ReviewMolecular biology reports2026
The dual role of pyroptosis in prostate cancer: new perspectives from molecular mechanisms to clinical translation.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
1 author.
Funding
Abstract
Pyroptosis, a gasdermin-mediated form of programmed inflammatory cell death, plays a complex and context-dependent dual role in the initiation, progression, and therapeutic response of prostate cancer. This review methodically elucidates canonical and non-canonical pyroptotic molecular pathways, emphasizing their dysregulation in prostate cancer. On one hand, the epigenetic silencing of key effector proteins, such as Gasdermin E (GSDME), weakens pyroptosis’s tumor-suppressive and immune-activating functions, thereby promoting therapeutic resistance. On the other hand, sustained pyroptosis-associated inflammatory signaling shapes an immunosuppressive microenvironment, driving tumor progression. The article further explores novel therapeutic strategies targeting pyroptosis pathways, including restoring GSDME expression, developing specific inducers, co-activation of pyroptosis and ferroptosis pathways, and combination applications with chemotherapy or immune checkpoint inhibitors, while highlighting the potential of nanodelivery systems for achieving tumor-selective activation. Notwithstanding the persistent difficulties in biomarker development, tumor selectivity, and clinical translation, the modulation of pyroptosis presents a remarkably promising new paradigm for surmounting therapeutic challenges in castration-resistant and neuroendocrine prostate cancers.
Indexed as
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41838288What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.