17 beta-estradiol stimulates generation of reactive species oxygen and nitric oxide in ovarian adenocarcinoma cells [OVCAR 3]

Experimental and epidemiological evidence supports a role for steroid hormones in the pathogenesis of ovarian cancer. Among steroid hormones, 17 beta -estradiol [E2] has the most potent effect on proliferation, apoptosis and metastasis. In the present study, we investigated the effect of E2 on production of ROS and NO in ovarian cancer cells. Ovarian adenocarcinoma cell line [OVCAR-3] was cultured and treated with various concentrations of E2, antioxidants [N-acetyle cysteine and Ebselen] and ICI182780 as an estrogen receptor antagonist. MTT test was performed to evaluate cell viability. NO and ROS levels were measured by Griess and DCFH-DA methods, respectively. ROS levels as well as NO levels were increased in OVCAR-3 cells treated with E2. The increase in ROS production was in parallel with increased cell viability which indicates that estrogen-induced ROS can participate in cancer progression. ICI182780 abolished E2-induced ROS production. Progesterone was also effective in reducing ROS and NO generation. NO and ROS are important molecules in signaling networks in cell. These molecules can be used as therapeutic targets for prevention and treatment of ovary cancer and other estrogen-induced malignancies