ArticleGut2025
NLRP6 deficiency enhances macrophage-mediated phagocytosis via E-Syt1 to inhibit hepatocellular carcinoma progression.
Article in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- Molecular mechanisms of tumor-associated macrophages in hepatocellular carcinoma development and therapy.World journal of gastroenterology · 2026Review
- Research progress on immune tolerance mechanisms in liver metastatic tumors and the "Liver-metastasis-oriented shared-mechanism therapeutic strategy" approach.Medical review (2021) · 2026Review
- Inflammasomes and pyroptosis in cancer: mechanisms and therapeutic advances.Journal of hematology & oncology · 2025Review
- Chimeric antigen receptor macrophages: a new frontier in hepatocellular carcinoma treatment.Cancer biology & medicine · 2025Article
- Engineered iron oxide nanoplatforms: reprogramming immunosuppressive niches for precision cancer theranostics.Molecular cancer · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCurrent treatments with tyrosine kinase inhibitors and immune checkpoint inhibitors have limited efficacy for hepatocellular carcinoma (HCC) due to drug resistance. Emerging therapies such as chimeric antigen receptor T (CAR-T) and macrophage-based cell therapies are promising but need to be improved.
objectivesThis study investigates the role of macrophage NOD-like receptor family pyrin domain containing 6 (NLRP6) in HCC progression and its therapeutic potential.
designImmunofluorescence staining was performed in patient samples. Liver tumour models (autonomous, orthotopic, subcutaneous) were developed, and RNA sequencing, flow cytometry and immunohistochemistry were performed in wild-type,
resultsCD68 (a macrophage marker) and NLRP6 expression were detected in patient HCC tissues, and patients with lower macrophage NLRP6 expression had longer survival. Compared with their wild-type mice,
conclusionsNLRP6 promotes HCC progression by inhibiting macrophage infiltration and suppressing phagocytosis via the interaction between its PYD domain and E-Syt1's SMP domain. Transfer of
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Registered trials
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