英国的一项新研究显示，目前常用于治疗艾滋病的药物——洛匹那韦也有助于治疗宫颈癌，实验显示它可以有选择地杀死即将癌变的细胞，却不会对正常细胞造成伤害。
英国曼彻斯特大学等机构的研究人员在新一期英国《抗病毒疗法》杂志上报告说，洛匹那韦对由人类乳头瘤病毒（HPV）引起的宫颈癌具有防治效果。研究人员在实验室中培养了人类细胞组织，结果发现洛匹那韦可杀死那些被HPV病毒感染且即将癌变的细胞，但同时对那些未被感染的正常细胞却没有什么不良影响。
研究人员伊恩·汉普森说，洛匹那韦已被证明是一种可安全口服的药物，不过本次研究显示如果要对付HPV病毒，用药浓度可能需达到现在口服药片所致浓度的10倍以上，这需要进一步开展临床研究加以确认。
人类乳头瘤病毒会造成皮肤或粘膜发生病变，是宫颈癌的主要诱因之一，此外它还会导致口腔癌和喉癌等癌症。（生物谷Bioon.com）
生物谷推荐原文出处：
Antiviral Therapy doi: 10.3851/IMP1786
Lopinavir up-regulates expression of the antiviral protein ribonuclease L in human papillomavirus-positive cervical carcinoma cells
Gavin Batman, Anthony W Oliver, Ingeborg Zehbe, Christina Richard, Lynne Hampson, Ian N Hampson
Abstract
Background: We have previously shown that the HIV protease inhibitor lopinavir has selective toxicity against human papillomavirus (HPV)-positive cervical carcinoma cells via an unknown mechanism.
Methods: SiHa cervical carcinoma cells were stably transfected with the proteasome sensor vector pZsProSensor-1 to confirm lopinavir inhibits the proteasome in these cells. The Panorama Xpress profiler 725 antibody array was then used to analyse specific changes in protein expression in lopinavir-treated versus control untreated SiHa cells followed by PCR and western blotting. Colorimetric growth assays of lopinavir-treated E6/E7 immortalised versus control human keratinocytes were performed. Targeted small interfering RNA gene silencing followed by growth assay comparison of lopinavir-treated/untreated SiHa cells was also used.
Results: Lopinavir induced an increase in the fluorescence of pZsProSensor-1 transfected SiHa cells, indicative of proteasomal inhibition. Ribonuclease L (RNASEL) protein was shown to be up-regulated in lopinavir-treated SiHa cells, which was confirmed by PCR and western blot. Targeted silencing of RNASEL reduced the sensitivity of SiHa cells to lopinavir. Selective toxicity against E6/E7 immortalised keratinocytes versus control cells was also seen with lopinavir and was associated with up-regulated RNASEL expression.
Conclusions: These data are consistent with the toxicity of lopinavir against HPV-positive cervical carcinoma cells being related to its ability to block viral proteasome activation and induce an up-regulation of the antiviral protein RNASEL. This is supported by the drug’s selective toxicity and up-regulation of RNASEL in E6/E7 immortalised keratinocytes combined with the increased resistance to lopinavir observed in SiHa cells following silencing of RNASEL gene expression.
