Table 2.
Anticancer activity of myricetin towards various cancer cell lines.
Cell line/Enzyme | Effect of Myricetin | Reference |
---|---|---|
Activity on Cell Lines | ||
Brain | ||
U251, NCH89 and LN229 cells | No effect when alone, since the IC50 value for each cell line was found to be >200 µM. A combination of myricetin (150 µM) and TRAIL (50 ng/mL) yielded a synergistic activity and increased cell death in U251, NCH89 and LN229 by 59%, 65% and 52%, respectively. | [78] |
Breast | ||
MCF-7 | IC50 2.70 μg/mL compared to vinblastine (IC50 45.6 μg/mL) | [79] |
Increased GSH content of cells and also increased the EROD reaction 2-fold at a concentration of 25 μM | [80] | |
Cervix | ||
HeLa cells | Cytotoxic with IC50 18.9 µg/mL | [81] |
Colon | ||
Epithelial adenocarcinoma cells | Proliferation of cells inhibited at 50 μM by decreasing COX-2 and cyclin D1 expression | [82] |
HCT116 | Inhibited the proliferation of human colon carcinoma cells by halting the cell cycle in G2/M phase and inducing apoptosis; LD50 28.2 μM | [83] |
COLO 205, COLO 320HSR, COLO 320DM, HT 29 and COLO 205-X | Inhibited the activation of MMP-2 enzyme in the cells with IC50 values of 7.82, 11.18, 11.56, 13.25 and 23.51 μM, respectively. It also suppressed TPA-induced MMP-2 protein expression in COLO 205 cells by blocking the translocation of PKCα from cytosol to membrane, phosphorylation of ERK1/2 protein and induction of c-Jun protein expression activated by TPA. | [84] |
Leukemia | ||
HL-60 | Alone, and in combination with piceatannol, induced apoptotic cell death through a ROS-independent cell death pathway. The effect was greater with the combined treatment | [85] |
Anti-proliferative activity and the effect was enhanced with increasing concentration | [70] | |
Prostate | ||
LNCaP | IC50 value 2.10 μg/mL while taxol (IC50 0.08 μg/mL) used as standard | [79] |
22Rv1 | Inhibition of TCDD-induced EROD activity in cancer cells; IC50 value 3.0 μM | [86] |
Uterus | ||
RL95-2 endometrial cancer cells | Inhibition of CYP1 activity of cancer cells; IC50 values 3 μM and lower | [87] |
Inhibition of enzyme/protein activity | ||
Thioredoxin reductase (TrxR) from mammals | Inhibitory effect on enzyme, which is overexpressed in many aggressive tumours; IC50 value 0.62 μM. Attacks the reduced COOH-terminal of -Cys-Sec-Gly, the active site of TrxR | [88] |
TrxR | At 50 μM, inhibited growth of A549 (human lung carcinoma) cells and reduced TrxR activity in the cell lysates, corresponding with the oxidization of thioredoxin | [88] |
Mammalian DNA polymerases | IC50 values ranged from 21.3 to 40.9 μM. Human DNA topoisomerase II activity inhibited; IC50 27.5 μM | [83] |
Phosphatidylinositol 3-kinase (PI3K) | Inhibited this enzyme (IC50 1.8 μM) that plays an important role in signal transduction and cell transformation. Also inhibited PKC and tyrosine kinase activity of EGF-R | [89,90] |
E6, a primary oncoprotein of human papillomaviruses | Inhibited E6, responsible for cervical cancer by inhibiting GST-E6 and His-caspase 8 binding | [91] |
CCAAT-enhancer-binding proteins-α, peroxisome proliferator-activated receptor-γ, lipoprotein lipase, fatty acid binding aP2 protein and adiponectin | At 30 μM, myricetin decreased mRNA levels of these enzymes. Inhibited adipogenesis in human adipose tissue-derived mesenchymal stem cells. | [92] |
Multidrug resistance-associated protein MRP1 and MRP2 mediated vincristine efflux in MDCKII cells | Inhibitory effects with IC50 30.5 and 24.6 μM, respectively. At a concentration of 25 μM, it increased the sensitivity of the cells towards vincristine toxicity towards MRP1 and MRP2 cells with IC50 values of 7.6 and 5.8 μM, respectively | [93] |