GPER stabilizes F-actin cytoskeleton and activates TAZ via PLCβ-PKC and Rho/ROCK-LIMK-Cofilin pathway

Zhen Wang; Li Sun; Shuang Liang; Zan chao Liu; Zeng yi Zhao; Jie Yang; Defeng Wang; DaQing Yang

doi:10.1016/j.bbrc.2019.06.132

GPER stabilizes F-actin cytoskeleton and activates TAZ via PLCβ-PKC and Rho/ROCK-LIMK-Cofilin pathway

Zhen Wang, Li Sun, Shuang Liang, Zan chao Liu, Zeng yi Zhao, Jie Yang, Defeng Wang, DaQing Yang

Hormel Institute

Research output: Contribution to journal › Article › peer-review

19 Scopus citations

Abstract

Actin 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.

Original language	English (US)
Pages (from-to)	976-982
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	516
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2019.06.132
State	Published - Aug 27 2019

Bibliographical note

Funding Information:
Funding: This work was supported by Hebei Natural Science Foundation Youth Fund ( C2019402141 ); Science and Technology Research Project of Hebei Education Department ( QN2019215 ); Innovation fund project of Hebei University of Engineering ( SJ010002098 ); Handan Science and Technology Research and Development Plan ( 1727201061 ); Hebei Cultivation of excellent clinical medical talents and basic research Projects ( 361037 ); and a Paint-The-Town-Pink (PTTP) Research Grant from The Hormel Institute of the University of Minnesota .

Funding Information:
Funding: This work was supported by Hebei Natural Science Foundation Youth Fund (C2019402141); Science and Technology Research Project of Hebei Education Department (QN2019215); Innovation fund project of Hebei University of Engineering (SJ010002098); Handan Science and Technology Research and Development Plan (1727201061); Hebei Cultivation of excellent clinical medical talents and basic research Projects (361037); and a Paint-The-Town-Pink (PTTP) Research Grant from The Hormel Institute of the University of Minnesota.

Publisher Copyright:
© 2019 Elsevier Inc.

Keywords

Breast cancer
F-actin cytoskeleton
GPER
TAZ

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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title = "GPER stabilizes F-actin cytoskeleton and activates TAZ via PLCβ-PKC and Rho/ROCK-LIMK-Cofilin pathway",

abstract = "Actin 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.",

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author = "Zhen Wang and Li Sun and Shuang Liang and Liu, {Zan chao} and Zhao, {Zeng yi} and Jie Yang and Defeng Wang and DaQing Yang",

note = "Funding Information: Funding: This work was supported by Hebei Natural Science Foundation Youth Fund ( C2019402141 ); Science and Technology Research Project of Hebei Education Department ( QN2019215 ); Innovation fund project of Hebei University of Engineering ( SJ010002098 ); Handan Science and Technology Research and Development Plan ( 1727201061 ); Hebei Cultivation of excellent clinical medical talents and basic research Projects ( 361037 ); and a Paint-The-Town-Pink (PTTP) Research Grant from The Hormel Institute of the University of Minnesota . Funding Information: Funding: This work was supported by Hebei Natural Science Foundation Youth Fund (C2019402141); Science and Technology Research Project of Hebei Education Department (QN2019215); Innovation fund project of Hebei University of Engineering (SJ010002098); Handan Science and Technology Research and Development Plan (1727201061); Hebei Cultivation of excellent clinical medical talents and basic research Projects (361037); and a Paint-The-Town-Pink (PTTP) Research Grant from The Hormel Institute of the University of Minnesota. Publisher Copyright: {\textcopyright} 2019 Elsevier Inc.",

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AU - Zhao, Zeng yi

AU - Yang, Jie

AU - Wang, Defeng

AU - Yang, DaQing

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N2 - Actin 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.

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GPER stabilizes F-actin cytoskeleton and activates TAZ via PLCβ-PKC and Rho/ROCK-LIMK-Cofilin pathway

Abstract

Bibliographical note

Keywords

UN SDGs

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