Kanerva Anna, Lavilla-Alonso Sergio, Raki Mari, Kangasniemi Lotta, Bauerschmitz Gerd J, Takayama Koichi, Ristimäki Ari, Desmond Renee A, Hemminki Akseli
Cancer Gene Therapy Group, Molecular Cancer Biology Program and Transplantation Laboratory and Finnish Institute for Molecular Medicine, University of Helsinki, Helsinki, Finland.
PLoS One. 2008 Aug 13;3(8):e2917. doi: 10.1371/journal.pone.0002917.
Clinical trials have confirmed the safety of selectively oncolytic adenoviruses for treatment of advanced cancers. However, increasingly effective viruses could result in more toxicity and therefore it would be useful if replication could be abrogated if necessary. We analyzed viruses containing the cyclooxygenase-2 (Cox-2) or vascular endothelial growth factor (VEGF) promoter for controlling replication. Anti-inflammatory agents can lower Cox-2 protein levels and therefore we hypothesized that also the promoter might be affected. As Cox-2 modulates expression of VEGF, also the VEGF promoter might be controllable. First, we evaluated the effect of anti-inflammatory agents on promoter activity or adenovirus infectivity in vitro. Further, we analyzed the oncolytic potency of the viruses in vitro and in vivo with and without the reagents. Moreover, the effect of on virus replication was analyzed. We found that RGD-4C or Ad5/3 modified fibers improved the oncolytic potency of the viruses in vitro and in vivo. We found that both promoters could be downregulated with dexamethasone, sodium salicylate, or salicylic acid. Oncolytic efficacy correlated with the promoter activity and in vitro virus production could be abrogated with the substances. In vivo, we saw good therapeutic efficacy of the viruses in a model of intravenous therapy of metastatic cervical cancer, but the inhibitory effect of dexamethasone was not strong enough to provide significant differences in a complex in vivo environment. Our results suggest that anti-inflammatory drugs may affect the replication of adenovirus, which might be relevant in case of replication associated side effects.
临床试验已证实选择性溶瘤腺病毒治疗晚期癌症的安全性。然而,病毒效力不断提高可能会导致更多毒性,因此如有必要能够废除病毒复制将很有用。我们分析了含有环氧合酶-2(Cox-2)或血管内皮生长因子(VEGF)启动子以控制复制的病毒。抗炎药可降低Cox-2蛋白水平,因此我们推测启动子也可能受到影响。由于Cox-2调节VEGF的表达,VEGF启动子也可能是可控的。首先,我们评估了抗炎药对体外启动子活性或腺病毒感染性的影响。此外,我们分析了有无这些试剂时病毒在体外和体内的溶瘤效力。而且,分析了对病毒复制的影响。我们发现RGD-4C或Ad5/3修饰的纤维提高了病毒在体外和体内的溶瘤效力。我们发现地塞米松、水杨酸钠或水杨酸均可下调这两种启动子。溶瘤效力与启动子活性相关,这些物质可废除体外病毒产生。在体内,我们在转移性宫颈癌静脉治疗模型中看到了病毒良好的治疗效果,但地塞米松的抑制作用在复杂的体内环境中不够强,无法产生显著差异。我们的结果表明,抗炎药可能会影响腺病毒的复制,这在复制相关的副作用情况下可能具有相关性。