Examination of the effects of bisphenol A on hepG2 cells

In this study, it was aimed to determine the effect of application Bisphenol A (BPA) and Fulvestrant (ICI) chemical to HepG2 human hepatoma cells on proliferation, wound healing, E-cadherin, N-cadherin, vimentin proteins and apoptosis (caspase 3/7) in cells. BPA is an endocrine disrupter commonly used in the industry and has an estrogen-like effect. Fulvestrant is an estrogen receptor antagonist. The% cell viability in HepG2 cells treated with BPA, ICI, BPA and ICI combination was determined by MTT assay. The effects of BPA and ICI combination on HepG2 cell viability were evaluated according to the Talalay-Chou method. Migration in HepG2 cells was determined by wound healing method. The protein levels of E-cadherin, N-cadherin and vimentin in cells were measured with the Elisa kits. Apoptosis in HepG2 cells was measured by ApoTox-Glo ™ Triplex Test. It was observed that 8 nM BPA applied to HepG2 cells increased cell viability, while 160 nM ICI and BPA and ICI combination treatment reduced cell viability. The Talalay-Chou method explained that the effect observed as a result of the combination of BPA and ICI against HepG2 cell viability is due to a synergistic interaction. It was also determined that BPA increased the cytotoxic effect of ICI. In wound-formed HepG2 cells, BPA, BPA and ICI combination treatment showed that % wound size is decreased. The protein level of E-cadherin in HepG2 cells decreased in BPA and ICI combination treatment. The protein level of N-cadherin increased with the combination of ICI and BPA; and ICI. No changes in the protein level of vimentin were observed. When apoptosis luminescence data were evaluated, it was determined that BPA and ICI combination application increased apoptosis and BPA application was found to affect necroptosis. The results of this thesis study explain that applying 8 nM BPA and 160 nM ICI to HepG2 cells affects the proliferation, wound healing and apoptosis in the cells. Keywords: Bisphenol A, epithelial mesenchymal transition, HepG2, E-cadherin, vimentin This thesis was supported by Hacettepe University Scientific Research Coordination Unit. Project Number: 17804