Nongenomic estrogen signaling of a plant isoflavone, tectoridin
- Nongenomic estrogen signaling of a plant isoflavone, tectoridin
- 강경수; 이샛별; 정상훈; 차광현; 박우동; 손영창; 노주원
- Tectoridin; phytoestrogen; ERK; nongenomic estrogen signaling; genistein; GPR30
- Issue Date
- 2009 한국응용생명화학회 춘계학술대회
- Phytoestrogens are the natural compounds isolated from plants, which are structurally similar to animal estrogen, 17β-estradiol(E2). Phytoestrogens often exert estrogenic effect in animal cells. They are ofter used for estrogen replacement therapy replacing E2 in menopausal women. Tectordin, a major isoflavone isolated from the rhizome of Belamecnda chinensis. Tectoridin is known as a phytoestrogen, however, the molecular mechanisms underlying its estrogenic effect are remained unclear. Tectoridin scarcely binds to ER α as compared to 17β-estradiol and genistein, a famous phytoestrogen. It also did not induce phosphorylation of ER α at Ser Despite poor binding to ER α, fectoridin did induce potent estrogenic effects showing recovery of the population of cells in the S-phase after serum starvation, transactivation of aht estrogen reponse element(ERE), and induction of MCF-7 cell proliferation. The rectoridin-induced estrogenic effect was severely abrogated ty treatment with U0126 or PD98059, a specific MEK1/2 inhibitor. Tectoridin rapidly induced phosphorylation of ERK1/2. It also increased cellular 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. Our data provide a new insight into the mechanisms of nongenomic estrogen signaling triggered by a poor ligand of ER, tectoridin.
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