Storey A, Banks L
International Center for Genetic Engineering and Biotechnology, Trieste, Italy.
Oncogene. 1993 Apr;8(4):919-24.
Human papillomaviruses (HPVs) are small DNA tumor viruses, a subset of which is closely associated with the development of cervical cancer. The viral E6 and E7 open reading frames encode multifunctional proteins that bind respectively to the p53 protein and to the product of the retinoblastoma tumor-suppressor gene. In this study we demonstrate that the HPV-16 E6 gene cooperates with EJ-ras to immortalize primary cultures of mouse kidney epithelial cells. HPV-16-immortalized cell lines expressing E6 but not E7 contained low levels of wild-type p53 protein. In contrast, those cells immortalized by EJ-ras alone contained elevated p53 protein levels, and were shown to contain a mutation in the gene. These results suggest that activating mutations in the p53 gene can functionally substitute for HPV-16 E6 in transforming primary cells.
人乳头瘤病毒（HPV）是一类小型DNA肿瘤病毒，其中一部分与宫颈癌的发生密切相关。病毒的E6和E7开放阅读框编码多功能蛋白，它们分别与p53蛋白以及视网膜母细胞瘤肿瘤抑制基因的产物相结合。在本研究中，我们证明HPV - 16 E6基因与EJ - ras协同作用可使小鼠肾上皮细胞原代培养物永生化。表达E6但不表达E7的HPV - 16永生化细胞系含有低水平的野生型p53蛋白。相比之下，那些仅由EJ - ras永生化的细胞含有升高的p53蛋白水平，并且显示该基因存在突变。这些结果表明，p53基因中的激活突变在转化原代细胞时可在功能上替代HPV - 16 E6。
