Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0578320090270030351
Molecules and Cells
2009 Volume.27 No. 3 p.351 ~ p.357
Tectoridin, a Poor Ligand of Estrogen Receptor, Exerts Its Estrogenic Effects via an ERK- Dependent Pathway
Kang Kyung-Su

Lee Saet-Byoul
Jung Sang-Hoon
Cha Kwang-Hyun
Nho Chu-Won
Sohn Young-Chang
Park Woo-Dong
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.
KEYWORD
ERK, genistein, GPR30, nongenomic estrogen signaling, tectoridin
FullTexts / Linksout information
Listed journal information
SCI(E) MEDLINE ÇмúÁøÈïÀç´Ü(KCI)