Carcinogenic effects of bisphenol A in breast and ovarian cancers.

Abstract

Endocrine-disrupting chemicals (EDCs) are exogenous chemical compounds ubiquitously found in everyday life of the modern world. EDCs enter the human body where they act similarly to endogenous hormones, altering the functions of the endocrine system and causing adverse effects on human health. Bisphenol A (BPA), the principal representative of this class, is a carbon-based synthetic plastic, and a key element in manufacturing cans, reusable water bottles and medical equipment. BPA mimics the actions of estrogen on multiple levels by activating estrogen receptors α and β. BPA regulates various processes, such as cell proliferation, migration and apoptosis, leading to neoplastic changes. Considering genetic mechanisms, BPA exerts its functions via multiple oncogenic signaling pathways, including the STAT3, PI3K/AKT and MAPK pathways. Furthermore, BPA is associated with various modifications of the reproductive system in both males and females. These alterations include benign lesions, such as endometrial hyperplasia, the development of ovarian cysts, an increase in the ductal density of mammary gland cells and other preneoplastic lesions. These benign lesions may continue to develop to breast or ovarian cancer; the effects of BPA depend on various molecular and epigenetic mechanisms that dictate whether the endocrine or reproductive system is impacted, wherein preexisting benign lesions can become cancerous. The present review supports the need for continuous research on BPA, considering its widespread use and most available data suggesting a carcinogenic effect of BPA on the female reproductive system. Although most studies on BPA have been conducted in vitro with human cells or in vivo with animal models, it can be argued that more studies should be conducted in vivo with humans to further promote understanding of the impact of BPA.