Cell junctions in the prostate: an overview about the effects of Endocrine Disrupting Chemicals (EDCS) in different experimental models

• Published in: Reproductive toxicology (Elmsford, N.Y.) Vol. 81; pp. 147 - 154
• Main Authors: Scarano, Wellerson R., Pinho, Cristiane F., Pissinatti, Lorenzo, Gonçalves, Bianca F., Mendes, Leonardo O., Campos, Silvana G.P.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.10.2018
• Subjects: Animals; Cell junctions; EDCs (Endocrine Disrupting Chemicals); EMT (epithelial-mesenchymal transition); Endocrine Disruptors - toxicity; Epithelial-Mesenchymal Transition - drug effects; Humans; Intercellular Junctions - drug effects; Male; Prostate - drug effects; Prostate - growth & development; Prostatitis - chemically induced; Toxicants; Xenobiotics - toxicity; Cell junctions; EDCs (Endocrine Disrupting Chemicals); Toxicants; EMT (epithelial-mesenchymal transition)
• ISSN: 0890-6238; 1873-1708
• DOI: 10.1016/j.reprotox.2018.08.009

•Toxicants exposure is associated with the occurrence of male reproductive disorders.•Prostate is highly sensible to hormonal unbalance caused by EDCs during its development.•EDCs are able to disrupt cell-cell adhesion in different experimental models and in different pathologic conditions.•Some EDCs can accelerate the epithelial-mesenchymal transition during oncogenic process and metastasis in the prostate. Throughout the last decades, increasing exposure to environmental Endocrine Disruptors Chemicals (EDCs) has been associated with the occurrence of male reproductive disorders, such as impairment of prostate development and function, increase of susceptibility to oncogenesis, Epithelial-Mesenchymal Transition and the metastatic invasive potential. Nevertheless, few studies address the mechanisms involved in these alterations, especially those related to cell junctions, which are hormonally regulated and, therefore, possible EDCs targets. The cellular mechanisms discussed in this review are addressed to EDCs actions on tight, gap and adherent junctions and its related genes and proteins, such as claudin-1, -3, -4 and -8, connexin-32 and -43, E-cadherin and β-catenin, respectively. The impairment of cell junction function, mainly due EDCs exposure during the prostate’s critical window of development, can corroborate to acquire a mesenchymal phenotype by epithelial cells and the prostate microenvironment becomes susceptible to development of lesions in the latter stages of life.