ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
15-Lipoxygenase-1 suppression of colitis-associated colon cancer through inhibition of the IL-6/STAT3 signaling pathway.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Regulatory role of PPAR in colorectal cancer.Cell death discovery · 2025Review
- Anti-inflammatory effects ofHeliyon · 2024Article
- The Role of Specialized Pro-Resolving Lipid Mediators in Inflammation-Induced Carcinogenesis.International journal of molecular sciences · 2023Review
- The role of peroxisome proliferator-activated receptors in the tumor microenvironment, tumor cell metabolism, and anticancer therapy.Frontiers in pharmacology · 2023Review
- PPAR-δ as a prognostic biomarker and its association with immune infiltrates in breast cancer PPAR-δ as a prognostic biomarker and its association with immune infiltrates in breast cancer.Journal of Cancer · 2023Article
- Rapid acceleration of KRAS-mutant pancreatic carcinogenesis via remodeling of tumor immune microenvironment by PPARδ.Nature communications · 2022Article
- Renal Cell Cancer and Obesity.International journal of molecular sciences · 2022Review
- Review
- Transcription Factors: The Fulcrum Between Cell Development and Carcinogenesis.Frontiers in oncology · 2021Review
- Molecular Targets in Precision Chemoprevention of Colorectal Cancer: An Update from Pre-Clinical to Clinical Trials.International journal of molecular sciences · 2020Review
- Influence of Lipoxygenase Inhibition on Glioblastoma Cell Biology.International journal of molecular sciences · 2020Article
- Suppression of Membranous LRP5 Recycling, Wnt/β-Catenin Signaling, and Colon Carcinogenesis by 15-LOX-1 Peroxidation of Linoleic Acid in PI3P.Cell reports · 2020Article
- PPAR Beta/Delta and the Hallmarks of Cancer.Cells · 2020Review
- The Role of PPAR-δ in Metabolism, Inflammation, and Cancer: Many Characters of a Critical Transcription Factor.International journal of molecular sciences · 2018Review
- Emerging cellular functions of the lipid metabolizing enzyme 15-Lipoxygenase-1.Cell proliferation · 2018Review
- The Role ofThe oncologist · 2018Review
- Frondanol, a Nutraceutical Extract fromMarine drugs · 2018Article
- PPAR-delta modulates membrane cholesterol and cytokine signaling in malignant B cells.Leukemia · 2018Article
- Expression ofBiochemistry and biophysics reports · 2017Article
- ALOX15 as a suppressor of inflammation and cancer: Lost in the link.Prostaglandins & other lipid mediators · 2017Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
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Abstract
The IL-6/signal transducer and activator of transcription 3 (STAT3) pathway is a critical signaling pathway for colitis-associated colorectal cancer (CAC). Peroxisome proliferator-activated receptor (PPAR)-δ, a lipid nuclear receptor, up-regulates IL-6. 15-Lipoxygenase-1 (15-LOX-1), which is crucial to production of lipid signaling mediators to terminate inflammation, down-regulates PPAR-δ. 15-LOX-1 effects on IL-6/STAT3 signaling and CAC tumorigenesis have not been determined. We report that intestinally targeted transgenic 15-LOX-1 expression in mice inhibited azoxymethane- and dextran sodium sulfate-induced CAC, IL-6 expression, STAT3 phosphorylation, and IL-6/STAT3 downstream target (Notch3 and MUC1) expression. 15-LOX-1 down-regulation was associated with IL-6 up-regulation in human colon cancer mucosa. Reexpression of 15-LOX-1 in human colon cancer cells suppressed IL-6 mRNA expression, STAT3 phosphorylation, IL-6 promoter activity, and PPAR-δ mRNA and protein expression. PPAR-δ overexpression in colonic epithelial cells promoted CAC tumorigenesis in mice and increased IL-6 expression and STAT3 phosphorylation, whereas concomitant 15-LOX-1 expression in colonic epithelial cells (15-LOX-1-PPAR-δ-Gut mice) suppressed these effects: the number of tumors per mouse (mean ± sem) was 4.22 ± 0.68 in wild-type littermates, 6.67 ± 0.83 in PPAR-δ-Gut mice (P = 0.026), and 2.25 ± 0.25 in 15-LOX-1-PPAR-δ-Gut mice (P = 0.0006). Identification of 15-LOX-1 suppression of PPAR-δ to inhibit IL-6/STAT3 signaling-driven CAC tumorigenesis provides mechanistic insights that can be used to molecularly target CAC.
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