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<p>Programmed cell death in cancer encompasses apoptosis, pyroptosis, necroptosis, ferroptosis, autophagy-dependent cell death and other interconnected programs. Within this broader landscape, apoptosis and pyroptosis are especially important because the same upstream anticancer pressure can generate different biological outputs: non-lytic apoptotic clearance, gasdermin-mediated lytic inflammation, or mixed death phenotypes. Rather than cataloguing these pathways as separate descriptions, this review integrates them as a cancer-specific switching network. It organizes the evidence around a sequence of determinants: the initiating tumor stress, the active caspase repertoire, the availability and cleavage site of gasdermin substrates, the cellular compartment in which death occurs, and the resulting immune or inflammatory output. The review discusses caspase-3-mediated cleavage of gasdermin E (GSDME), caspase-8-mediated regulation or cleavage of GSDMD and GSDMC, canonical and noncanonical inflammasome signaling, cFLIP, granzyme-mediated gasdermin cleavage, and autophagy-dependent removal of inflammasome stimuli. It distinguishes mechanisms shown in infection or myeloid-cell models from evidence demonstrated in tumor cells or tumor microenvironment models. This framework highlights when pyroptosis may overcome apoptotic resistance and enhance antitumor immunity, and when excessive or poorly localized pyroptosis may promote tissue injury, immune suppression or chronic tumor-supportive inflammation. A mechanistic, cancer-specific interpretation of apoptosis-pyroptosis crosstalk may support biomarker-guided therapeutic strategies that exploit immunogenic tumor-cell death while limiting inflammatory toxicity.</p>

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Molecular switches in cell death: the interplay of apoptosis and pyroptosis in cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月9日

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  • Yanfang Liu,
  • Yi Xie

摘要

Programmed cell death in cancer encompasses apoptosis, pyroptosis, necroptosis, ferroptosis, autophagy-dependent cell death and other interconnected programs. Within this broader landscape, apoptosis and pyroptosis are especially important because the same upstream anticancer pressure can generate different biological outputs: non-lytic apoptotic clearance, gasdermin-mediated lytic inflammation, or mixed death phenotypes. Rather than cataloguing these pathways as separate descriptions, this review integrates them as a cancer-specific switching network. It organizes the evidence around a sequence of determinants: the initiating tumor stress, the active caspase repertoire, the availability and cleavage site of gasdermin substrates, the cellular compartment in which death occurs, and the resulting immune or inflammatory output. The review discusses caspase-3-mediated cleavage of gasdermin E (GSDME), caspase-8-mediated regulation or cleavage of GSDMD and GSDMC, canonical and noncanonical inflammasome signaling, cFLIP, granzyme-mediated gasdermin cleavage, and autophagy-dependent removal of inflammasome stimuli. It distinguishes mechanisms shown in infection or myeloid-cell models from evidence demonstrated in tumor cells or tumor microenvironment models. This framework highlights when pyroptosis may overcome apoptotic resistance and enhance antitumor immunity, and when excessive or poorly localized pyroptosis may promote tissue injury, immune suppression or chronic tumor-supportive inflammation. A mechanistic, cancer-specific interpretation of apoptosis-pyroptosis crosstalk may support biomarker-guided therapeutic strategies that exploit immunogenic tumor-cell death while limiting inflammatory toxicity.