ArticleJournal of experimental & clinical cancer research : CR2019
Inhibition of lung cancer growth and metastasis by DHA and its metabolite, RvD1, through miR-138-5p/FOXC1 pathway.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 91 citations in OpenAlex.
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- Comparative Effect of African Walnut Oil and Docosahexaenoic Acid on Hematological and Oxidative Stress Markers of Female Wistar Rats With 7,12-Dimethylbenz[a]anthracene-Induced Breast Cancer.Food science & nutrition · 2026Article
- FOXC1 drives lung cancer metastasis and functions as a target for AI-enabled anti-metastatic drug discovery.Frontiers in pharmacology · 2026Article
- Docosahexaenoic Acid Inhibits Osteoclastogenesis via FFAR4-Mediated Regulation of Inflammatory Cytokines.Molecules (Basel, Switzerland) · 2025Review
- Mode and Mechanism of Action of Omega-3 and Omega-6 Unsaturated Fatty Acids in Chronic Diseases.Nutrients · 2025Review
- Roles and therapeutic opportunities of ω-3 long-chain polyunsaturated fatty acids in lung cancer.iScience · 2025Review
- miRNA Expression Profile in Primary Limbal Epithelial Cells of Aniridia Patients.Investigative ophthalmology & visual science · 2025Article
- Omega-6/Omega-3 Ratio as a Protective Factor in Lung Cancer: A Mendelian Randomization Study on Polyunsaturated Fatty Acids and Lung Adenocarcinoma Risk.Journal of Cancer · 2025Article
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- Engineered extracellular vesicles for targeted reprogramming of cancer-associated fibroblasts to potentiate therapy of pancreatic cancer.Signal transduction and targeted therapy · 2024Article
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- Metabolic Alterations in Canine Mammary Tumors.Animals : an open access journal from MDPI · 2023Review
- Docosahexaenoic Acid as Master Regulator of Cellular Antioxidant Defenses: A Systematic Review.Antioxidants (Basel, Switzerland) · 2023Review
- The Potential of DHA as Cancer Therapy Strategies: A Narrative Review of In Vitro Cytotoxicity Trials.Nutrients · 2023Review
- Aspirin-Triggered Resolvin D1 (AT-RvD1) Protects Mouse Skin against UVB-Induced Inflammation and Oxidative Stress.Molecules (Basel, Switzerland) · 2023Article
- Targeting EGFR in Combination with Nutritional Supplements on Antitumor Efficacy in a Lung Cancer Mouse Model.Marine drugs · 2022Article
- Evaluating adipose-derived stem cell exosomes as miRNA drug delivery systems for the treatment of bladder cancer.Cancer medicine · 2022Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundNon small cell lung cancer (NSCLC) is one of the most common cancers in the world. DHA is known to be capable of suppressing NSCLC cell proliferation and metastasis. However, the mechanisms by which DHA exhibits its antitumor effects are unknown. Here we aimed to identify the effects and mechanisms of DHA and its metabolites on lung cancer cell growth and invasion.
methodsAs measures of cell proliferation and invasion ability, the cell viability and transwell assays were used in vitro. Transgenic mfat-1 mice, which convert ω-6 PUFAs to ω-3 PUFAs, were used to detect the effect of endogenous DHA on tumor transplantation. An LC - MS/MS analysis identified the elevation of several eicosanoid metabolites of DHA. By using qPCR miRNA microarray, online prediction software, luciferase reporter assays and Western blot analysis, we further elucidated the mechanisms.
resultsAddition of exogenous DHA inhibited the growth and invasion in NSCLC cells in vitro. Endogenously produced DHA attenuated LLC-derived tumor growth and metastasis in the transgenic mfat-1 mice. Among the elevation of DHA metabolites, resolvin D1 (RvD1) significantly contributed to the inhibition in cell growth and invasion. MiRNA microarray revealed that the level of miR-138-5p was significantly increased after RvD1 treatment. MiR-138-5p mimics decreased cell viability and invasion; while miR-138-5p inhibitor abolished RvD1-mediated suppression of cell viability and invasion. The expression of FOXC1 was significantly reduced upon overexpression of miR-138-5p while luciferase reporter assay showed that FOXC1 was a direct target of miR-138-5p. In vivo, endogenous DHA by the mfat-1 transgene enhanced miR-138-5p expression and decreased FOXC1 expression. Furthermore, overexpression of FOXC1 reversed the inhibition in cell viability and invasion induced by RvD1 treatment.
conclusionsThese data identified the RvD1/miR-138-5p/FOXC1 pathway as a novel mechanism by DHA and its metabolite, RvD1, and the potential of targeting such pathway as a therapeutic strategy in treating NSCLC.
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