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Review uncovers nuanced impact of nuclear factor κB on immune responses and tumor interactions, highlighting potential for cancer immunotherapy.
Inflammation plays a pivotal role in every stage of cancer development, from tumor initiation to progression, largely by influencing the balance between immune surveillance and immune evasion. At the heart of this inflammatory signaling is the transcription factor Nuclear Factor κB (NFκB), widely recognized as a key orchestrator of immune responses in malignancies. Within the framework of cancer immunoediting, comprising the three key phases Elimination, Equilibrium, and Escape, NFκB emerges as a double-edged sword. While it can enhance the activity and infiltration of effector immune cells that promote tumor destruction, it can also reprogram these cells into immunosuppressive subsets, thereby facilitating tumor immune evasion and growth. This dual functionality makes NFκB both a promising and challenging target in cancer immunotherapy. Despite its significance, comprehensive insights into NFκB’s roles across the immunoediting continuum remain limited. This review aims to bridge that gap by systematically exploring the multifaceted contributions of NFκB in modulating tumor-immune interactions, from immune-mediated tumor surveillance to immune escape, highlighting its potential and complexity as a therapeutic target.
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Mukherjee et al. (2025) studied this question.
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