scholarly journals Resveratrol modulates the phosphoinositide 3-kinase pathway through an estrogen receptor α-dependent mechanism: Relevance in cell proliferation

2003 ◽  
Vol 109 (2) ◽  
pp. 167-173 ◽  
Author(s):  
Eulalia Pozo-Guisado ◽  
M. Jesús Lorenzo-Benayas ◽  
Pedro M. Fernández-Salguero
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Phosphoinositide 3 Kinase ◽  
Kinase Pathway ◽  
Dependent Mechanism

scholarly journals Rapid Estrogen Receptor-α Activation Improves Ischemic Tolerance in Aged Female Rats through a Novel Protein Kinase Cε-Dependent Mechanism

Endocrinology ◽  
2009 ◽  
Vol 150 (2) ◽  
pp. 889-896 ◽  
Author(s):  
Jennifer L. Novotny ◽  
Amy M. Simpson ◽  
Nanette J. Tomicek ◽  
Timothy S. Lancaster ◽  
Donna H. Korzick
Keyword(s):  
Estrogen Receptor ◽  
Protein Kinase ◽  
Estrogen Receptor Α ◽  
Ischemic Tolerance ◽  
Female Rats ◽  
Dependent Mechanism ◽  
Novel Protein

scholarly journals Palmitoylation-dependent Estrogen Receptor α Membrane Localization: Regulation by 17β-Estradiol

2005 ◽  
Vol 16 (1) ◽  
pp. 231-237 ◽  
Author(s):  
Filippo Acconcia ◽  
Paolo Ascenzi ◽  
Alessio Bocedi ◽  
Enzo Spisni ◽  
Vittorio Tomasi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Plasma Membrane ◽  
Estrogen Receptor Α ◽  
Membrane Localization ◽  
Target Cells ◽  
Dependent Manner ◽  
Caveolin 1 ◽  
17Β Estradiol

A fraction of the nuclear estrogen receptor α (ERα) is localized to the plasma membrane region of 17β-estradiol (E2) target cells. We previously reported that ERα is a palmitoylated protein. To gain insight into the molecular mechanism of ERα residence at the plasma membrane, we tested both the role of palmitoylation and the impact of E2 stimulation on ERα membrane localization. The cancer cell lines expressing transfected or endogenous human ERα (HeLa and HepG2, respectively) or the ERα nonpalmitoylable Cys447Ala mutant transfected in HeLa cells were used as experimental models. We found that palmitoylation of ERα enacts ERα association with the plasma membrane, interaction with the membrane protein caveolin-1, and nongenomic activities, including activation of signaling pathways and cell proliferation (i.e., ERK and AKT activation, cyclin D1 promoter activity, DNA synthesis). Moreover, E2 reduces both ERα palmitoylation and its interaction with caveolin-1, in a time- and dose-dependent manner. These data point to the physiological role of ERα palmitoylation in the receptor localization to the cell membrane and in the regulation of the E2-induced cell proliferation.

scholarly journals The Antitumor Peptide ERα17p Exerts Anti-Hyperalgesic and Anti-Inflammatory Actions Through GPER in Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Christophe Mallet ◽  
Ludivine Boudieu ◽  
Sylvain Lamoine ◽  
Catherine Coudert ◽  
Yves Jacquot ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Systemic Administration ◽  
Mice Model ◽  
Persistent Inflammation ◽  
Human Estrogen Receptor ◽  
Anti Inflammatory ◽  
G Protein Coupled ◽  
Inflammatory Action ◽  
Dependent Mechanism

Persistent inflammation and persistent pain are major medical, social and economic burdens. As such, related pharmacotherapy needs to be continuously improved. The peptide ERα17p, which originates from a part of the hinge region/AF2 domain of the human estrogen receptor α (ERα), exerts anti-proliferative effects in breast cancer cells through a mechanism involving the hepta-transmembrane G protein-coupled estrogen receptor (GPER). It is able to decrease the size of xenografted human breast tumors, in mice. As GPER has been reported to participate in pain and inflammation, we were interested in exploring the potential of ERα17p in this respect. We observed that the peptide promoted anti-hyperalgesic effects from 2.5 mg/kg in a chronic mice model of paw inflammation induced by the pro-inflammatory complete Freund’s adjuvant (CFA). This action was abrogated by the specific GPER antagonist G-15, leading to the conclusion that a GPER-dependent mechanism was involved. A systemic administration of a Cy5-labeled version of the peptide allowed its detection in both, the spinal cord and brain. However, ERα17p-induced anti-hyperalgesia was detected at the supraspinal level, exclusively. In the second part of the study, we have assessed the anti-inflammatory action of ERα17p in mice using a carrageenan-evoked hind-paw inflammation model. A systemic administration of ERα17p at a dose of 2.5 mg/kg was responsible for reduced paw swelling. Overall, our work strongly suggests that GPER inverse agonists, including ERα17p, could be used to control hyperalgesia and inflammation.

scholarly journals Estrogenic Activity of Mycoestrogen (3β,5α,22E)-Ergost-22-en-3-ol via Estrogen Receptor α-Dependent Signaling Pathways in MCF-7 Cells

Molecules ◽  
2021 ◽  
Vol 27 (1) ◽  
pp. 36
Author(s):  
Dahae Lee ◽  
Yuri Ko ◽  
Changhyun Pang ◽  
Yoon-Joo Ko ◽  
You-Kyoung Choi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Methanol Extract ◽  
Estrogenic Activity ◽  
Cancer Cell Line ◽  
Estrogen Receptor Α ◽  
Bile Secretion ◽  
Bioassay Guided Fractionation ◽  
Positive Breast Cancer Cell ◽  
Mcf 7

Armillariella tabescens (Scop.) Sing., a mushroom of the family Tricholomataceae, has been used in traditional oriental medicine to treat cholecystitis, improve bile secretion, and regulate bile-duct pressure. The present study evaluated the estrogen-like effects of A. tabescens using a cell-proliferation assay in an estrogen-receptor-positive breast cancer cell line (MCF-7). We found that the methanol extract of A. tabescens fruiting bodies promoted cell proliferation in MCF-7 cells. Using bioassay-guided fractionation of the methanol extract and chemical investigation, we isolated and identified four steroids and four fatty acids from the active fraction. All eight compounds were evaluated by E-screen assay for their estrogen-like effects in MCF-7 cells. Among the tested isolates, only (3β,5α,22E)-ergost-22-en-3-ol promoted cell proliferation in MCF-7 cells; this effect was mitigated by the ER antagonist, ICI 182,780. The mechanism underlying the estrogen-like effect of (3β,5α,22E)-ergost-22-en-3-ol was evaluated using Western blot analysis to detect the expression of extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase (PI3K), Akt, and estrogen receptor α (ERα). We found that (3β,5α,22E)-ergost-22-en-3-ol induced an increase in phosphorylation of ERK, PI3K, Akt, and ERα. Together, these experimental results suggest that (3β,5α,22E)-ergost-22-en-3-ol is responsible for the estrogen-like effects of A. tabescens and may potentially aid control of estrogenic activity in menopause.

Estrogen receptor α/β isoforms, but not βcx, modulate unique patterns of gene expression and cell proliferation in Hs578T cells

2007 ◽  
Vol 101 (5) ◽  
pp. 1125-1147 ◽  
Author(s):  
Frank J. Secreto ◽  
David G. Monroe ◽  
Shamit Dutta ◽  
James N. Ingle ◽  
Thomas C. Spelsberg
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Estrogen Receptor Α
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