Myricetin is a potent anticarcinogen and antimutagen, but it has been shown to promote mutagenesis with the use of the Ames Test. Although the anticancer property of myricetin has been attributed mainly to its antioxidant action, it has additional protective mechanisms such as inhibition of STAT1 (signal transducer and activator of transcription 1) activation . JAK1/STAT3 pathway may play a role in cell transformation and carcinogenesis. An in-vitro study by the Kagoshima University, Japan, on epidermal growth factor-activated mouse epidermal cells indicated that myricetin might directly target JAK1 to block cell transformation, by directly binding to JAK1/STAT3 molecules and thereby inhibiting cell transformation . From the three tested flavonols (myricetin, quercetin and kaempferol) myricetin showed the strongest inhibitory effect on cell transformation.
Jung and coworkers at the Seoul National University also found a protective effect of myricetin in mouse skin epidermal cells . This study demonstrated that myricetin suppressed UVB-induced cyclooxygenase-2 expression. Abnormal expression of cyclooxygenase-2 has been implicated in the development of cancer. Myricetin inhibited FYN kinase activity and attenuated UVB-induced phosphorylation of mitogen-activated protein kinases. FYN, is a human gene that encodes a membrane-associated tyrosine kinase that has been implicated in the control of cell growth. A study by Seoul National University also found that myricetin inhibited phorbol ester-induced COX-2 expression in mouse epidermal cells by suppressing activation of nuclear factor kappa B . The phytochemicals also attenuated the phorbol ester-induced production of prostaglandin E 2.
A study by the University of Quebec showed the inhibition of Met activity by myricetin may explain its chemopreventive properties . The team of researchers, lead by D. Labbé, investigated the inhibition of dietary-derived flavonols quercetin, kaempferol and myricetin on tyrosine kinase Met, the tyrosine kinase Met, which is a key factor in the development of medulloblastoma, the most common malignant brain tumor in children. They found that quercetin, kaempferol, and myricetin inhibited HGF/Met signaling in a medulloblastoma cell line. Lee KW an co-workers of University of Minnesota demonstrated that myricetin had a stronger anticancer-promoting activity than resveratrol, a phytochemical known for the possible chemopreventive activity of red wine . But red wine contains 30 times more flavonols, mainly myricetin, than resveratrol. This study demonstrated that myricetin is a novel inhibitor of mitogen-activated protein kinase kinase 1 activity and transformation in mouse epidermal cells. Myricetin inhibited 12-O-tetradecanoylphorbol-13-acetate or epidermal growth factor -induced cell transformation by about 75%. Myricetin also attenuated tumor promoter-induced activation of c-fos or activator protein-1. The study concluded that myricetin may have potent anticancer-promoting activity and may contribute to the chemopreventive potential red wine and other foods.
Studies have indicated an association between wine consumption and the incidence of breast cancer in postmenopausal women, which could be explained by the estrogenic properties of red wine phytochemicals. Maggiolini M and co-workers of the University of Calabria, Italy, evaluated the estrogenic properties of two abundant wine-derived phytochemicals, named piceatannol and myricetin, on hormone-sensitive MCF7 and the endocrine-independent SKBR3 breast cancer cells . They found that both phytochemicals might contribute to the estrogenicity of red wine, since the phytochemicals transactivated endogenous estrogen receptor alpha and competed with 17beta-estradiol for binding estrogen receptors alpha and beta. They conluded that the estrogenic activity of piceatannol and myricetin might explain the association of red wine intake and the risk of breast cancer.
Ko CH and coworkers of the Graduate Institute of Pharmaceutical Sciences, School of Pharmacy, Taipei, investigated the protective effect of myricetin on human colon cancer cells. Colon cancer is a leading cause of human mortality due to its high metastatic ability. The activation of matrix metalloproteinases (MMP) is a key factor in this metastatic process. The found that among the 36 flavonoids tested myricetin had the strongest inhibitory effect on MMP-2 enzyme activity in COLO 205 cells and showed also an inhibitory effect in other human colon cancer cell lines. In contrast, the myricetin glycoside in myricitrin (myricetin-3-rhamnoside) showed no such effect. Myricetin blocked endogenous and TPA-induced MMP-2 enzyme activity by inhibiting its protein expression and enzyme activity.
 Targeting STAT1 by myricetin and delphinidin provides efficient protection of the heart from ischemia/reperfusion-induced injury. FEBS Lett. 2009 Feb 4;583(3):531-41.
 The flavonols quercetin, kaempferol, and myricetin inhibit hepatocyte growth factor-induced medulloblastoma cell migration. Journal of Nutrition. 2009 Apr;139(4):646-52.
 Myricetin directly targets JAK1 to inhibit cell transformation. Cancer Lett. 2009 Mar 8;275(1):17-26.
 Myricetin suppresses UVB-induced skin cancer by targeting FYN. Cancer Res. 2008 Jul 15;68(14):6021-9.
 Myricetin down-regulates phorbol ester-induced cyclooxygenase-2 expression in mouse epidermal cells by blocking activation of nuclear factor kappa. J Agric Food Chem. 2007 Nov 14;55(23):9678-84.
 Myricetin is a novel natural inhibitor of neoplastic cell transformation and MEK1. Carcinogenesis. 2007 Sep;28(9):1918-27.
 The red wine phenolics piceatannol and myricetin act as agonists for estrogen receptor alpha in human breast cancer cells. J Mol Endocrinol. 2005 Oct;35(2):269-81.
 Myricetin inhibits matrix metalloproteinase 2 protein expression and enzyme activity in colorectal carcinoma cells.
Mol Cancer Ther. 2005 Feb;4(2):281-90.