ArticleCell death & disease2025
NLRP12 decreases TRIM25-mediated HK2 degradation to promote glycolysis and H3K18la in gastric cancer.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Review
- Expression of the NLRP12/NF-κB/iNOS axis in lung tissues across stages of non-small cell lung cancer and its mechanism in mediating immune cell regulation.Translational cancer research · 2026Article
- The evolving landscape of the Warburg effect in gastric cancer: From molecular mechanisms to targeted therapy.Clinical and translational medicine · 2026Review
- Crosstalk between lactylation and other post-translational modifications in health and diseases.Molecular biomedicine · 2026Review
- Role of histone modifications in gastric cancer (Review).International journal of oncology · 2026Review
- TRIM25 promotes glioblastoma progression by stabilizing HIF-1α expression in normoxia through K11/K29 polyubiquitination.Cell death & disease · 2026Article
- Enhancing platinum-based chemotherapy efficacy and safety through combination therapy-mediated remodeling of autophagic homeostasis in gastric cancer.Cell death & disease · 2026Article
- YAP1 converts circELP2-mediated biochemical signals to mechanical forces through promoting cytoskeleton remodeling in pulmonary fibrosis.International journal of biological sciences · 2026Article
- NLRP12 in cancer: a context-dependent regulator of tumor progression, immunity, and metabolism.Frontiers in oncology · 2026Review
- Inflammasomes and pyroptosis in cancer: mechanisms and therapeutic advances.Journal of hematology & oncology · 2025Review
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8 authors.
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Abstract
Gastric cancer is the most common primary malignant tumor of the digestive system. Recent studies have shown that targeting tumor cell metabolic reprogramming is a key cancer treatment strategy. NLR family pyrin domain containing 12 (NLRP12) is related to innate immunity, inflammation and tumorigenesis, but its role in the progression of gastric cancer remains unclear. The present study revealed that NLRP12 was highly expressed in gastric cancer tissues and cells, as well as positively correlated with poor patient prognosis and survival. NLRP12 promoted the progression of gastric cancer mainly by promoting the metabolic reprogramming of gastric cancer cells, the expression of histone H3 lysine 18 lactylation (H3K18la) and the stabilization of hexokinase 2 (HK2), a crucial enzyme in glycolysis. In the present study, NLRP12 competes with HK2 for binding to TRIM25, selectively reducing the K63-linked ubiquitination of HK2. Moreover, NLRP12 also exerted a significant cancer-promoting effect in mouse models. In summary, the present study demonstrated that NLRP12 prevents TRIM25 from mediating the K63-linked ubiquitination of HK2, which inhibits HK2 degradation through the autophagosome-lysosome pathway, thereby increasing its protein stability. These changes increase lactic acid production and induce H3K18la, which increases Myc transcription, thereby advancing gastric cancer progression. These findings reveal a novel cancer-promoting mechanism of NLRP12, potentially leading to the identification of new therapeutic targets for gastric cancer treatment.
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