{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tian R"],"funding":["National Cancer Institute","National Institutes of Health through Cancer Center","NCI NIH HHS","Cancer Prevention Research Institute of Texas"],"pagination":["77-83"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5509529"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["132"],"pubmed_abstract":["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-α, IL-1β/NF-κB, and IL-6/STAT3 sign"],"journal":["Prostaglandins & other lipid mediators"],"pubmed_title":["ALOX15 as a suppressor of inflammation and cancer: Lost in the link."],"pmcid":["PMC5509529"],"funding_grant_id":["R01 CA195686","CA016672","R01-CA 195686","P30 CA016672","RP140224","R01 CA206539","R01-CA 206539","RP150195"],"pubmed_authors":["Jaoude J","Shureiqi I","Zuo X","Tian R","Colby J","Mao F"],"additional_accession":[]},"is_claimable":false,"name":"ALOX15 as a suppressor of inflammation and cancer: Lost in the link.","description":"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-α, IL-1β/NF-κB, and IL-6/STAT3 sign","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Sep","modification":"2025-04-19T22:40:50.646Z","creation":"2019-03-26T23:53:00Z"},"accession":"S-EPMC5509529","cross_references":{"pubmed":["28089732"],"doi":["10.1016/j.prostaglandins.2017.01.002"]}}