Dehazya P, Bell J, Sirover M A
Carcinogenesis. 1986 Apr;7(4):621-5. doi: 10.1093/carcin/7.4.621.
The effect of SV-40 viral transformation of human cells on the proliferation-dependent regulation of base excision repair was examined. Normal human diploid WI-38 fibroblasts and SV-40 transformed WI-38 cells were used to examine whether the process of transformation perturbed the regulation of base excision repair. The regulation of excision repair enzymes in each cell type was examined by quantitating: the specific activities of the base excision repair enzymes uracil DNA glycosylase and hypoxanthine DNA glycosylase as a function of cell growth; and immunological analysis of the uracil DNA glycosylase using monoclonal antibodies to human uracil DNA glycosylase. In each cell type, both DNA glycosylase activities were increased as a function of cell proliferation; the extent of enhancement being greater in the transformed cells. As defined by ELISA and immunoblot analysis, the induced uracil DNA glycosylases in both cell types share the same determinants. Although other repair processes are altered upon SV-40 transformation, these results suggest that the proliferation-dependent regulation of these base excision repair enzymes is retained in SV-40 transformed human cells.
研究了SV - 40病毒对人细胞的转化作用对碱基切除修复的增殖依赖性调节的影响。使用正常人二倍体WI - 38成纤维细胞和SV - 40转化的WI - 38细胞来检测转化过程是否扰乱了碱基切除修复的调节。通过定量分析每种细胞类型中切除修复酶的调节:作为细胞生长函数的碱基切除修复酶尿嘧啶DNA糖基化酶和次黄嘌呤DNA糖基化酶的比活性;以及使用抗人尿嘧啶DNA糖基化酶单克隆抗体对尿嘧啶DNA糖基化酶进行免疫分析。在每种细胞类型中,两种DNA糖基化酶活性均随着细胞增殖而增加;转化细胞中的增强程度更大。通过ELISA和免疫印迹分析确定,两种细胞类型中诱导的尿嘧啶DNA糖基化酶具有相同的决定簇。尽管在SV - 40转化后其他修复过程发生了改变,但这些结果表明,这些碱基切除修复酶的增殖依赖性调节在SV - 40转化的人细胞中得以保留。