Abstract
Oncolytic virus therapy of cancer is an actively pursued field of research. Viruses that were once considered as pathogens threatening the wellbeing of humans and animals alike are with every passing decade more prominently regarded as vehicles for genetic and oncolytic therapies. Oncolytic viruses kill cancer cells, sparing healthy tissues, and provoke an anticancer immune response. Among these viruses, recombinant adenoviruses are particularly attractive agents for oncolytic immunotherapy of cancer. Different approaches are currently examined to maximize their therapeutic effect. Here, knowledge of virus–host interactions may lead the way. In this regard, viral and host microRNAs are of particular interest. In addition, cellular factors inhibiting viral replication or dampening immune responses are being discovered. Therefore, applying RNA interference is an attractive approach to strengthen the anticancer efficacy of oncolytic viruses gaining attention in recent years. RNA interference can be used to fortify the virus’ cancer cell-killing and immune-stimulating properties and to suppress cellular pathways to cripple the tumor. In this review, we discuss different ways of how RNA interference may be utilized to increase the efficacy of oncolytic adenoviruses, to reveal their full potential.
Highlights
Oncolytic virus therapy of cancer is an actively pursued field of research
The latter group includes oncolytic viruses derived from adenovirus, herpes simplex virus (HSV), and vesicular stomatitis virus (VSV), as well as an attenuated and genetically modified strain of poliovirus [11,12,13]
This review focuses on oncolytic adenoviruses, but the general concepts discussed apply to other oncolytic viruses as well
Summary
Despite many different types of treatments used to combat cancer, cancer is still one of the leading causes of death worldwide. The third group consists of viruses that were genetically engineered by introducing mutations in their genome to ensure selective replication in cancer cells The latter group includes oncolytic viruses derived from adenovirus, HSV, and vesicular stomatitis virus (VSV), as well as an attenuated and genetically modified strain of poliovirus [11,12,13]. Replication-deficient adenovirus vectors lack genes from the E1 region and may have E3 genes deleted to accommodate newly introduced genes [16] These adenoviruses showed low toxicity and promising results compared to conventional therapy, their efficacy in clinical trials remained low, which minimizes their use. There is a clear need to increase the efficacy of OVT This could be achieved using more effective delivery methods or by enhancing the potency of CRAds to kill cancer cells or to induce an antitumor immune response. While most efforts are on improving anticancer treatment efficacy, studies are undertaken to more stringently control CRAd replication in healthy cells
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