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
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 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.
Kyungsu Kang, Saet Byoul Lee, Sang Hoon Jung, Kwang Hyun Cha, Woo Dong Park, Young Chang Sohn, and Chu Won Nho
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
Ki-Hong Jang, Chloe R. Heras, and Gina Lee
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