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Abstract Pyroptosis, a caspase-dependent form of inflammatory programmed cell death, is driven by inflammasome activation and gasdermin-mediated membrane pore formation. Its immunogenic nature has attracted increasing attention in oncology, particularly for overcoming therapeutic challenges such as chemoresistance, radiotherapy failure, and immune checkpoint blockade non-responsiveness. By promoting the release of pro-inflammatory cytokines and damage-associated molecular patterns (DAMPs), pyroptosis can enhance antitumor immunity and reshape the tumor microenvironment (TME). However, sustained or dysregulated pyroptosis can lead to chronic inflammation, radiotherapy-induced tissue injury, and tumorigenesis, making it a double-edged sword. Emerging evidence shows that pyroptosis exhibits cancer-type-specific roles, depending on the molecular context and the extent of activation. Therefore, understanding the molecular regulators, tumor-specific signaling, and temporal dynamics of pyroptosis is essential for its therapeutic modulation. This review comprehensively outlines the dual roles of pyroptosis in cancer progression and treatment, discusses its molecular mechanisms, and highlights recent strategies to harness or suppress pyroptosis for therapeutic gain. Targeting pyroptosis offers a promising, yet complex, avenue for immune-enhancing cancer therapies. Graphical abstract
Aram et al. (Tue,) studied this question.