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Fludioxonil is an antifungal agent used in agricultural applications that is present at measurable amounts in fruits and vegetables. In this study, the effects of fludioxonil on cancer cell viability, epithelial-mesenchymal transition (EMT) and metastasis were examined in BG-1 ovarian cancer cells with estrogen receptors (ERs). BG-1 cells were cultured with 0.1% DMSO (control), 17β-estradiol (E2; 1x10-9 M), or fludioxonil (10-5-10-8 M). MTT assay revealed that fludioxonil increased BG-1 cell viability 1.2 to 1.5 times compared to the control, while E2 markedly increased BG-1 cell viability by about 3.5 times. When the samples were co-treated with ICI 182,780 (10-8 M), an ER antagonist, fludioxonil-induced BG-1 cell viability was reversed to the level of the control. Protein levels of cyclin E, cyclin D1, snail and N-cadherin increased in response to fludioxonil as E2 did, but these increases were not observed when fludioxonil was administered with ICI 182,780. Moreover, the protein level of p21 and E-cadherin decreased in response to treatment with fludioxonil, but remained at the control level when co-treated with ICI 182,780. In xenografted mouse models transplanted with BG-1 cells, fludioxonil significantly increased the tumor mass formation by about 2.5 times as E2 did when compared to vehicle (0.1% DMSO) during the experimental period (80 days). Immunohistochemistry revealed that the protein level of proliferating cell nuclear antigen (PCNA), snail and cathepsin D increased in response to fludioxonil as E2 did. These results imply that fludioxonil may have disruptive effects on ER expressing cancers by inducing alterations in the expression of cell cycleand EMTrelated genes via the ER dependent pathway. Abstract Results

endocrine abstracts

An estrogen receptor-dependent pathway is involved in fludioxonil-induced cancer growth and metastasis linked with epithelial mesenchymal transition in cellular and xenografted ovarian cancer models