Mantovani F, Banks L
International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
Oncogene. 1999 Jun 3;18(22):3309-15. doi: 10.1038/sj.onc.1202688.
The E6 proteins derived from tumour associated papillomavirus types target the cellular tumour suppressor protein p53 for ubiquitin mediated degradation. In cell lines derived from cervical tumours the p53 protein is present in very low amounts, but it can be activated by appropriate DNA damaging agents, indicating that functional p53 is present within these lines. Recent studies have also shown that different polymorphic forms of the p53 protein are differentially susceptible to E6 mediated degradation. Therefore we have been interested in analysing the effects of different HPV E6 proteins upon p53 levels in a variety of cervical tumour derived cell lines. We show that inhibition of E6 mediated degradation of p53 frequently results in increased levels of p53 expression. However, there are notable exceptions to this where increased p53 levels are only obtained following DNA damage and proteasome inhibition. We also show in E6 expressing cells, that as well as p53 being targeted for degradation, the localization of p53 to the nucleus is also inhibited, consistent with previous observations which indicate that degradation of p53 is not essential for E6 mediated inhibition of p53 function. These results have important implications for any potential therapies which might aim to block E6 mediated degradation of p53.
源自肿瘤相关乳头瘤病毒类型的E6蛋白将细胞肿瘤抑制蛋白p53作为泛素介导降解的靶点。在源自宫颈肿瘤的细胞系中,p53蛋白含量极低,但它可被适当的DNA损伤剂激活,这表明这些细胞系中存在功能性p53。最近的研究还表明,p53蛋白的不同多态形式对E6介导的降解敏感性不同。因此,我们一直对分析不同的人乳头瘤病毒E6蛋白对多种源自宫颈肿瘤的细胞系中p53水平的影响感兴趣。我们发现,抑制E6介导的p53降解常常导致p53表达水平升高。然而,也有明显的例外情况,即只有在DNA损伤和蛋白酶体抑制后才会出现p53水平升高。我们还在表达E6的细胞中发现,除了p53被靶向降解外,p53向细胞核的定位也受到抑制,这与之前的观察结果一致,即p53的降解对于E6介导的p53功能抑制并非必不可少。这些结果对于任何旨在阻断E6介导的p53降解的潜在治疗方法都具有重要意义。