{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T06:46:35Z","timestamp":1789454795215,"version":"build-2803163510"},"reference-count":70,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T00:00:00Z","timestamp":1761091200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Ulcerative colitis (UC), a type of inflammatory bowel disease (IBD), is a chronic inflammatory disorder of the colon. Chronic intestinal inflammation plays a critical role in the increased risk of developing colitis-associated cancer (CAC). CU06-1004, an endothelial dysfunction blocker, can alleviate acute colitis by suppressing inflammation and regulating colonic vascular dysfunction. However, whether CU06-1004 suppresses chronic intestinal inflammation and prevents the development of CAC remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In this study, we investigated the protective effects of CU06-1004 by suppressing inflammation in both the dextran sulfate sodium (DSS)-induced chronic colitis model and the azoxymethane (AOM)\/DSS-induced colorectal cancer mouse models. We evaluated the expression of key pro-inflammatory cytokines, assessed histological characteristics in the animals, and examined the expression of key genes associated with inflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In the DSS-induced chronic colitis model, our results showed that CU06-1004 treatment suppressed inflammation, as evidenced by disease activity index scores, colon length, colon damage, and histological analysis. Furthermore, CU06-1004 administration reduced the levels of various inflammatory cytokines and factors (tumor necrosis factor-\u03b1, interleukin (IL)-1\u03b2, IL-6, cyclooxygenase-2, and inducible nitric oxide synthase), decreased immune cell infiltration (F4\/80+ macrophages and CD177+ neutrophils), and alleviated inflammation by inhibiting vascular adhesion molecules. Moreover, in the AOM\/DSS-induced colorectal cancer model as well, CU06-1004 significantly reduced the severity of colitis. CU06-1004 treatment also significantly reduced both the number and size of AOM\/DSS-induced colorectal tumors, suppressed inflammation, and inhibited the malignant proliferation of epithelial cells. Additionally, CU06-1004 treatment downregulated the expression of the key colorectal cancer marker \u03b2-catenin and its target gene c-Myc in AOM\/DSS-induced mice, thereby inhibiting tumor growth.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings suggest that CU06-1004 inhibits inflammation-induced tumorigenesis by modulating the inflammatory response in the colon. Consequently, CU06-1004 could represent a promising therapeutic candidate for the prevention of colorectal cancer through modulation of inflammation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2025.1684870","type":"journal-article","created":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T09:34:07Z","timestamp":1761125647000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":5,"title":["CU06-1004 inhibits the progression of chronic colitis and colitis-associated colorectal cancer by suppressing inflammation"],"prefix":"10.3389","volume":"16","author":[{"given":"Dongyeop","family":"Kim","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yeomyeong","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haiying","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ye-Seul","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minyoung","family":"Noh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cho-Rong","family":"Bae","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young-Guen","family":"Kwon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sang-Jun","family":"Ha","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2025,10,22]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"114","DOI":"10.5217\/ir.2021.00037","article-title":"Incidence comparison of adverse events in patients with inflammatory bowel disease receiving different biologic agents: retrospective long-term evaluation","volume":"20","author":"Barberio","year":"2022","journal-title":"Intest. 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