Evidence map›Paper›PMID 41838288›Full record

ReviewMolecular biology reports2026

The dual role of pyroptosis in prostate cancer: new perspectives from molecular mechanisms to clinical translation.

Wenjian Li

Abstract readReview
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Wenjian LiThe Affiliated Changzhou Hospital of Xuzhou Medical University, Changzhou Third People's Hospital, Changzhou, Jiangsu, China. bolite@163.com.ORCID http://orcid.org/0000-0002-7650-8842

Funding

Changzhou Municipal Science and Technology Bureau CJ20253108
6 · The paper itself

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

Prostatic NeoplasmsPyroptosisAnimalsGasderminsGene Expression Regulation, NeoplasticHumansMaleSignal TransductionTumor MicroenvironmentGasderminsGSDME protein, humanCombination therapyGasdermin proteinProstate cancerPyroptosisTherapeutic resistance

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.