Crook T, Fisher C, Vousden K H
Ludwig Institute for Cancer Research, St. Mary's Hospital Medical School, London, United Kingdom.
J Virol. 1991 Jan;65(1):505-10. doi: 10.1128/JVI.65.1.505-510.1991.
The E7 protein is one of the principle transforming proteins encoded by human papillomavirus type 16 (HPV16), a virus strongly associated with the development of cervical carcinoma. In the present study we show that cotransfection of wild-type human or murine p53 sequences with E7 and ras markedly reduces transformation in baby rat kidney cells, although no effect of p53 is seen on the ability of E7 to transform an established mouse line to anchorage independence. In contrast, expression of mutant p53 strongly potentiates the transforming function of E7 and confers marked growth factor independence to cells cotransformed by E7 and ras. These data suggest that E7 and p53 function in separate yet complementary biochemical pathways.
E7蛋白是16型人乳头瘤病毒(HPV16)编码的主要转化蛋白之一,该病毒与宫颈癌的发生密切相关。在本研究中,我们发现,野生型人或鼠p53序列与E7和ras共转染可显著降低幼鼠肾细胞的转化,尽管未观察到p53对E7将已建立的小鼠细胞系转化为不依赖贴壁生长能力的影响。相反,突变型p53的表达可强烈增强E7的转化功能,并赋予由E7和ras共转化的细胞显著的生长因子非依赖性。这些数据表明,E7和p53在不同但互补的生化途径中发挥作用。