Interferon Regulation in Cancer: Tumor Vulnerabilities, Oncolytic Virus Exploitation, and Emerging Immunotherapeutic Strategies

Interferons (IFNs) are central regulators of antitumor immunity, cellular stress responses, and host defense mechanisms, yet their functions in cancer are highly context dependent. This review examines the dual role of IFN signaling in cancer, highlighting how tumors exploit defects in IFN pathways to escape immune surveillance while also exposing therapeutic vulnerabilities that can be targeted for treatment. Alterations in IFN production, signaling networks, and downstream effector mechanisms influence tumor initiation, progression, immune evasion, and therapeutic resistance. We discuss the molecular mechanisms by which cancer cells reshape IFN responses, including disruptions in antigen presentation, immune recognition, and tumor microenvironment interactions. Furthermore, oncolytic viruses exploit tumor-specific defects in antiviral signaling pathways, particularly IFN-related vulnerabilities, to selectively infect and eliminate malignant cells while stimulating antitumor immunity. Recent advances in immunotherapeutic strategies, including immune checkpoint blockade, adoptive cell therapies, and combination approaches integrating IFN modulation with viral-based therapies, have expanded opportunities for exploiting IFN biology in precision oncology. This review summarizes current mechanistic insights, therapeutic strategies, and emerging challenges associated with targeting IFN regulation in cancer. By integrating molecular mechanisms with translational applications, we provide a comprehensive framework for understanding how IFN pathways can be manipulated to improve cancer therapy.

Hali tarjima qilinmagan