Coumestrol exerts chemotherapeutic effects via PI3K and ERK1/2 MAPK pathways. Coumestrol inhibits viability and invasion, and induces apoptosis of ES2 (clear cell-/serous carcinoma origin) cells. In addition, immunoreactive PCNA and ERBB2, markers of proliferation of ovarian carcinoma, are attenuated in their expression in coumestrol-induced death of ES2 cells. Phosphorylation of AKT, p70S6K, ERK1/2, JNK1/2 and p90RSK is inactivated by coumestrol treatment in a dose- and time-dependent manner[1]. Coumestrol inhibits proliferation and induces apoptosis in MCF-7 cells, which is prevented by copper chelator neocuproine and ROS scavengers. Coumestrol treatment induces ROS generation coupled to DNA fragmentation, up-regulation of p53/p21, cell cycle arrest at G1/S phase, mitochondrial membrane depolarization and caspases 9/3 activation[2].
Kinase Assay
Cell Assay
To determine dose-dependent effects of coumestrol, ES2 cells are treated with different concentrations (0, 1, 10, 20, 50 or 100 μM) of coumestrol[1]. Coumestrol is dissolved in DMSO to prepare a 3 mM stock. Breast cancer MCF-7 cells are treated with increasing concentrations of coumestrol for 24, 48 and 72 h. Then, 20 μL of MTT (5 mg/mL) is added each well and re-incubated for additional 3 h. Formazan blue crystals formed are dissolved in 100 μL of DMSO. Absorbance is read at 570 nm using ELISA plate reader[2].
Animal Administration
References
[1]. Lim W, et al. Coumestrol suppresses proliferation of ES2 human epithelial ovarian cancer cells. J Endocrinol. 2016 Mar;228(3):149-60.
[2]. Zafar A, et al. Cytotoxic activity of soy phytoestrogen coumestrol against human breast cancer MCF-7 cells: Insights into the molecular mechanism. Food Chem Toxicol. 2017 Jan;99:149-161.
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