干扰素 --(IFN-) 广泛地在癌症治疗被使用了,但是临床的试用结果通常是令人失望的。我们的以前的研究证明了带 IFN-(ZD55-IFN-) 的 oncolytic 侵入人体气管粘膜的病菌展出重要反肿瘤活动。然而,内在的机制不是清楚的。这里,我们由激活混乱毛细管扩张以一种 p53 依赖的方式显示出那 ZD55-IFN- 导致感染的 S 阶段房间周期拘捕变异依赖者的 DNA 损坏小径。另外, ZD55-IFN- 感染能在癌症房间开始 caspase 依赖的 apoptosis 和 necroptosis。更重要地, ZD55-IFN- 在癌症房间上看了 synergistic 效果什么时候与 doxorubicin 结合了。这些结果建议有 doxorubicin 的 ZD55-IFN- 的联合可以在癌症治疗代表有希望的临床的策略。
Interferon-β (IFN-β) has been widely used in cancer therapy, but the clinical trial results are generally disappointing. Our previous studies have shown that an oncolytic adenovirus carrying IFN-β (ZD55-IFN-β) exhibits significant anti-tumor activities. However, the underlying mechanisms are not clear. Here we showed that ZD55- IFN-β infection-induced S-phase cell cycle arrest in a p53-dependent manner by activating the ataxia telangiectasia mutated-dependent DNA damage pathway. In addition, ZD55-IFN-β infection could initiate both caspase-dependent apoptosis and necroptosis in cancer cells. More importantly, ZD55-IFN-β showed a synergistic effect on cancer cells when combined with doxorubicin. These results suggest that the combination of ZD55-IFN- β with doxorubicin may represent a promising clinical strategy in cancer therapy.