细胞凋亡
异种雌激素
内分泌干扰物
细胞生物学
细胞周期
化学
细胞生长
伤口愈合
细胞周期检查点
程序性细胞死亡
癌症研究
生物
内科学
生物化学
雌激素受体
免疫学
医学
内分泌系统
激素
癌症
乳腺癌
作者
Junhui Song,Byungdo Hwang,Su-Bin Kim,Yung Hyun Choi,Wun-Jae Kim,Sung‐Kwon Moon
标识
DOI:10.1016/j.ecoenv.2022.114358
摘要
Bisphenol A (BPA) is commonly used to produce epoxy resins and polycarbonate plastics. BPA is an endocrine-disrupting chemical that is leaked from the polymer and absorbed into the body to disrupt the endocrine system. Although BPA may cause cytotoxicity in the prostate, a hormone-dependent reproductive organ, its underlying mechanism has not yet been elucidated. Here, we investigated the effects of BPA on cell proliferation, apoptosis, and the wound healing process using prostate epithelial cells (RWPE-1) and stromal cells (WPMY-1). Observations revealed that BPA induced G2/M cell cycle arrest in both cell types through the ATM−CHK1/CHK2–CDC25c−CDC2 signaling pathway, and the IC50 values were estimated to be 150 μM. Furthermore, BPA was found to induce caspase-dependent apoptosis through initiator (caspase-8 and −9) and executioner (caspase-3 and −7) caspase cascades. In addition, BPA interfered with the wound healing process through inhibition of MMP-2 and − 9 expression, accompanied by reductions in the binding activities of AP-1 as well as NF-κB motifs. Phosphorylation of MAPKs was associated with the BPA-mediated toxicity of prostate cells. These results suggest that BPA exhibits prostate toxicity by inhibiting cell proliferation, inducing apoptosis, and interfering with the wound healing process. Our study provided new insights into the precise molecular mechanisms of BPA-induced toxicity in human prostate cells.
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