IC50: 50 μM

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. 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.