Nakayama T, Hashimoto Y, Kaneko Y, Yoshida M, Beppu T, Ohmi K, Yamashita S, Nonomura Y, Kurokawa K
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Experientia. 1993 Oct 15;49(10):876-80. doi: 10.1007/BF01952601.
The administration of 200 nM K252a to HuH7 suppressed the proliferation of the cells almost completely. The uptake of [3H]thymidine was inhibited, and flow cytometry revealed only one peak at 2C on day 3 after treatment with 100 nM K252a. The expression of proto-oncogene c-myc was not reduced. Despite the blockage at G1, both the size of the cells and the amount of cell protein had increased by 4 times by day 3 after treatment with K252a, while the cells secreted albumin and alpha-fetoprotein into the medium as usual. These results show that K252a can increase the cell size of HuH7 without losing its function by blocking the cell cycle at G1 phase.
向HuH7细胞施用200 nM的K252a几乎完全抑制了细胞的增殖。[3H]胸苷的摄取受到抑制，流式细胞术显示在用100 nM K252a处理后第3天，仅在2C处有一个峰。原癌基因c-myc的表达没有降低。尽管在G1期受阻，但在用K252a处理后第3天，细胞大小和细胞蛋白量均增加了4倍，而细胞仍像往常一样向培养基中分泌白蛋白和甲胎蛋白。这些结果表明，K252a可以通过在G1期阻断细胞周期来增加HuH7细胞的大小，而不会丧失其功能。
