Pu H, Tsuji T, Kondo A, Fushimi K, Ohashi R, Inoue Y, Mimura T, Hamazaki K, Miyazaki M, Namba M
Department of Cell Biology, Okayama University Medical School, Japan.
Acta Med Okayama. 1997 Dec;51(6):313-9. doi: 10.18926/AMO/30772.
Characteristics of human hepatoma cell lines with the wild-type p53 were compared with those of human hepatoma cell lines with the mutant-type p53. The p21 protein located downstream of p53 was expressed in cell lines with the wild-type p53 but was not expressed in cell lines with the mutant-type p53. As to other tumor suppressor genes such as p16 and p27, there was no difference in their expression between both types of cell lines. In addition, no marked difference was observed in the activities of CDK2 and CDK4 between cell lines with the wild-type and the mutant-type p53. Phosphorylated Rb protein was detected in all cell lines except the HLE line, indicating that this cell line may have a deletion of and/or a mutation of the Rb gene. These results indicate that abnormalities of tumor suppressor genes other than p53, p16, p27, and Rb may be involved in hepatocarcinogenesis. The population doubling time of the wild-type p53 cells was significantly longer than that of the mutant p53 cells. Neither type of cell line showed a specific chromosome distribution which would indicate karyotype instability. The cell lines expressing the wild-type p53 produced tumors at lower frequency than those with the mutant p53 gene. Although there was no significant difference in effects of TGF-beta 1, EGF, cholera toxin, and db-cAMP on cell growth between the two types of cells, all three cell lines with the wild-type p53 were resistant to cytotoxicity of TNF-alpha, while two of the three with the mutant p53 were very sensitive to its cytotoxic effects.
将具有野生型p53的人肝癌细胞系的特征与具有突变型p53的人肝癌细胞系的特征进行了比较。位于p53下游的p21蛋白在具有野生型p53的细胞系中表达,但在具有突变型p53的细胞系中不表达。至于其他肿瘤抑制基因,如p16和p27,在这两种类型的细胞系之间其表达没有差异。此外,在具有野生型和突变型p53的细胞系之间,未观察到CDK2和CDK4活性有明显差异。除HLE细胞系外,在所有细胞系中均检测到磷酸化Rb蛋白,这表明该细胞系可能存在Rb基因的缺失和/或突变。这些结果表明,除p53、p16、p27和Rb之外的肿瘤抑制基因异常可能参与肝癌发生。野生型p53细胞的群体倍增时间明显长于突变型p53细胞。两种类型的细胞系均未显示出表明核型不稳定的特定染色体分布。表达野生型p53的细胞系产生肿瘤的频率低于具有突变型p53基因的细胞系。尽管两种类型的细胞之间,TGF-β1、EGF、霍乱毒素和db-cAMP对细胞生长的影响没有显著差异,但所有三个具有野生型p53的细胞系对TNF-α的细胞毒性具有抗性,而三个具有突变型p53的细胞系中有两个对其细胞毒性非常敏感。