EA inhibited ovarian carcinoma cells mainly through G1 phase arrest of the cell cycle, through elevating the levels of p53 and Cip1/p21 and suppressing the levels of cyclin D1 and E. EA also induced apoptosis by inhibiting the Bcl-2 level and altering the Bax : Bcl-2 ratio and activating caspase 3. This evidence concerns the gene CCND1 and ovarian carcinoma.