ArticleJournal of gastrointestinal oncology2026
Silencing OTUB1 induces pyroptosis to inhibit the growth of liver cancer HepG2 cells via the NLRP3/caspase/GSDM signaling pathway.
Article in Journal of gastrointestinal oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Linking deubiquitination to pyroptosis: new perspectives from OTUB1 in hepatocellular carcinoma.Journal of gastrointestinal oncology · 2026Article
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10 authors.
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Abstract
Background: Liver cancer is one of the most common malignant tumors worldwide. Pyroptosis, a novel form of programmed cell death, plays an important role in the occurrence and development of liver cancer. The deubiquitinase OTUB1 is associated with various types of programmed cell death, but its relationship with pyroptosis is unclear. To study the role and mechanism of OTUB1 in pyroptosis in liver cancer, we conducted this study. Methods: First, we searched for survival data of liver cancer patients in The Cancer Genome Atlas (TCGA) database and performed Kaplan-Meier analysis to evaluate the impact of OTUB1 expression on liver cancer prognosis. Then, OTUB1 small interfering RNA (siRNA) was transfected into HepG2 cells, and cell growth was subsequently measured using a Cell Counting Kit-8 (CCK-8) assay. At 72 hours after transfection, the morphology and structure of the pyroptotic cells were observed via transmission electron microscopy (TEM), and the protein levels of pyroptosis-related and signaling pathway-related proteins were measured via Western blotting. Results: The Kaplan-Meier curve indicated that patients with high OTUB1 expression had significantly lower survival rates compared to those with low expression, suggesting that high OTUB1 expression is associated with tumor progression and poor prognosis. In HepG2 cells, CCK-8 assays revealed that cell growth was inhibited, and pyroptosis was promoted in HepG2 cells at 72 hours after transfection. Moreover, OTUB1 knockdown increased NLRP3, cleaved caspase-1, -3, -4, -8, Smad4 and transforming growth factor beta (TGF-β) levels and reduced the protein expression of gasdermin D (GSDMD), GSDME, interleukin (IL)-1β, IL-18, β-catenin and STAT3. Conclusions: These results reveal that silencing OTUB1 induces pyroptosis to inhibit the growth of HepG2 cells via the NLRP3/caspase/GSDM signaling pathway, which may be related to OTUB1 regulation of the β-catenin, STAT3, TGF-β/Smad signaling pathways. These findings improve our understanding of the pathogenesis of liver cancer and reveal OTUB1 as a potential therapeutic target.
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