殖受阻，且NDGA液浓度越高，这种作用越明显，即呈明显的剂量依赖性；②NDGA对细胞周期抑制作用主要表现于G1→期；③NDGA处理后，SHG－44细胞CDK4蛋白激酶的活性降低，且这种作用与NDGA的处理浓度呈正相关，与NDGA对SHG－44细胞的增殖抑制作用相一致；④NDGA处理后，SHG－44细胞CDK4基因的蛋白表达明显减弱。结论：CDK4蛋白激酶活性降低在NDGA抑制SHG－44细胞增殖中起着十分重要的作用。

Roles of cyclin-dependent kinase 4 (CDK4) in nordihydroguaiaretic acid-induced inhibitory effect on proliferation of human malignant glioma cells

Objective　To investigate roles of cyclin-dependent kinase 4 (CDK4) in nordihydroguaiaretic acid (NDGA)-induced inhibitory effect on proliferation of human malignant glioma cells. Methods　The techniques of cell culture, cell counts, flow cytometry, immunoprecipitation, immunohistochemistry and image analysis were employed in this study. Results　①A concentration-dependent inhibition of proliferation was demonstrated in the SHG-44 cells incubated for 24 hours in the presence of NDGA, and cell proliferation was blocked in the G1→S phase. ②The activity of CDK4 was decreased apparently in the SHG-44 cells treated for 24 hours with 10 to 200 μmol/L NDGA in a concentration-dependent way. ③The expression of CDK4 gene was downregulated in the cells after NDGA treatment. Conclusion　CDK4 plays an important role in NDGA-induced inhibition of glioma cell proliferation.