Abstract
Absence in melanoma 2 (AIM2) protein functions as a double-stranded DNA sensor and is critical for host defense against intracellular bacterial and viral pathogens. Recent research has highlighted the significance of AIM2 in the pathogenesis of diverse malignancies. Through its recognition of foreign or intracellular dsDNA, AIM2 triggers inflammasome activation, resulting in the release of pro-inflammatory cytokines such as IL-1β, IL-18, and induction of pyroptosis. Additionally, AIM2 can engage alternative signaling pathways, such as AKT and NF-κB, independent of inflammasome activation, to modulate cancer progression. This review provides a comprehensive overview of recent advancements in understanding the involvement of AIM2 in the pathogenesis of different types of cancer through both inflammasome-dependent and inflammasome-independent mechanisms. Furthermore, we discuss the potential applications and challenges associated with targeting AIM2 in cancer therapy.