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A novel role and mechanism of cystic fibrosis transmembrane conductance regulator in bisphenol A‐induced prostate cancer
Author(s) -
Zhu Xiaonian,
Gao Li,
Yan Chengmei,
He Yonghua
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28156
Subject(s) - lncap , prostate cancer , cystic fibrosis transmembrane conductance regulator , cancer research , apoptosis , viability assay , chemistry , cell growth , medicine , prostate , carcinogenesis , cancer , endocrinology , biology , cystic fibrosis , biochemistry
Bisphenol A (BPA) is a well known environmental endocrine disruptor that may cause human prostate cancer through disturbing cell mitosis, proliferation, and apoptosis. As one of the most important anion channels in organisms, cystic fibrosis transmembrane conductance regulator (CFTR) is proposed as a tumor suppressor in carcinogenesis and development of prostate cancer in recent studies. Whether CFTR plays a role in BPA‐induced prostate cancer needs to be further identified. In this study, two prostate cancer cell lines PC‐3 and LNCaP were exposed to BPA for detecting the cytotoxic reactions by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide and enzyme‐linked immunosorbent assays. After the treatment with BPA for 24 hours, the cell viability was decreased significantly with increased cell apoptosis in the two cell lines. Moreover, both PC‐3 and LNCaP cells had a reduced expression level of cAMP, CFTR, and adenosine triphosphate upon BPA treatment. In addition, AMPKα kinase was found upregulated to promote cell apoptosis through increasing Bax expression and decreasing Bcl‐2 expression. Our study suggests a role and mechanism of CFTR in BPA‐induced prostate cancer via cell apoptosis for the first time.