蛋白激酶B
三阴性乳腺癌
PI3K/AKT/mTOR通路
癌症研究
沃特曼宁
乳腺癌
化学
双酚
磷酸化
双酚S
双酚A
转移
上皮-间质转换
内科学
信号转导
生物
医学
癌症
生物化学
有机化学
环氧树脂
作者
Jinmi Liu,Haiping Wang,Xiaoying Hou,Limei Fan,Fang Yang,Yuhang Dai,Yih–Charng Deng,Zhengqi Fu,Xiji Shu,Binlian Sun,Yuchen Liu
标识
DOI:10.1016/j.scitotenv.2023.164748
摘要
Bisphenol P (BPP) and bisphenol M (BPM) are increasing in our living environment as analogues of bisphenol A (BPA), but little is known about their biological effect. In this study, we investigated the effects of low to medium dose exposure of BPP and BPM on triple negative breast cancer (TNBC). We found that BPP and BPM exposure didn't affect proliferation of TNBC cell lines MDA-MB-231 and 4 T1, but significantly promoted cells migration and invasion. The effect of BPP and BPM on promoting TNBC metastasis was further confirmed in mouse models. Low concentrations of BPP and BPM significantly increased the expression of epithelial-mesenchymal transition (EMT) marker and related proteins such as N-cadherin, MMP-9, MMP-2 and Snail, and also enhanced phosphorylation of AKT both in vitro and in vivo. When PI3K inhibitor wortmannin was applied to specifically inhibit phosphorylation of AKT, the expression of target genes markedly decreased, and the TNBC metastasis induced by low-concentration BPP and BPM were reversed. In conclusion, these results showed that PI3K/AKT signaling regulate BPP/BPM-induced metastasis of TNBC by triggering EMT. This study provides insights into the effects and the potential mechanisms of BPP and BPM on TNBC, raising concerns about the risk of using these two bisphenols as the alternative of BPA.
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