Pyroptosis plays a complex dual role in colorectal cancer—sometimes fueling, sometimes killing tumors.

Pyroptosis, a gasdermin-driven inflammatory cell death, can promote CRC via chronic inflammation and immunosuppressive TME, or suppress tumors through direct cancer cell killing and anti-tumor immunity activation. This review synthesizes molecular mechanisms, pathway crosstalk (apoptosis,…

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Pyroptosis plays a complex dual role in colorectal cancer—sometimes fueling, sometimes killing tumors.

Pyroptosis plays a complex dual role in colorectal cancer—sometimes fueling, sometimes killing tumors.

Pyroptosis, a gasdermin-driven inflammatory cell death, can promote CRC via chronic inflammation and immunosuppressive TME, or suppress tumors through direct cancer cell killing and anti-tumor immunity activation. This review synthesizes molecular mechanisms, pathway crosstalk (apoptosis, ferroptosis, PANoptosis), and regulatory networks including gut microbiota and epigenetics. Therapeutic strategies include nanomedicines, PDT/SDT, and chemosensitization.

Key Findings

  • Pyroptosis has context-dependent dual roles in CRC
  • Gasdermin family drives the process
  • Crosstalk with apoptosis, ferroptosis, and PANoptosis
  • Gut microbiota, metabolism, and epigenetics regulate pyroptosis
  • Emerging therapies include nanomedicines and PDT/SDT

Implications

New therapeutic targets for chemo-resistant CRC via context-sensitive pyroptosis manipulation.

Caveats

Review article; abstract-only. Most evidence preclinical. Dual-role complexity requires precise therapeutic control.

Source: Apoptosis : an international journal on programmed cell death — 2026-04-12

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