ArticleCell death discovery2025
Gasdermin E in glioblastoma -pyroptosis resistance and tumor-promoting functions.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
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Who cites it
4 citing papers in PubMed.
- GSDME upregulation predicts poor prognosis in gastric cancer.Molecular biology reports · 2026Article
- Review
- Gasdermin as a Molecular Signature and Predictor of Adult-Type Diffuse Glioma Severity and Grading.Journal of clinical medicine · 2026Article
- Pyroptosis in cancer therapy: a double-edged sword for immune activation and tumor progression.Molecular cancer · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Treatment of glioblastoma (GB), the most common and most aggressive malignant brain tumor, has made little progress over the past two decades. Despite extensive research on apoptosis and autophagy, necrotic cell death mechanisms like pyroptosis, which have the potential to stimulate anti-tumor immune responses, remain largely underexplored in GB. Here, we investigated whether Gasdermin E (GSDME)-mediated pyroptosis can be induced in GB by employing the drug raptinal, an inducer of cytochrome c release. Using human patient-derived and mouse GB cell lines, we showed that raptinal promotes GSMDE cleavage. However, although a strong pyroptotic response was observed in mouse cell lines, it was weak in human cell lines. This resistance was partially reversed by the calcium chelator BAPTA-AM, indicating that membrane repair mechanisms may counteract the pyroptotic response. Gsdme knockout (KO) in mouse GB cells unexpectedly prolonged the survival of immunocompetent mice, demonstrating a tumor-promoting role of GSDME independent of its pyroptotic function. Analysis of the immune microenvironment revealed that Gsdme KO promoted infiltration of T cells, which was confirmed by spatial transcriptomic analysis of GB patient samples. In addition, Gsdme/GSMDE KO reduced the invasive capacity of mouse/human GB cells. In conclusion, active membrane repair mechanisms may impair the pyroptotic efficacy in GB. GSDME has a tumor-promoting role in GB by suppressing T cell infiltration and increasing tumor cell invasion.
Identifiers
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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 OpenQuestion graph.