Vousden K H
Ludwig Institute for Cancer Research, St Mary's Hospital Medical School, London, UK.
Semin Cancer Biol. 1995 Apr;6(2):109-16. doi: 10.1006/scbi.1995.0014.
Human papillomavirus (HPVs) adenovirus and simian virus 40 (SV40) are small DNA viruses which can show oncogenic activity. Although not otherwise related, all three have adopted very similar strategies to deregulate cell growth; each virus encoding oncoproteins which interact with the same cellular targets. Of particular interest are the interactions with the cell encoded pRB and p53 proteins, products of tumour suppressor genes. Somatic mutation results in the loss of the pRB and p53 function in many cancers and the contribution of the viruses to tumour development appears to reflect their ability to inactivate these cellular proteins. Both pRB and p53 negatively regulate progress through the cell cycle and the action of the viral proteins has highlighted the central importance of these tumour suppressor proteins in maintaining normal cell growth.
人乳头瘤病毒（HPV）、腺病毒和猴病毒40（SV40）是能显示致癌活性的小型DNA病毒。尽管它们在其他方面并无关联，但这三种病毒都采用了非常相似的策略来解除对细胞生长的调控；每种病毒都编码与相同细胞靶点相互作用的癌蛋白。特别值得关注的是它们与细胞编码的pRB和p53蛋白（肿瘤抑制基因的产物）的相互作用。体细胞突变导致pRB和p53功能在许多癌症中丧失，而病毒对肿瘤发展的作用似乎反映了它们使这些细胞蛋白失活的能力。pRB和p53都通过细胞周期对进程进行负调控，病毒蛋白的作用凸显了这些肿瘤抑制蛋白在维持正常细胞生长中的核心重要性。
