Yutsudo M, Okamoto Y, Hakura A
Department of Tumor Virology, Osaka University, Suita, Japan.
Virology. 1988 Oct;166(2):594-7. doi: 10.1016/0042-6822(88)90532-6.
Human papillomavirus (HPV) type 16 is thought to be responsible for development of cervical carcinomas, but the mechanism of its carcinogenic action is unknown. To determine which viral genes are involved in cellular transformation, we constructed recombinant murine retrovirus DNAs containing various subgenomic fragments of the HPV 16 early region and examined their transforming activities. The results show that the E6 and E7 ORFs are the transforming genes of HPV 16; the former governs the tumorigenicity in nude mice and the latter influences cell growth properties such as saturation density and colony formation in soft agar. There may also be a tumor-suppressing gene in the E1-E2 ORF region, because the tumorigenic activity of recombinant DNA containing the E1 ORF and the 5' portion of the E2 ORF in addition to the E6 and E7 ORFs was much lower than that of recombinant DNA containing only the E6 and E7 ORFs.
人乳头瘤病毒16型（HPV-16）被认为是宫颈癌发生的病因，但致癌作用机制尚不清楚。为了确定哪些病毒基因参与细胞转化，我们构建了包含HPV-16早期区域各种亚基因组片段的重组鼠逆转录病毒DNA，并检测其转化活性。结果表明，E6和E7开放阅读框是HPV-16的转化基因；前者决定裸鼠中的致瘤性，后者影响细胞生长特性，如饱和密度和软琼脂中的集落形成。在E1-E2开放阅读框区域可能也存在一个肿瘤抑制基因，因为除E6和E7开放阅读框外，还包含E1开放阅读框和E2开放阅读框5'部分的重组DNA的致瘤活性远低于仅包含E6和E7开放阅读框的重组DNA。
