Miyasaka M, Takami Y, Inoue H, Hakura A
Department of Tumor Virology, Osaka University, Japan.
J Virol. 1991 Jan;65(1):479-82. doi: 10.1128/JVI.65.1.479-482.1991.
The E6 and E7 genes of human papillomavirus type 16 (HPV-16) transform established lines of rat cells but not rat cells in primary culture irrespective of the expression of the two genes. The reason for this difference between the susceptibilities of cell lines and primary cells was examined by using hybrid cells obtained by somatic cell fusion of rat cell lines transformed by the E6 and E7 genes of HPV-16 and freshly isolated rat embryo fibroblast cells. In these hybrid cells, transformed phenotypes, including colony formation in soft agar, saturation density, and tumorigenicity in nude mice, were suppressed, whereas hybrid cells between E6/E7-transformed cell lines and normal rat cell lines retained these transformed phenotypes. RNA analysis showed that the E6 and E7 genes were transcribed in both types of hybrid cells. These results suggest that primary rat cells possess intracellular functions that cause posttranscriptional suppression of induction of the transformed phenotypes by the E6 and E7 genes of HPV-16.
人乳头瘤病毒16型（HPV - 16）的E6和E7基因可转化已建立的大鼠细胞系，但无论这两个基因的表达情况如何，都不能转化原代培养的大鼠细胞。利用由HPV - 16的E6和E7基因转化的大鼠细胞系与新鲜分离的大鼠胚胎成纤维细胞进行体细胞融合获得的杂交细胞，研究了细胞系和原代细胞易感性存在这种差异的原因。在这些杂交细胞中，包括软琼脂中集落形成、饱和密度和裸鼠致瘤性在内的转化表型受到抑制，而E6/E7转化细胞系与正常大鼠细胞系之间的杂交细胞则保留了这些转化表型。RNA分析表明，E6和E7基因在两种杂交细胞中均有转录。这些结果表明，原代大鼠细胞具有细胞内功能，可导致HPV - 16的E6和E7基因对转化表型诱导的转录后抑制。
