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Mol. Cells 2009; 27(3): 351-357

Published online March 19, 2009

https://doi.org/10.1007/s10059-009-0045-8

© The Korean Society for Molecular and Cellular Biology

Tectoridin, a Poor Ligand of Estrogen Receptor, Exerts Its Estrogenic Effects via an ERK-Dependent Pathway

Kyungsu Kang, Saet Byoul Lee, Sang Hoon Jung, Kwang Hyun Cha, Woo Dong Park, Young Chang Sohn, and Chu Won Nho

Received: November 21, 2008; Revised: December 22, 2008; Accepted: December 24, 2008

Abstract

Phytoestrogens are the natural compounds isolated from plants, which are structurally similar to animal estrogen, 17?-estradiol. Tectoridin, a major isoflavone isolated from the rhizome of Belamcanda chinensis. Tectoridin is known as a phytoestrogen, however, the molecular mechanisms underlying its estrogenic effect are remained unclear. In this study we investigated the estrogenic signaling triggered by tectoridin as compared to a famous phytoestrogen, genistein in MCF-7 human breast cancer cells. Tectoridin scarcely binds to ER ? as compared to 17?-estradiol and genistein. Despite poor binding to ER ?, tectoridin induced potent estrogenic effects, namely recovery of the population of cells in the S-phase after serum starvation, transactivation of the estrogen response element, and induction of MCF-7 cell proliferation. The tectoridin-induced estrogenic effect was severely abrogated by treatment with U0126, a specific MEK1/2 inhibitor. Tectoridin promoted phosphorylation of ERK1/2, but did not affect phosphorylation of ER ? at Ser118. It also increased cellu-lar accumulation of cAMP, a hallmark of GPR30-mediated estrogen signaling. These data imply that tectoridin exerts its estrogenic effect mainly via the GPR30 and ERK-mediated rapid nongenomic estrogen signaling pathway. This property of tectoridin sets it aside from genistein where it exerts the estrogenic effects via both an ER-dependent genomic pathway and a GPR30-dependent nongenomic pathway.

Keywords ERK, genistein, GPR30, nongenomic estrogen signaling, tectoridin

Article

Research Article

Mol. Cells 2009; 27(3): 351-357

Published online March 31, 2009 https://doi.org/10.1007/s10059-009-0045-8

Copyright © The Korean Society for Molecular and Cellular Biology.

Tectoridin, a Poor Ligand of Estrogen Receptor, Exerts Its Estrogenic Effects via an ERK-Dependent Pathway

Kyungsu Kang, Saet Byoul Lee, Sang Hoon Jung, Kwang Hyun Cha, Woo Dong Park, Young Chang Sohn, and Chu Won Nho

Received: November 21, 2008; Revised: December 22, 2008; Accepted: December 24, 2008

Abstract

Phytoestrogens are the natural compounds isolated from plants, which are structurally similar to animal estrogen, 17?-estradiol. Tectoridin, a major isoflavone isolated from the rhizome of Belamcanda chinensis. Tectoridin is known as a phytoestrogen, however, the molecular mechanisms underlying its estrogenic effect are remained unclear. In this study we investigated the estrogenic signaling triggered by tectoridin as compared to a famous phytoestrogen, genistein in MCF-7 human breast cancer cells. Tectoridin scarcely binds to ER ? as compared to 17?-estradiol and genistein. Despite poor binding to ER ?, tectoridin induced potent estrogenic effects, namely recovery of the population of cells in the S-phase after serum starvation, transactivation of the estrogen response element, and induction of MCF-7 cell proliferation. The tectoridin-induced estrogenic effect was severely abrogated by treatment with U0126, a specific MEK1/2 inhibitor. Tectoridin promoted phosphorylation of ERK1/2, but did not affect phosphorylation of ER ? at Ser118. It also increased cellu-lar accumulation of cAMP, a hallmark of GPR30-mediated estrogen signaling. These data imply that tectoridin exerts its estrogenic effect mainly via the GPR30 and ERK-mediated rapid nongenomic estrogen signaling pathway. This property of tectoridin sets it aside from genistein where it exerts the estrogenic effects via both an ER-dependent genomic pathway and a GPR30-dependent nongenomic pathway.

Keywords: ERK, genistein, GPR30, nongenomic estrogen signaling, tectoridin

Mol. Cells
Nov 30, 2023 Vol.46 No.11, pp. 655~725
COVER PICTURE
Kim et al. (pp. 710-724) demonstrated that a pathogen-derived Ralstonia pseudosolanacearum type III effector RipL delays flowering time and enhances susceptibility to bacterial infection in Arabidopsis thaliana. Shown is the RipL-expressing Arabidopsis plant, which displays general dampening of the transcriptional program during pathogen infection, grown in long-day conditions.

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