## 2 Bioactive Compounds
### Myricetin  
Myricetin is a flavonoid found in a number of common foods including tomatoes [131], oranges, berries, and grapes [132]. Myricetin's antioxidant properties and anti-cancer effects have been widely studied [133]. [PERSON] et al. (2018) demonstrated that myricetin kills prostate cancer cells, with ONCOMINE database mining and prostate cancer tissue immunohistochemistry analysis indicating that the compound suppresses PIM1 while interrupting the PIM1/CXCR4 interaction, thereby inducing selective cell toxicity and apoptosis [134]. The flavonoid thereby enhanced chemosensitivity in A2780 and OVCAR3 ovarian cancer cells (IC50 value = 25 \(\upmu\)M), with treatment also regulating specific pro- and anti-apoptotic markers resulting in the induction of apoptosis. Such effects mediated by myricetin appear to be associated with MDR-1 down-regulation in these cell models [135]. [PERSON] et al. (2018) investigated the anti-carcinogenic effects of myricetin in skin cancer using the A431 cell line and found that myricetin-mediated anti-cancer activity was attributable to reactive oxygen species (ROS)-prompted mitochondrial membrane potential modulation and the initiation of apoptosis, events that were associated with myricetin-mediated alterations in Bcl-2 and Bax expression. Myricetin also caused cell cycle arrest and inhibited the migration and invasion of A431 cells [136]. The compound has also been reported to inhibit angiogenesis, as well as breast tumor growth via down-regulation of VEGF/VEGF2 and the p38 MAPK signaling pathway [137]. Myricetin also inhibits mTOR activation in HepG2 cells, thereby inducing protective autophagy, providing another avenue for potential anti-cancer effects [138]. Treatment with an inflammatory cytokine mixture (IL-6, interferon-\(\gamma\), and TNF-\(\alpha\)) in CCA KKU-100 cells induced migration and invasion via activation of the STAT3 pathway, which was reversed by myricetin treatment. Myricetin also suppressed STAT3-mediated downstream genes, including intercellular adhesion molecule-1, matrix metalloproteinase-9, iNOS, and COX-2 in CCA KKU-100 cells [139]. The myricetin derivative M10 exhibits protective effects against ulcerative colitis and colorectal cancer, with the chronic anti-inflammatory activity of M10 protecting against colorectal tumorigenesis while increasing CD8+ and CD4+ T cells, as well as reducing IL-6 and TNF-\(\alpha\) levels [140]. Myricetin-induced cell apoptosis has been observed in T47D breast cancer cells, associated with increased expression of apoptotic genes including caspase-3, -8, -9, BAX/Bcl-2, p53, BRCA1, and GADD45. In particular, the BRCA1-GADD45 pathway was involved in the apoptotic death of the T47D cells [141]. Myricetin has also been reported to inhibit the migration and invasion of hepatocellular carcinoma MHCC97H cells and weaken filopodia and lamellipodia [142]. Myricetin also up-regulates E-cadherin expression while down-regulating N-cadherin [142]. Collectively, these findings suggest that myricetin suppresses the process of epithelial-mesenchymal transition (EMT), thereby impeding the migration and invasion of hepatocellular carcinoma cells [142]. Myricetin also protects against thyroid cancer cells by inducing apoptosis, which is associated with caspase activation and enhancement of the Bax/Bcl-2 ratio, while regulating mitochondrial dysfunction [143].