• Zhen Wang, Li Sun, Shuang Liang, Zan-Chao Liu, Zeng-Yi Zhao, Jie Yang, Defeng Wang, and Da-Qing Yang.
• The Affiliated Hospital and the Medical College, Hebei University of Engineering, Handan, Hebei Province, PR China; The Hormel Institute, University of Minnesota, Austin, MN, USA; The Shijiazhuang Second Hospital, Shijiazhuang, Hebei, PR China.
• Biochem. Biophys. Res. Commun. 2019 Aug 27; 516 (3): 976-982.

AbstractActin is a highly abundant cytoskeletal protein that is essential for all eukaryotic cells and participates in many structural and functional roles. It has long been noted that estrogen affects cellular morphology. However, recent studies observed that both estrogen and tamoxifen induce a remarkable cytoskeletal remodeling independent of ER. In addition to ER, G protein-coupled estrogen receptor 1 (GPER, also known as GPR30) also binds to estrogen with high affinity and mediates intracellular estrogenic signaling. Here, we show that activation of GPER by its specific agonist G-1 induces re-organization of F-actin cytoskeleton. We further demonstrate that GPER acts through PLCβ-PKC and Rho/ROCK-LIMK-Cofilin pathway, which are upstream regulators of F-actin cytoskeleton assembly, thereby enhancing TAZ nuclear localization and activation. Furthermore, we find that LIMK1/2 is critical for GPER activation-induced breast cancer cell migration. Together, our results suggest that GPER mediates G-1-induced cytoskeleton assembly and GPER promotes breast cancer cell migration via PLCβ-PKC and Rho/ROCK-LIMK-Cofilin pathway.Copyright © 2019 Elsevier Inc. All rights reserved.

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