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首页> 外文期刊>Cellular Signalling >The G protein estrogen receptor (GPER) is regulated by endothelin-1 mediated signaling in cancer cells
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The G protein estrogen receptor (GPER) is regulated by endothelin-1 mediated signaling in cancer cells

机译：G蛋白雌激素受体（GPER）受内皮素1介导的癌细胞信号调节

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摘要

Endothelin-1 (ET-1) is a potent endogenous vasoconstrictor involved in many diseases, including certain cardiovascular disorders and cancer. As previous studies have shown that the G protein estrogen receptor (GPER) may regulate ET-1 dependent effects on the vascular system, we evaluated whether GPER could contribute to the effects elicited by ET-1 in breast cancer and hepatocarcinoma cells. Here, we demonstrate that ET-1 increases GPER expression through endothelin receptor A (ETAR) and endothelin receptor B (ETBR) along with the activation of PI3K/ERK/c-Fos/AP1 transduction pathway. In addition, we show that GPER is involved in important biological responses observed upon ET-1 exposure, as the migration of the aforementioned tumor cells and the formation of tube-like structures in human umbilical vein endothelial cells (HUVECs). Our data suggest that GPER may contribute to ET-1 action toward the progression of some types of tumor. (C) 2015 Elsevier Inc. All rights reserved.
机译：内皮素-1（ET-1）是一种有效的内源性血管收缩药，涉及多种疾病，包括某些心血管疾病和癌症。正如先前的研究表明，G蛋白雌激素受体（GPER）可能调节ET-1对血管系统的依赖作用，我们评估了GPER是否可以促进ET-1在乳腺癌和肝癌细胞中引起的作用。在这里，我们证明了ET-1通过内皮素受体A（ETAR）和内皮素受体B（ETBR）以及PI3K / ERK / c-Fos / AP1转导途径的激活来增加GPER表达。此外，我们表明GPER参与了在ET-1暴露下观察到的重要生物学反应，因为上述肿瘤细胞的迁移和人脐静脉内皮细胞（HUVECs）的管状结构的形成。我们的数据表明，GPER可能有助于ET-1促进某些类型肿瘤的进展。 （C）2015 Elsevier Inc.保留所有权利。

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