Jones D L, Münger K
Department of Pathology, Harvard Medical School, Boston, MA, USA.
Semin Cancer Biol. 1996 Dec;7(6):327-37. doi: 10.1006/scbi.1996.0042.
Human papillomavirus (HPVs) critically depend on the cellular machinery for the replication of their genome. Viral replication is restricted to the differentiated strata of the skin that are normally growth arrested. Hence, the HPVs have developed strategies to subvert cellular growth regulatory pathways and are able to uncouple cellular proliferation and differentiation. The HPV E7 protein can overcome the activity of some cyclin-dependent kinase inhibitors, associate with cyclin/cyclin dependent kinase complexes and bind to and destabilize the retinoblastoma tumor suppressor protein. These biological activities contribute to the carcinogenic potential of the high risk HPV E7 proteins which are consistently expressed in HPV-positive cervical carcinomas.
人乳头瘤病毒（HPV）的基因组复制严重依赖细胞机制。病毒复制局限于通常处于生长停滞状态的皮肤分化层。因此，HPV已形成策略来颠覆细胞生长调节途径，并能够使细胞增殖与分化解偶联。HPV E7蛋白可克服某些细胞周期蛋白依赖性激酶抑制剂的活性，与细胞周期蛋白/细胞周期蛋白依赖性激酶复合物结合，并与视网膜母细胞瘤肿瘤抑制蛋白结合并使其不稳定。这些生物学活性促成了高危型HPV E7蛋白的致癌潜力，而该蛋白在HPV阳性宫颈癌中持续表达。
