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Abstract
Myricetin is a natural dietary flavonoid compound. We evaluated the efficacy of myricetin against intestinal tumorigenesis in adenomatous polyposis coli multiple intestinal neoplasia (APCMin/+) mice. Myricetin was given orally once a day for 12 consecutive weeks. APCMin/+ mice fed with myricetin developed fewer and smaller polyps without any adverse effects. Histopathological analysis showed a decreased number of dysplastic cells and degree of dysplasia in each polyp. Immunohistochemical and western blot analysis revealed that myricetin selectively inhibits cell proliferation and induces apoptosis in adenomatous polyps. The effects of myricetin were associated with a modulation the GSK-3β and Wnt/β-catenin pathways. ELISA analysis showed a reduced concentration of pro-inflammatory cytokines IL-6 and PGE2 in blood, which were elevated in APCMin/+ mice. The effect of myricetin treatment was more prominent in the adenomatous polyps originating in the colon. Further studies showed that myricetin downregulates the phosphorylated p38 MAPK/Akt/mTOR signaling pathways, which may be the mechanisms for the inhibition of adenomatous polyps by myricetin. Taken together, our data show that myricetin inhibits intestinal tumorigenesis through a collection of biological activities. Given these results, we suggest that myricetin could be used preventatively to reduce the risk of developing colon cancers.
Highlights
Colon cancer is the second leading cause of cancer death in Western countries and the third most common cancer in other parts of the world
We evaluated the efficacy of myricetin against intestinal tumorigenesis in adenomatous polyposis coli multiple intestinal neoplasia (APCMin/+) mice
Further studies showed that myricetin downregulates the phosphorylated p38 mitogen-activated protein kinase (MAPK)/Akt/mammalian target of rapamycin (mTOR) signaling pathways, which may be the mechanisms for the inhibition of adenomatous polyps by myricetin
Summary
Colon cancer is the second leading cause of cancer death in Western countries and the third most common cancer in other parts of the world. Somatic mutations and deletions that inactivate both copies of APC are present in most sporadic colorectal adenomas and cancers. Patients with these genetic changes are 330 times more likely to develop colon cancer than their normal counterparts [3]. Clinical studies have indicated that half of the population develops www.impactjournals.com/oncotarget at least one benign adenomatous colonic polyp, with about 3% of these progressing to colon cancer [1]. The presence of intestinal adenomatous polyps has been considered as a major precursor of colon cancer. Removing adenomatous polyps at this stage could prevent the development and progression to colon cancer. Chemoprevention of intestinal adenomatous polyposis has emerged as a pragmatic approach to reduce the risk of colon cancer
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