Endocrine disrupting chemicals (EDCs) are man-made substances widespread in the environment that include, among many others, bisphenol A (BPA), organochlorinated pesticides and hormone derivatives detectable in meat from animals raised in concentrated animal feeding operations. Increasing evidence indicates that EDCs have a negative impact on human health as well as on male and female fertility. They may also be associated with some endocrine diseases and increased incidence of breast and prostate cancer. This review aims to summarize available data on the (potential) impact of some common EDCs, focusing particularly on BPA, prostate cancer and their mechanisms of action. These compounds interfere with normal hormone signal pathway transduction, resulting in prolonged exposure of receptors to stimuli or interference with cellular hormone signaling in target cells. Understanding the effects of BPA and other EDCs as well as their molecular mechanism(s) may be useful in sensitizing the scientific community and the manufacturing industry to the importance of finding alternatives to their indiscriminate use.

Endocrine disrupting chemicals (EDCs) are natural or synthetic compounds that interfere with normal functions of natural hormones in the body, leading to a disruption of the endocrine system. Specifically, EDCs have the potential to cause formation of several hormone-dependent cancers, including breast, ovarian, and prostate cancers. Epithelial mesenchymal transition (EMT) process by which epithelial cells lose their cell polarity and cell-cell adhesion and acquire mesenchymal phenotype is closely associated with malignant transformation and the initiation of cancer metastasis. As a key epithelial marker responsible for adherens junction, E-cadherin enables the cells to maintain epithelial phenotypes. EMT event is induced by E-cadherin loss which can be carried out by many transcription factors (TFs), including Snail, Slug, ZEB1, ZEB2, Kruppel-like factor 8 (KLF8), and Twist. N-cadherin, fibronectin, and vimentin are mesenchymal markers needed for cellular migration. The EMT process is regulated by several signaling pathways mediated by transforming growth factor β (TGF-β), Wnt-β-catenin, Notch, Hedgehog, and receptor tyrosine kinases. In the present article, we reviewed the current understanding of cancer progression effects of synthetic chemical EDCs such as bisphenol A (BPA), phthalates, tetrachlorodibenzo-p-dioxin (TCDD), and triclosan by focusing their roles in the EMT process. Collectively, the majority of previous studies revealed that BPA, phthalates, TCDD, and triclosan have the potential to induce cancer metastasis through regulating EMT markers and migration via several signaling pathways associated with the EMT program. Therefore, it is considered that the exposure to these EDCs can increase the risk aggravating the disease for the patients suffering cancer and that more regulations about the use of these EDCs are needed.

BPA, a chemical used in the preparation of polycarbonate plastics, is an endocrine disruptor. Exposure to BPA has been suggested to be a risk factor for breast cancer because of its potential to induce estrogen receptor signaling in breast cancer cells. More recently, it has been recognized that BPA also binds to the G protein-coupled estrogen receptor and other nuclear receptors, in addition to estrogen receptors, and acts on immune cells, adipocytes, and fibroblasts, potentially modulating the TME. The TME significantly impacts the behavior of cancer cells. Therefore, understanding how BPA affects stromal components in breast cancer is imperative to adequately assess the association between exposure to BPA and the risk of breast cancer. This review examines the effects of BPA on stromal components of tumors to highlight their potential role in the carcinogenic effect of BPA. As a result, I propose considerations for the risk assessment of BPA exposure and studies needed to improve understanding of the TME-mediated, breast cancer-promoting effect of BPA.

Polycystic ovary syndrome (PCOS) is the most common and the most heterogeneous endocrine disorder in premenopausal women. Apart from signs of hyperandrogenism such as acne, hirsutism and hair loss, women with PCOS usually present with menstrual irregularities and fertility problems.Additionally, they are often characterized by impaired glucose tolerance, which usually leads to the development of type 2 diabetes mellitus (T2DM). This review article describes current and novel approach to the pathomechanisms of PCOS and the potential role of an endocrine disrupting chemical ("endocrine disruptor" - ED) - bisphenol A (BPA), which is commonly used as a plasticizer and due to its molecular structure can interact with estrogen receptors (ERs). Recent observations point to the higher levels of BPA in biological fluids of women with PCOS and its role in the pathogenesis of hyperandrogenism and hyperinsulinemia. It seems that mother's exposure to BPA during pregnancy may also lead to the development of PCOS in the female offspring.

Bisphenol A (BPA; 4,4'-isopropylidenediphenol) is an endocrine disruptor that is used as a material for the production of phenol resins, polyacrylates, polyesters, epoxy resins, and polycarbonate plastics. Endocrine-disruptive or toxic effects of BPA on living organisms through a number of cell signaling pathways have been reported. BPA induces carcinogenesis, reproductive toxicity, abnormal inflammatory or immune response, and developmental disorders of brain or nervous system through various cell signaling pathways. This review considers the literature concerning BPA and its association with cancer-related cell signaling pathways, reproductive toxicity-related cell signaling pathways, inflammatory or immune response-related cell signaling pathways, and brain and nervous system-related cell signaling pathways.

Bisphenol A (BPA) is an organic synthetic compound serving as a monomer to produce polycarbonate plastic, widely used in the packaging for food and drinks, medical devices, thermal paper, and dental materials. BPA can contaminate food, beverage, air, and soil. It accumulates in several human tissues and organs and is potentially harmful to human health through different molecular mechanisms. Due to its hormone-like properties, BPA may bind to estrogen receptors, thereby affecting both body weight and tumorigenesis. BPA may also affect metabolism and cancer progression, by interacting with GPR30, and may impair male reproductive function, by binding to androgen receptors. Several transcription factors, including PPARγ, C/EBP, Nrf2, HOX, and HAND2, are involved in BPA action on fat and liver homeostasis, the cardiovascular system, and cancer. Finally, epigenetic changes, such as DNA methylation, histones modification, and changes in microRNAs expression contribute to BPA pathological effects. This review aims to provide an extensive and comprehensive analysis of the most recent evidence about the potential mechanisms by which BPA affects human health.