Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 EP159 | DOI: 10.1530/endoabs.37.EP159

ECE2015 Eposter Presentations Reproduction, endocrine disruptors and signalling (92 abstracts)

Treatment with antifungal agents, fenhexamid and cyprodinil, resulted in an increase of cell cycle- and metastasis-related genes in an oestrogen receptor-dependent pathway in cellular and xenografted mouse models with BG-1 ovarian cancer cells

Ryeo-Eun Go & Kyung-Chul Choi


Laboratory of Biochemistry and Immunology, College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk, Republic of Korea.


Fenhexamid and cyprodinil are antifungal agents used in agricultural applications and present at measurable amounts in fruits and vegetables. In this study, the effects of fenhexamid and cyprodinil on cancer cell viability and metastasis were examined and the expression levels of proteins such as cyclins D1 and E, and cathepsins B and D were analysed in BG-1 ovarian cancer cells with oestrogen receptors (ERs). BG-1 cells were cultured with 0.1% DMSO (control), 17β-oestradiol (E2; 1×10−9 M), fenhexamid or cyprodinil (10−5–10−8 M). As results, in MTT assay, E2 as a positive control markedly increased BG-1 cell viability about five times and these antifungal agents increased BG-1 cell viability about 1.5–2 times compared to control. When the respective treatment was co-treated with ICI 182 780, an ER antagonist, BG-1 cell viability was reversed to the level of control. In wound-healing scratch assay, the scratched area was reduced by BG-1 cells treated with E2 or these antifungal agents compared with control. However, when BG-1 cells were treated with ICI 182 780, the scratched area was maintained to the level of control. Protein levels of cyclins D1 and E, cathepsins B and D were induced by E2 and these antifungal agents, but when co-treated with ICI 182 780, the increased protein levels were reversed. In xenografted mouse models transplanted with BG-1 cells, E2 significantly increased the tumour mass formation about six times and cyprodinil also induced tumor formation about two times compared to vehicle (0.1% DMSO) during 80 days. However, fenhexamid did not increase the tumour mass formation. These results imply that the fenhexamid and cyprodinil may have disruptive effects on ER expressing cancer by alteration of cell cycle- and metastasis-related genes via ER dependent pathway. This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (MEST) of the Republic of Korea (2014R1A1A2055295).

Disclosure: This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (MEST) of the Republic of Korea (2014R1A1A2055295).

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