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Bisphenol A suppresses proliferation and induces apoptosis in colonic epithelial cells through mitochondrial and MAPK/AKT pathways

Wei Qu, Zhenguo Zhao, Sijin Chen, Lijin Zhang, Danlian Wu, Zhigao Chen
Life sciences 2018 v.208 pp. 167-174
apoptosis, bisphenol A, cell proliferation, colorectal neoplasms, epithelial cells, epithelium, gene expression, gene expression regulation, humans, hydrogen peroxide, malondialdehyde, membrane potential, mitochondria, mitochondrial membrane, mitogen-activated protein kinase, models, neoplasm cells, pathogens, signal transduction, toxicity, viability
Bisphenol A (BPA) can act as pathogenic agent on mammalian cells. However, whether BPA induces colonic epithelial cell damage remains unexplored. We used HCT116 cells as a model to investigate the negative effect of BPA on human colon cancer cells and explore the potential mechanism. Our results suggest that BPA decreased viability of HCT116 cells. BPA also caused serious oxidative damage to the colonic epithelium, as indicated by increased mitochondrial and intracellular reactive oxygen species (ROS) content and elevated malondialdehyde and H2O2 levels. Moreover, BPA depolarized the mitochondrial membrane potential and caused loss of mitochondrial integrity. Furthermore, BPA induced colonic epithelial cell apoptosis accompanied by upregulation of caspase3 and bax gene expression. Additionally, cell proliferation was inhibited significantly in HCT116 cells after the BPA treatment. We also studied the molecular mechanism involved in these effects and found that BPA inhibited proliferation of colonic epithelial cells through the mitogen activated protein kinase (MAPK) and AKT signaling pathways. Our data suggest that BPA triggers ROS generation as an initial step, followed by mediation of mitochondrial dysfunction, apoptosis, and proliferation of HCT116 cells. Moreover, MAPK/AKT signaling pathways were involved in BPA-induced toxicity of human colon cancer cells.