Boulet Gaëlle, Horvath Caroline, Vanden Broeck Davy, Sahebali Shaira, Bogers Johannes
AMBIOR, Laboratory for Cell Biology & Histology, University of Antwerp, Groenenborgerlaan 171, BE-2020 Antwerp, Belgium.
Int J Biochem Cell Biol. 2007;39(11):2006-11. doi: 10.1016/j.biocel.2007.07.004. Epub 2007 Jul 19.
The recognition of a causal relationship between human papillomaviruses and cancer almost 30 years ago led to a rapid expansion of knowledge in the field, resulting in the description of the main mediators of HPV-induced carcinogenesis, the viral proteins E6 and E7. These oncoproteins show a remarkable pleiotropism in binding host-cell proteins, with the tumour suppressor genes p53 and pRb as their major targets. These interactions induce proliferation, immortalization and malignant transformation of infected cells. The link between HPV and cervical cancer led to the development of molecular methods, often based on the detection of E6 and E7, for screening and diagnosis. Therapeutic vaccines and gene therapy are primarily directed at E6 and E7. Although prophylactic vaccines are available, further understanding of the viral life cycle and the mechanisms underlying HPV-induced oncogenesis is necessary to face the many challenges in the field of HPV and cancer.
大约30年前，人类乳头瘤病毒与癌症之间因果关系的确认促使该领域知识迅速扩充，从而得以描述HPV诱导致癌作用的主要介质，即病毒蛋白E6和E7。这些癌蛋白在结合宿主细胞蛋白方面表现出显著的多效性，主要靶标是肿瘤抑制基因p53和pRb。这些相互作用诱导受感染细胞的增殖、永生化和恶性转化。HPV与宫颈癌之间的联系促使了分子方法的发展，这些方法通常基于对E6和E7的检测，用于筛查和诊断。治疗性疫苗和基因疗法主要针对E6和E7。尽管已有预防性疫苗，但要应对HPV与癌症领域的诸多挑战，仍有必要进一步了解病毒生命周期以及HPV诱导肿瘤发生的潜在机制。
