Abstract
In recent years, oncolytic virotherapy became a promising therapeutic approach, leading to the introduction of a novel generation of anticancer drugs. However, despite evoking an antitumor response, introducing an oncolytic virus (OV) to the patient is still inefficient to overcome both tumor protective mechanisms and the limitation of viral replication by the host. In cancer treatment, nuclear factor (NF)-κB has been extensively studied among important therapeutic targets. The pleiotropic nature of NF-κB transcription factor includes its involvement in immunity and tumorigenesis. Therefore, in many types of cancer, aberrant activation of NF-κB can be observed. At the same time, the activity of NF-κB can be modified by OVs, which trigger an immune response and modulate NF-κB signaling. Due to the limitation of a monotherapy exploiting OVs only, the antitumor effect can be enhanced by combining OV with NF-κB-modulating drugs. This review describes the influence of OVs on NF-κB activation in tumor cells showing NF-κB signaling as an important aspect, which should be taken into consideration when targeting tumor cells by OVs.
Highlights
Since its discovery in 1986, nuclear factor (NF)-κB has been widely studied and is well known as a pleiotropic transcription factor, which orchestrates inflammation, innate and adaptive immune responses, cell growth, and apoptosis
Canonical NF-κB signaling pathway, which results in nuclear translocation of RelA/p50 and c-Rel/p50 dimers, is triggered by certain receptors activated by proinflammatory cytokines, such as tumor necrosis factor (TNF)-α
Since NF-κB is a key player in tumorigenesis, NF-κB activation level may indicate the effectiveness of oncolytic virotherapy
Summary
Since its discovery in 1986, nuclear factor (NF)-κB has been widely studied and is well known as a pleiotropic transcription factor, which orchestrates inflammation, innate and adaptive immune responses, cell growth, and apoptosis. NF-κB is considered a good candidate for the therapeutic target, becoming an important focus in cancer research [1,2,3,4]. Cellular senescence, resulting from chemotherapy treatment, involves NF-κB activation. This suggests that blockage of NF-κB would prevent this outcome. Apoptotic defects of cancer cells are responsible for chemoresistance. These factors should be considered when targeting NF-κB in cancer treatment [1]
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