ArticleScientific reports2025
Gpr109A in TAMs promoted hepatocellular carcinoma via increasing PKA/PPARγ/MerTK/IL-10/TGFβ induced M2c polarization.
Article in Scientific reports, 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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Who cites it
5 citing papers in PubMed.
- Macrophage programming in systemic sclerosis: Niches, networks, and translational horizons.Seminars in immunopathology · 2026Review
- GPCRs in CAR-T Cell Immunotherapy: Expanding the Target Landscape and Enhancing Therapeutic Efficacy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- GPR109a-AMPK axis mediates the Attenuation of uric acid-induced M1 macrophage polarization by β-hydroxybutyrate from Lacticaseibacillus rhamnosus M2b.Scientific reports · 2026Article
- Polysaccharides-gut microbiota interaction: mechanisms regulating the hepatocellular carcinoma immune microenvironment.Frontiers in immunology · 2026Review
- Microbiome-macrophage crosstalk in the tumor microenvironment: implications for oral squamous cell carcinoma progression and therapy.Frontiers in immunology · 2025Review
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Authors and funding
5 authors.
Funding
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Abstract
To delineate Gpr109A's role and mechanisms in modulating the immune microenvironment of hepatocellular carcinoma. Employing Gpr109A-knockout mice and in vitro co-cultures of hepatocellular carcinoma cells with macrophages, this study utilized a suite of techniques, including lentiviral vectors for stable cell line establishment, Western blotting, cell scratch, CCK-8, transwell assays, flow cytometry, immunohistochemistry and phagocytosis assay to assess various cellular behaviors and interactions. Gpr109A deletion markedly reduced the oncogenic potential of H22 cells, both in vivo and when co-cultured with knockout macrophages, impairing their growth, invasion, and migration. In Gpr109A-knockout macrophages, an upregulation of MerTK and a reduction in immunosuppressive cytokine release were observed, indicating a shift towards an M2c macrophage phenotype. This shift is linked to Gpr109A's role in promoting protease overexpression and inhibiting SHP2 phosphorylation, crucial for enhancing cancer cell proliferation and invasiveness. Gpr109A significantly influences macrophage polarization to the M2c type, augmenting hepatocellular carcinoma cell aggressiveness.
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