ArticleOncoimmunology
Formyl peptide receptor 1 suppresses gastric cancer angiogenesis and growth by exploiting inflammation resolution pathways.
Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- Pro-resolving lipid mediators in diseases: exploring the molecular basis and clinical implication.Molecular biomedicine · 2026Review
- Assessing the potential of bacterial signal peptides for radiopharmaceutical applications.Scientific reports · 2025Article
- The neutrophil extracellular trap-related gene FPR1 (formyl peptide receptor 1) as a potential prognostic and therapeutic target in osteosarcoma.BMC musculoskeletal disorders · 2025Article
- TheFrontiers in immunology · 2025Review
- Aspirin-triggered DHA metabolites inhibit angiogenesis.Frontiers in pharmacology · 2025Article
- Tumor suppressor function of formyl peptide receptor 1 in gastrointestinal cancers: a focus on the underlying signaling.Frontiers in cell and developmental biology · 2025Review
- Molecular Mechanisms and Therapeutic Potential of Resolvins in Cancer - Current Status and Perspectives.Current medicinal chemistry · 2024Review
- Review
- Development of potent isoflavone-based formyl peptide receptor 1 (FPR1) antagonists and their effects in gastric cancer cell models.European journal of medicinal chemistry · 2023Article
- Harnessing Ferroptosis to Overcome Drug Resistance in Colorectal Cancer: Promising Therapeutic Approaches.Cancers · 2023Review
- The Role of Specialized Pro-Resolving Lipid Mediators in Inflammation-Induced Carcinogenesis.International journal of molecular sciences · 2023Review
- Protective and Pain-Killer Effects of AMC3, a Novel N-Formyl Peptide Receptors (FPRs) Modulator, in Experimental Models of Rheumatoid Arthritis.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Aspirin-Triggered Resolvin D1 (AT-RvD1) Protects Mouse Skin against UVB-Induced Inflammation and Oxidative Stress.Molecules (Basel, Switzerland) · 2023Article
- Targeting Angiogenesis via Resolution of Inflammation.Cold Spring Harbor perspectives in medicine · 2023Review
- An Update of G-Protein-Coupled Receptor Signaling and Its Deregulation in Gastric Carcinogenesis.Cancers · 2023Review
- Probiotic Lactobacillus rhamnosus GG (LGG) restrains the angiogenic potential of colorectal carcinoma cells by activating a proresolving program via formyl peptide receptor 1.Molecular oncology · 2022Article
- The Impact of Resolution of Inflammation on Tumor Microenvironment: Exploring New Ways to Control Cancer Progression.Cancers · 2022Review
- The Role of Lipid Metabolism in Gastric Cancer.Frontiers in oncology · 2022Review
- Toll-Like Receptor 7 Mediates Inflammation Resolution and Inhibition of Angiogenesis in Non-Small Cell Lung Cancer.Cancers · 2021Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation can result from inadequate engagement of resolution mechanisms, mainly accomplished by specialized pro-resolving mediators (SPMs) arising from the metabolic activity of lipoxygenases (ALOX5/15) on ω-6 or ω-3 essential polyunsaturated fatty acids (PUFA). We previously demonstrated that formyl peptide receptor 1 (FPR1) suppresses gastric cancer (GC) by inhibiting its inflammatory/angiogenic potential. In this study, we asked whether FPR1 exploits inflammation resolution pathways to suppress GC angiogenesis and growth. Here, we demonstrate that genetic or pharmacologic modulation of FPR1 in GC cells regulated ALOX5/15 expression and production of the SPMs Resolvin D1 (RvD1) and Lipoxin B4 (LXB4). SPM treatment of GC cells abated their angiogenic potential. Genetic deletion of ALOX15 or of the RvD1 receptor GPR32 increased the angiogenic and tumorigenic activity of GC cells thereby mimicking FPR1 loss. Deletion/inhibition of ALOX5/15 or GPR32 blocked FPR1-mediated anti-angiogenic activities, indicating that ALOX5/15 and GPR32 are required for FPR1's pro-resolving action. An ω-3- or ω-6-enriched diet enforced SPM endogenous production in mice and inhibited growth of shFPR1 GC xenografts by suppressing their angiogenic activity. These data implicate that FPR1 and/or pro-resolving pathway components might be used as risk/prognostic markers for GC; ω-6/3-enriched diets, and targeting FPR1 or SPM machinery may be exploited for GC management.
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