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首页> 外文期刊>Human and Experimental Toxicology >2,2 ',4,4 '-Tetrabromodiphenyl ether promotes human neuroblastoma SH-SYSY cells migration via the GPER/PI3K/Akt signal pathway
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2,2 ',4,4 '-Tetrabromodiphenyl ether promotes human neuroblastoma SH-SYSY cells migration via the GPER/PI3K/Akt signal pathway

机译：2,2'，4,4'-四溴二苯醚通过GPER / PI3K / Akt信号通路促进人神经母细胞瘤SH-SYSY细胞迁移

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摘要

Neuroblastoma is the predominant tumor of early childhood. 2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) has the highest concentration among all polybrominated diphenyl ether (PBDE) congeners in human body, particularly for children. Considering that accumulating evidences showed developmental neurotoxicity of PBDE, there is an urgent need to investigate the effects of BDE-47 on the development of neuroblastoma. This study revealed that BDE-47 had limited effects on the cytotoxicity while significantly increased the in vitro migration and invasion of human neuroblastoma SH-SY5Y cells. This was further confirmed by the results that BDE-47 treatment significantly downregulated the expression of E-cadherin and zona occludin-1 and upregulated the expression of matrix metalloproteinase-9 (MMP-9). Silencing of MMP-9 by specific small interfering RNA significantly abolished the BDE-47-induced migration and invasion of SH-SY5Y cells. Further, the signals G protein-coupled estrogen receptor I (GPER)/phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (Akt) mediated the BDE-47-induced upregulation of MMP-9 and in vitro migration of SH-SY5Y cells since G15 (GPER inhibitor) and LY 294002 (PI3K/Akt inhibitor) significantly abolished the effects of BDE- 47. Our results revealed that BDE-47 significantly triggered the metastasis of human neuroblastoma SH-SY5Y cells via upregulation of MMP-9 by the GPER/PI3K/Akt signal pathway. This study revealed for the first time that BDE-47 can promote the migration of SH-SY5Y cells. It also provided a better understanding about the metastasis of human neuroblastoma induced by environmental endocrine disruptors.
机译：神经母细胞瘤是儿童早期的主要肿瘤。 2,2'，4,4'-四溴二苯醚（BDE-47）在人体中所有多溴二苯醚（PBDE）同系物中的浓度最高，特别是对于儿童。考虑到越来越多的证据显示了多溴二苯醚的发育神经毒性，迫切需要研究BDE-47对成神经母细胞瘤发展的影响。这项研究表明，BDE-47对细胞毒性的作用有限，同时显着增加了人类神经母细胞瘤SH-SY5Y细胞的体外迁移和侵袭。结果进一步证实，BDE-47处理可显着下调E-钙粘蛋白和Zona occludin-1的表达，并上调基质金属蛋白酶9（MMP-9）的表达。特定的小干扰RNA沉默MMP-9大大消除了BDE-47诱导的SH-SY5Y细胞的迁移和侵袭。此外，信号G蛋白偶联雌激素受体I（GPER）/磷脂酰肌醇-4,5-双磷酸3-激酶（PI3K）/蛋白激酶B（Akt）介导了BDE-47诱导的MMP-9上调和体外自G15（GPER抑制剂）和LY 294002（PI3K / Akt抑制剂）起SH-SY5Y细胞迁移显着消除了BDE-47的作用。我们的结果表明BDE-47通过上调显着触发了人类神经母细胞瘤SH-SY5Y细胞的转移。 GPER / PI3K / Akt信号通路对MMP-9的检测这项研究首次揭示了BDE-47可以促进SH-SY5Y细胞的迁移。它还提供了对由环境内分泌干扰物诱导的人神经母细胞瘤转移的更好的理解。

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