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,…
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