ArticleJournal of pharmaceutical analysis2025
USP50-mediated NLRP3 deubiquitination enhances NLRP3 inflammasome activation to suppress HCC metastasis.
Article in Journal of pharmaceutical analysis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Nifuroxazide Pretreatment Protects Against Acute CdClAntioxidants (Basel, Switzerland) · 2026Article
- Reprogramming of the hepatic ubiquitin‑immune axis: A unifying mechanism in liver disease progression (Review).Molecular medicine reports · 2026Review
- Hepatocellular carcinoma metastasis-immune microenvironment crosstalk: emerging mechanisms and immunotherapy.Cellular & molecular biology letters · 2026Review
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Authors and funding
14 authors.
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Abstract
The nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome is downregulated in hepatocellular carcinoma (HCC), and its stability is regulated by ubiquitination. However, the regulatory mechanisms underlying NLRP3 deubiquitination and its role in HCC metastasis remains unclear. We demonstrated that ubiquitin-specific protease 50 (USP50) directly interacts with NLRP3, exhibiting deubiquitinase (DUB) activity through specific cleavage of K48-linked polyubiquitination chains to stabilize NLRP3 by preventing proteasomal degradation. Clinically, we observed that low NLRP3 and high β-catenin levels were negatively correlated in HCC specimens. Subsequent mechanistic exploration confirmed that NLRP3 exerts negative regulation on β-catenin by binding with glycogen synthase kinase 3 beta (GSK3β), reversing the downstream epithelial-mesenchymal transition (EMT) process, and inhibiting HCC metastasis. Notably, USP50 was found to activate NLRP3 inflammasome by promoting nuclear factor-kappa B (NF-κB) signaling, consequently enhancing proinflammatory cytokines. Furthermore, USP50 overexpression negatively regulated β-catenin, reversed EMT process and inhibited HCC metastasis
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