Chang Z F, Cheng S M
Department of Biochemistry, Chang Gung Medical College, Tao-Yuan, Taiwan, Republic of China.
Cancer Res. 1993 Jul 15;53(14):3253-6.
We have used the sequence of the cell-cycle regulatory region of human thymidine kinase promoter to study the DNA-protein interaction in human tumor and normal cells. By performing band-shift assays and DNase I footprint analysis, we have demonstrated that human tumor cells exhibited an elevated level of binding activity to the distal CCAAT box of human thymidine kinase promoter. The expression of human thymidine kinase CCAAT-binding activity was serum or independent in human tumor cells but serum dependent in normal human diploid fibroblasts. Our results present the fact that the constitutive interaction of CCAAT-binding factor with the promoter of a cell growth-controlled gene, such as thymidine kinase, is consistent with the loss of stringent cell growth regulation associated with tumorigenic phenotype.
我们利用人胸苷激酶启动子的细胞周期调控区域序列来研究人肿瘤细胞和正常细胞中的DNA-蛋白质相互作用。通过进行凝胶迁移实验和DNase I足迹分析,我们证明人肿瘤细胞对人胸苷激酶启动子的远端CCAAT盒的结合活性水平升高。人胸苷激酶CCAAT结合活性的表达在人肿瘤细胞中是血清非依赖性的,但在正常人二倍体成纤维细胞中是血清依赖性的。我们的结果表明,CCAAT结合因子与细胞生长调控基因(如胸苷激酶)启动子的组成性相互作用与肿瘤发生表型相关的严格细胞生长调控的丧失是一致的。