Moens U, Van Ghelue M, Johannessen M
Department of Microbiology and Virology, Faculty of Medicine, University of Tromsø, N-9037, Tromsø, Norway.
Cell Mol Life Sci. 2007 Jul;64(13):1656-78. doi: 10.1007/s00018-007-7020-3.
The polyomaviruses BK, JC and SV40 are common in the human population. Their DNA genomes encode large T-antigen, small t-antigen, agnoprotein, and the capsid proteins VP1-3. Studies with these viruses have contributed extensively to the understanding of processes such as replication, transcriptional and posttranscriptional regulation, and cell cycle control. All three viruses can transform human cells in vitro, can induce tumours in animal models, and are strongly association with certain human cancers. It is generally assumed that large T-antigen is the major protein involved in neoplastic processes and that large T-antigen predominantly exerts its effect through deregulation of the tumour suppressors p53 and the retinoblastoma family members. However, additional properties of large T-antigen as well as the other viral proteins contribute to oncogenic processes. This review presents the different mechanisms by which the polyomavirus proteins can induce transformation and discusses which mechanisms may be operational in polyomavirus-positive cancers.
多瘤病毒BK、JC和SV40在人群中很常见。它们的DNA基因组编码大T抗原、小t抗原、agnoprotein和衣壳蛋白VP1 - 3。对这些病毒的研究极大地促进了人们对复制、转录和转录后调控以及细胞周期控制等过程的理解。这三种病毒都能在体外转化人类细胞，能在动物模型中诱导肿瘤，并且与某些人类癌症密切相关。一般认为大T抗原是参与肿瘤形成过程的主要蛋白质，并且大T抗原主要通过解除肿瘤抑制因子p53和视网膜母细胞瘤家族成员的调控来发挥作用。然而，大T抗原以及其他病毒蛋白的其他特性也有助于致癌过程。本综述介绍了多瘤病毒蛋白诱导转化的不同机制，并讨论了哪些机制可能在多瘤病毒阳性癌症中起作用。
