ArticleThe Journal of pharmacology and experimental therapeutics2015
Omega-3 fatty acids and other FFA4 agonists inhibit growth factor signaling in human prostate cancer cells.
Article in The Journal of pharmacology and experimental therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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47 citing papers in PubMed, 100 citations in OpenAlex.
- Role of Host GPR120 in Mediating Dietary Omega-3 Fatty Acid Inhibition of Prostate Cancer.Journal of the National Cancer Institute · 2019Trial
- Structural mechanisms underlying distinct binding and activities of 18:0 and 18:1 lysophosphatidic acids at LPA1 receptor.PLoS computational biology · 2026Article
- The role of lysophosphatidic acid metabolism in castration-resistant prostate cancer progression.Frontiers in oncology · 2026Review
- Review
- G-protein coupled receptors in metabolic reprogramming and cancer.Pharmacology & therapeutics · 2025Review
- The Impact of Polyunsaturated Fatty Acids in Cancer and Therapeutic Strategies.Current nutrition reports · 2025Review
- Synthetic free fatty acid receptor (FFAR) 2 agonist 4-CMTB and FFAR4 agonist GSK13764 inhibit colon cancer cell growth and migration and regulate FFARs expression in in vitro and in vivo models of colorectal cancer.Pharmacological reports : PR · 2024Article
- Role for CCN1 in lysophosphatidic acid response in PC-3 human prostate cancer cells.Journal of cell communication and signaling · 2024Article
- Global Proteomics Analysis of Lysophosphatidic Acid Signaling in PC-3 Human Prostate Cancer Cells: Role of CCN1.International journal of molecular sciences · 2024Article
- FFAR4 activation inhibits lung adenocarcinoma via blocking respiratory chain complex assembly associated mitochondrial metabolism.Cellular & molecular biology letters · 2024Article
- From outside to inside and back again: the lysophosphatidic acid-CCN axis in signal transduction.Journal of cell communication and signaling · 2023Article
- PHF8-GLUL axis in lipid deposition and tumor growth of clear cell renal cell carcinoma.Science advances · 2023Article
- The role of lipid metabolism in cancer radioresistance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- The Involvement of Polyunsaturated Fatty Acids in Apoptosis Mechanisms and Their Implications in Cancer.International journal of molecular sciences · 2023Review
- Physicochemical and Biopharmaceutical Controllability of New Self-Assembled Fatty Acid Conjugated Leuprolide for the Enhanced Anticancer Activity.International journal of nanomedicine · 2023Article
- Upregulation of G-protein Coupled Receptor 120 in Rats Following Spinal Cord Injury.Neurochemical research · 2022Article
- GPR120 prevents colorectal adenocarcinoma progression by sustaining the mucosal barrier integrity.Scientific reports · 2022Article
- Serum Free Fatty Acids and G-Coupled Protein Receptors Are Associated With the Prognosis of Epithelial Ovarian Cancer.Frontiers in oncology · 2022Article
- Novel GPR120 Agonists with Improved Pharmacokinetic Profiles for the Treatment of Type 2 Diabetes.Molecules (Basel, Switzerland) · 2021Article
- Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Omega-3 fatty acids (n-3 FAs) are proposed to have many beneficial effects on human health. However, the mechanisms underlying their potential cancer preventative effects are unclear. G protein-coupled receptors (GPCRs) of the free fatty acid receptor (FFAR) family, FFA1/GPR40 and FFA4/GPR120, specifically bind n-3 FAs as agonist ligands. In this study, we examined the effects of n-3 FAs in human prostate cancer cell lines. Initial studies established that the long-chain n-3 FAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid, inhibit proliferation of DU145 cells in response to lysophosphatidic acid (LPA), a mitogenic lipid mediator. When added alone to serum-starved DU145 cells, EPA transiently activates signaling events, including p70S6K phosphorylation. However, when added 15 minutes prior to LPA, EPA suppresses LPA-induced activating phosphorylations of ERK, FAK, and p70S6K, and expression of the matricellular protein CCN1. The rapid onset of the inhibitory action of EPA suggested involvement of a GPCR. Further studies showed that DU145 and PC-3 cells express mRNA and protein for both FFA4 and FFA1. TUG-891 (4-[(4-fluoro-4'-methyl[1,1'-biphenyl]-2-yl)methoxy]-benzenepropanoic acid), a selective agonist for FFA4, exerts inhibitory effects on LPA- and epidermal growth factor-induced proliferation and migration, similar to EPA, in DU145 and PC-3 cells. The effects of TUG-891 and EPA are readily reversible. The FFA1/FFA4 agonist GW9508 (4-[[(3-phenoxyphenyl)methyl]amino]-benzenepropranoic acid) likewise inhibits proliferation at doses that block FFA4. Knockdown of FFA4 expression prevents EPA- and TUG-891-induced inhibition of growth and migration. Together, these results indicate that activation of FFA4 initiates signaling events that can inhibit growth factor-induced signaling, providing a novel mechanism for suppression of cancer cell proliferation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.