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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
Mar 31, 2023 Vol.46 No.3, pp. 131~189
COVER PICTURE
The physiologically important cytoprotective signaling in normal cells (background area in turquoise) mediated by NRF2 (blue chain) is often hijacked by cancer cells (red ball) in the tumor microenvironment (yellow area). However, the differential roles of NRF2 throughout the multistage carcinogenesis remains largely unresolved (white-colored overlapping misty areas).

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