| Autor: |
Liu J; Department of Epidemiology and Statistics, School of Public Health, 74716Guilin Medical University, Guilin, China., Ou C; Department of Toxicology, School of Public Health, 74716Guilin Medical University, Guilin, China., Zhu X; Department of Toxicology, School of Public Health, 74716Guilin Medical University, Guilin, China., Tan C; Department of Epidemiology and Statistics, School of Public Health, 74716Guilin Medical University, Guilin, China., Xiang X; Department of Urology, Affiliated Hospital of 74716Guilin Medical University, Guilin, China., He Y; Department of Epidemiology and Statistics, School of Public Health, 74716Guilin Medical University, Guilin, China. |
| Abstrakt: |
Bisphenol A (BPA) is an environmental endocrine disruptor and a risk factor for prostate cancer. The cystic fibrosis transmembrane conductance regulator (CFTR) is proposed to be a prostate cancer suppressor in some recent researches. However, the potential role and mechanism of CFTR in BPA-induced prostate cancer cells has not been well identified. In this study, BPA decreased the viability of human normal prostate RWPE-1 cells detected with a CCK-8 kit. The capacity of the cell line on soft agar colony formation, wound healing, and transwell invasion indicated malignant transformation induced by BPA. Western blot analysis demonstrated that the levels of CFTR and Bcl-2 decreased, whereas Bax level increased, and ELISA detection showed a decreased ATP level in BPA-exposed cells. Cell apoptosis was analyzed with Annexin V-FITC Detection Kit by flow cytometry. However, no significant difference was observed in cell viability and apoptosis rates compared to normal RWPE-1 cells. Our research revealed a potential role of CFTR in BPA-induced malignant transformation via mitochondrial apoptosis of normal prostate cells. |
