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CFTR 在双酚 A 诱导前列腺细胞癌变中的潜在作用:通过线粒体凋亡。

Potential role of CFTR in bisphenol A-induced malignant transformation of prostate cells via mitochondrial apoptosis.

机构信息

Department of Epidemiology and Statistics, School of Public Health, 74716Guilin Medical University, Guilin, China.

Department of Toxicology, School of Public Health, 74716Guilin Medical University, Guilin, China.

出版信息

Toxicol Ind Health. 2020 Aug;36(8):531-539. doi: 10.1177/0748233720943750. Epub 2020 Jul 30.

Abstract

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.

摘要

双酚 A (BPA) 是一种环境内分泌干扰物,也是前列腺癌的一个风险因素。最近的一些研究表明,囊性纤维化跨膜电导调节因子 (CFTR) 是前列腺癌的一种抑制因子。然而,CFTR 在 BPA 诱导的前列腺癌细胞中的潜在作用和机制尚未得到很好的确定。在这项研究中,CCK-8 试剂盒检测到 BPA 降低了人正常前列腺 RWPE-1 细胞的活力。细胞系在软琼脂集落形成、伤口愈合和 Transwell 侵袭方面的能力表明 BPA 诱导了恶性转化。Western blot 分析表明,CFTR 和 Bcl-2 的水平降低,而 Bax 水平升高,ELISA 检测显示暴露于 BPA 的细胞中 ATP 水平降低。通过流式细胞术用 Annexin V-FITC 检测试剂盒分析细胞凋亡。然而,与正常 RWPE-1 细胞相比,细胞活力和凋亡率没有显著差异。我们的研究揭示了 CFTR 在 BPA 诱导的正常前列腺细胞线粒体凋亡导致恶性转化中的潜在作用。

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