Chen W, Lee Y, Wang H, Yu G G, Jiao W, Zhou W, Zeng Y
Department of Tumor Virus and HIV, Institute of Virology, Chinese Academy of Preventive Medicine, Beijing.
J Cancer Res Clin Oncol. 1992;119(1):46-8. doi: 10.1007/BF01209487.
Wild-type and mutant human p53 genes were transfected into the nasopharyngeal carcinoma (NPC) cell line CNE-3. Tumorigenicity in nude mice showed that the tumor resulting from the cells transfected with the wild-type p53 gene grew more slowly and was smaller than that from the cells transfected with mutant p53 gene and that from control CNE-3 cells. In contrast, the tumor from the cells transfected with the mutant p53 gene grew faster than that produced by cells transfected with the wild-type p53 gene and that produced by control CNE-3 cells. The results demonstrate that the wild-type p53 gene could inhibit the NPC cell growth in nude mice and the mutant p53 gene could enhance the NPC cell growth in nude mice. The p53 gene may also play an important role in the pathogenesis of NPC.
将野生型和突变型人p53基因转染至鼻咽癌(NPC)细胞系CNE - 3中。裸鼠致瘤性实验表明,野生型p53基因转染细胞形成的肿瘤生长更缓慢且体积小于突变型p53基因转染细胞及对照CNE - 3细胞形成的肿瘤。相反,突变型p53基因转染细胞形成的肿瘤比野生型p53基因转染细胞及对照CNE - 3细胞形成的肿瘤生长更快。结果表明,野生型p53基因可抑制裸鼠体内NPC细胞生长,而突变型p53基因可促进裸鼠体内NPC细胞生长。p53基因可能在NPC的发病机制中也发挥重要作用。