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Polycystic ovary syndrome (PCOS) is a common endocrine disease characterized by hyperandrogenic phenotype in women of reproductive age. The pathogenesis of PCOS remains unclear, and androgen is now thought to have an essential impact on the pathogenesis of PCOS. Bisphenol A (BPA), an environmental endocrine disruptor, can increase the relevant androgen synthetase and induce PCOS through excessive androgen exposure. Studies have shown that BPA exposure can inhibit the activity of aromatase, prevent the binding of androgen and receptor, thus inducing hyperandrogenemia. BPA can also regulate the ovarian function of PCOS through oxidative stress, estrogen-related pathways, hypothalamic-pituitary-ovarian axis, regulation of obesity and insulin resistance, and other routes. This article aims to review the neuroendocrine mechanism and related signal pathways of BPA-induced PCOS by regulating hyperandrogen, clarify the specific biological functions of BPA and provide a reference for follow-up research. [ABSTRACT FROM AUTHOR]

Objective：To explore the mechanism of bisphenol A on the proliferation in human endometrial cancer cells (Ishikawa and RL952) via PI3K/AKT signaling pathway. Methods：CCK8 assay was used to detect the proliferation in Ishikawa and RL952 cells, and Western blotting was applied to observe the expression of phosphorylation-AKT. Results：Ishikawa and RL952 cells proliferation increased significantly with treatment of 1 μmol/L BPA after 48 h, and cell proliferation was (0.758±0.023) and (0.692±0.042) respectively (P＜0.01). The proliferation effect decreased when BPA was more than 1 μmol/L. Ishikawa and RL952 cells did not increase after treated for 24 h. Cytotoxic effects were showed after BPA treated for 72 h. After 1 μmol/L BPA treated for 48 h, p-AKT expression was increased significantly compared with controls （P＜0.05）. When PI3K was blocked by LY294002, p- AKT expression was decreased, but it is not significant compared to controls (P＞0.05). Conclusions：Bisphenol A induced endometrial cancer cell proliferation by activating PI3K/AKT pathway. [ABSTRACT FROM AUTHOR]