title: Genistein, a soy phytoestrogen, prevents the growth of BG-1 ovarian             cancer cells induced by 17β-estradiol or bisphenol A via the inhibition of cell             cycle progression.
abstract: An endocrine disrupting chemical (EDC) is a global health concern. In this             study, we examined the effects of genistein (GEN) on bisphenol A (BPA) or 17β-estradiol             (E2)-induced cell growth and gene alterations of BG-1 ovarian cancer cells expressing             estrogen receptors (ERs). In an in vitro cell viability assay, E2 or BPA significantly             increased the growth of BG-1 cells. This increased proliferative activity was             reversed by treatment with ICI 182,780, a well-known ER antagonist, while cell             proliferation was further promoted in the presence of propyl pyrazole triol (PPT),             an ERα agonist. These results imply that cell proliferation increased by E2 or             BPA was mediated by ERs, particularly ERα. BPA clearly acted as a xenoestrogen             in BG-1 ovarian cancer cells by mimicking E2 action. In contrast, GEN effectively             suppressed BG-1 cell proliferation promoted by E2 or BPA by inhibiting cell cycle             progression. E2 and BPA increased the expression of cyclin D1, a factor responsible             for the G1/S cell cycle transition. They also decreased the expression of p21,             a potent cyclin-dependent kinase (CDK) inhibitor that arrests the cell cycle in             G1 phase, and promoted the proliferation of BG-1 cells. As shown by its repressive             effect on cell growth, GEN decreased the expression of cyclin D1 augmented by             E2 or BPA. On the other hand, GEN increased the p21 expression downregulated by             E2 or BPA. Collectively, our findings suggest that GEN, a dietary phytoestrogen,             has an inhibitory effect on the growth of estrogen-dependent cancers promoted             by E2 or BPA.
authors.affiliation: Laboratory of Veterinary Biochemistry and Immunology, College                     of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk                     361-763, Republic of Korea.
authors.forename: Kyung-A
authors.initials: KA
authors.lastname: Hwang
authors.forename: Nam-Hee
authors.initials: NH
authors.lastname: Kang
authors.forename: Bo-Rim
authors.initials: BR
authors.lastname: Yi
authors.forename: Hye-Rim
authors.initials: HR
authors.lastname: Lee
authors.forename: Min-Ah
authors.initials: MA
authors.lastname: Park
authors.forename: Kyung-Chul
authors.initials: KC
authors.lastname: Choi
mesh_terms: D001559:Benzhydryl Compounds / Q000494:pharmacology; D002453:Cell Cycle / Q000187:drug effects / Q000235:genetics; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D019833:Genistein / Q000008:administration & dosage*; D006801:Humans; D010051:Ovarian Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D010636:Phenols / Q000494:pharmacology; D048789:Phytoestrogens / Q000008:administration & dosage*; D011960:Receptors, Estrogen / Q000378:metabolism; D013025:Glycine max; D020741:rho GTP-Binding Proteins / Q000378:metabolism; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D004958:Estradiol; D019833:Genistein; D010636:Phenols; D048789:Phytoestrogens; D011960:Receptors, Estrogen; D020741:rho GTP-Binding Proteins; C006780:bisphenol A; D000098826:Bisphenol A Compounds