Low-dose bisphenol A (BPA)-induced DNA damage and tumorigenic events in MCF-10A cells

Nasir Jalal, Jing Wei, Yaxin Jiang, J. Pathak, A. R. Surendranath, Chang Y. Chung
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引用次数: 2

Abstract

Abstract The carcinogenic capacity of Bisphenol A (BPA) at nano-molar concentrations of 8.73 and 17.47 nM (in culture) was evaluated on both normal breast epithelial cells (MCF-10A) and breast cancer cells (MCF-7). The highest DNA damage was recorded at 6 h and MCF-10A cells showed significant increase of IGF1R protein while mRNA expression was unchanged; however, the converse was true for MCF-7 cells. Homology modeling predicted the structure of SPCA1/2 and indicated BPA binding within catalytic domain. Our data indicated that BPA caused detectable DNA damage, inhibited cellular SPCA1/2 protein which eventually dysregulated Ca2+-dependent IGF1R.
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低剂量双酚A (BPA)诱导MCF-10A细胞的DNA损伤和致瘤事件
研究了双酚A (BPA)在8.73和17.47 nM(培养)纳米摩尔浓度下对正常乳腺上皮细胞(MCF-10A)和乳腺癌细胞(MCF-7)的致癌能力。DNA损伤在6 h时达到最大,MCF-10A细胞IGF1R蛋白显著升高,mRNA表达不变;然而,MCF-7细胞的情况正好相反。同源性模型预测了SPCA1/2的结构,并指出了BPA在催化域中的结合。我们的数据表明,BPA引起可检测的DNA损伤,抑制细胞SPCA1/2蛋白,最终失调Ca2+依赖性IGF1R。
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