Journal
PROSTAGLANDINS & OTHER LIPID MEDIATORS
Volume 132, Issue -, Pages 77-83Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.prostaglandins.2017.01.002
Keywords
ALOX15; Colon cancer; Colitis-associated colorectal cancer
Categories
Funding
- National Cancer Institute [R01-CA 206539, R01-CA 195686]
- Cancer Prevention Research Institute of Texas [RP140224, RP150195]
- National Institutes of Health through Cancer Center Support Grant [CA016672]
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Mounting evidence supports a mechanistic link between inflammation and cancer, especially colon cancer. ALOX15 (15-lipoxygenase-1) plays an important role in the formation of key lipid mediators (e.g., lipoxins and resolvins) to terminate inflammation. ALOX15 expression is downregulated in colorectal cancer (CRC). Intestinally-targeted transgenic expression of ALOX15 in mice inhibited dextran sodium sulfate-induced colitis from promoting azoxymethane-induced colorectal tumorigenesis, demonstrating that ALOX15 can suppress inflammation-driven promotion of carcinogen-induced colorectal tumorigenesis and therefore ALOX15 downregulation during tumorigenesis is likely to enhance the link between colitis and colorectal tumorigenesis. ALOX15 suppressed the TNF-alpha, IL-1 beta/NF-kappa B, and IL-6/STAT3 signaling pathways, which play major roles in promotion of colorectal cancer by chronic inflammation. Defining ALOX15's regulatory role in colitis-associated colorectal cancer could identify important molecular regulatory events that could be targeted to suppress promotion of tumorigenesis by chronic inflammation. (C) 2017 Elsevier Inc. All rights reserved.
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