ArticleCancer research2012
The proinflammatory myeloid cell receptor TREM-1 controls Kupffer cell activation and development of hepatocellular carcinoma.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.
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Who cites it
153 citing papers in PubMed, 227 citations in OpenAlex.
- Neupogen/MSCs conditioned media inhibit HEp-2 laryngeal cancer cells proliferation by down regulating miRNA 21expression and ROS production.Molecular biology reports · 2026Article
- Exercise reduces hepatic pre-metastatic niche formation via TREM-1 signaling in kupffer cells.BMC medicine · 2026Article
- Overexpression of TREM1 predicts poor prognosis and chemotherapy resistance in Egyptian acute myeloid leukemia associated with FLT3 internal tandem duplication and CD123 expression and stemness signatures.Discover oncology · 2026Article
- Integrative Analysis Reveals Genes Causal Relation with Ovarian Cancer and aging.Current topics in medicinal chemistry · 2026Article
- Review
- MEF2D-expressing cancer precursors reprogram tissue-resident macrophages to support liver tumorigenesis.Nature cancer · 2025Article
- Triggering Receptor Expressed on Myeloid Cells-1 (TREM-1) in Inflammation and Disease: Mechanisms, Therapeutic Potential, and Future Directions.International journal of molecular sciences · 2025Review
- TREM-1 Interacts with Rotavirus Proteins and Drives Inflammatory Responses: A Combined Experimental and Computational Approach.Pathogens (Basel, Switzerland) · 2025Article
- The tumor microenvironment's role in the response to immune checkpoint blockade.Nature cancer · 2025Review
- A novel 5-differentially expressed gene (DEG) signature predicting the prognosis in patients with metastatic liver malignancies and the prognostic and therapeutic potential of SPP1.International journal of clinical oncology · 2025Article
- Shortened PGLYRP1 Peptides Regulate Antitumor Activity of Cytotoxic Lymphocytes via TREM-1 Receptor: From Biology to Bioinformatics.International journal of molecular sciences · 2025Article
- Tissue-resident CCR2Cell reports · 2025Article
- CAT and CXCL8 are crucial cofactors for the progression of nonalcoholic steatohepatitis to hepatocellular carcinoma, the immune infiltration and prognosis of hepatocellular carcinoma.Discover oncology · 2025Article
- The properties of TREM1 and its emerging role in pain-related diseases.Molecular brain · 2025Review
- Small molecules as ligands in the tuning of immune regulatory receptors.Frontiers in immunology · 2025Review
- TREM1 is essential for maintaining stemness of liver cancer stem-like cells in hepatocellular carcinoma.Frontiers in immunology · 2025Article
- Biological impact and therapeutic implication of tumor-associated macrophages in hepatocellular carcinoma.Cell death & disease · 2024Review
- Article
- The roles of tissue resident macrophages in health and cancer.Experimental hematology & oncology · 2024Review
- Triggering receptor expressed on myeloid cells-1 in sepsis, and current insights into clinical studies.Critical care (London, England) · 2024Review
93 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic inflammation drives liver cancer pathogenesis, invasion, and metastasis. Liver Kupffer cells have crucial roles in mediating the inflammatory processes that promote liver cancer, but the mechanistic basis for their contributions are not fully understood. Here we show that expression of the proinflammatory myeloid cell surface receptor TREM-1 expressed by Kupffer cells is a crucial factor in the development and progression of liver cancer. Deletion of the murine homolog Trem1 in mice attenuated hepatocellular carcinogenesis triggered by diethylnitrosamine (DEN). Trem1 deficiency attenuated Kupffer cell activation by downregulating transcription and protein expression of interleukin (IL)-6, IL-1β, TNF, CCL2, and CXCL10. In addition, Trem1 ablation diminished activation of the p38, extracellular regulated kinase 1/2, JNK, mitogen-activated protein kinase, and NF-κB signaling pathways in Kupffer cells, resulting in diminished liver injury after DEN exposure. Adoptive transfer of wild-type Kupffer cells to Trem1-deficient mice complemented these defects and reversed unresponsiveness to DEN-induced liver injury and malignant development. Together, our findings offer causal evidence that TREM-1 is a pivotal determinant of Kupffer cell activation in liver carcinogenesis, deepening mechanistic insights into how chronic inflammation underpins the development and progression of liver cancer.
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