Pipas J M, Levine A J
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA 15260, USA.
Semin Cancer Biol. 2001 Feb;11(1):23-30. doi: 10.1006/scbi.2000.0343.
SV40 induces neoplastic transformation by disabling several key cellular growth regulatory circuits. Among these are the Rb- and p53-families of tumor suppressors. The multifunctional, virus-encoded large T antigen blocks the function of both Rb and p53. Large T antigen uses multiple mechanisms to block p53 activity, and this action contributes to tumorigenesis, in part, by blocking p53-mediated growth suppression and apoptosis. Since the p53 pathway is inactivated in most human tumors, T antigen/p53 interactions offer a possible mechanism by which SV40 contributes to human cancer.
猴空泡病毒40（SV40）通过破坏几个关键的细胞生长调节回路来诱导肿瘤转化。其中包括肿瘤抑制因子Rb家族和p53家族。多功能的、病毒编码的大T抗原会阻断Rb和p53的功能。大T抗原利用多种机制来阻断p53的活性，这种作用部分地通过阻断p53介导的生长抑制和细胞凋亡而促进肿瘤发生。由于p53通路在大多数人类肿瘤中失活，T抗原/p53相互作用提供了一种可能的机制，通过该机制SV40促成人类癌症。
