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Drug: Estradiol

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Total 353 results found since Jan 2013.

Ginsenoside Rg1 activates ligand-independent estrogenic effects via rapid estrogen receptor signaling pathway
Conclusions Ginsenoside Rg1 exerted estrogenic actions by rapidly inducing the formation of ER containing signalosome in MCF-7 cells. Additionally, Rg1 could activate EGFR and c-Src ER-independently and exert estrogenic effects via rapid activation of membrane-associated ER and GPER.
Source: Journal of Ginseng Research - March 31, 2018 Category: Complementary Medicine Source Type: research

Mechanisms of canalicular transporter endocytosis in the cholestatic rat liver
In conclusion, our findings show that CME is the mechanism responsible for the internalization of the canalicular transporters BSEP and MRP2 in E17G-induced cholestasis. The shift of these transporters from raft to non-raft microdomains could be a prerequisite for the transporters to be endocytosed under cholestatic conditions.
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - March 1, 2018 Category: Molecular Biology Source Type: research

Mechanisms of canalicular transporter endocytosis in the cholestatic rat liver.
In conclusion, our findings show that CME is the mechanism responsible for the internalization of the canalicular transporters BSEP and MRP2 in E17G-induced cholestasis. The shift of these transporters from raft to non-raft microdomains could be a prerequisite for the transporters to be endocytosed under cholestatic conditions. PMID: 29355600 [PubMed - as supplied by publisher]
Source: Biochimica et Biophysica Acta - January 17, 2018 Category: Biochemistry Authors: Miszczuk GS, Barosso IR, Larocca MC, Marrone J, Marinelli RA, Boaglio AC, Sánchez Pozzi EJ, Roma MG, Crocenzi FA Tags: Biochim Biophys Acta Source Type: research

Estrogen receptor β1 activation accelerates resistance to epidermal growth factor receptor-tyrosine kinase inhibitors in non-small cell lung cancer.
In conclusion, ERβ1 was activated in EGFR-TKI secondary resistance. The downregulation of ERβ1 sensitized the cells to EGFR-TKIs. ERβ1 may be a key molecule in EGFR-TKI therapy. In addition, anti-ERβ1 treatment may reverse TKI resistance. PMID: 29328407 [PubMed - as supplied by publisher]
Source: Oncology Reports - January 14, 2018 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Neonatal cardiomyocyte hypertrophy induced by endothelin-1 is blocked by estradiol acting on GPER.
In conclusion, E2 plays a key role in antagonizing ET-1-induced hypertrophy in cultured neonatal cardiomyocytes through GPER signaling by mechanism involving activation of PDK1 pathway, which would prevent the increase of ERK1/2 activity and consequently the development of hypertrophy. PMID: 29167148 [PubMed - as supplied by publisher]
Source: Am J Physiol Cell Ph... - November 22, 2017 Category: Cytology Authors: Goncalves GK, Scalzo S, Alves AP, Agero U, Guatimosim S, Reis AM Tags: Am J Physiol Cell Physiol Source Type: research

Nonsteroidal estrogen receptor isoform ‐selective biphenyls
Estrogen receptor (ER) has been a therapeutic target to treat ER‐positive breast cancer, most notably by agents known as selective estrogen receptor modulators (SERMs). However, resistance and severe adverse effects of known drugs gave impetus to the search for newer agents with better therapeutic profile. ERα and ERβ are two isoforms sharing 56% identity and having different physiological functions and expressions in various tissues. Only two residues differ in the active sites of the two isoforms motivating us to design isoform‐selective ligands. Guided by computational docking and molecular dynamics simulations, w...
Source: Chemical Biology and Drug Design - November 10, 2017 Category: Biology Authors: Seema Bhatnagar, Anjali Soni, Swati Kaushik, Megha Rikhi, Thankayyan Retnabai Santhoshkumar, Bhyravabhotla Jayaram Tags: RESEARCH ARTICLE Source Type: research

Estrogen receptor {beta}-dependent Notch1 activation protects vascular endothelium against tumor necrosis factor {alpha} (TNF{alpha})-induced apoptosis Molecular Bases of Disease
Unlike age-matched men, premenopausal women benefit from cardiovascular protection. Estrogens protect against apoptosis of endothelial cells (ECs), one of the hallmarks of endothelial dysfunction leading to cardiovascular disorders, but the underlying molecular mechanisms remain poorly understood. The inflammatory cytokine TNFα causes EC apoptosis while dysregulating the Notch pathway, a major contributor to EC survival. We have previously reported that 17β-estradiol (E2) treatment activates Notch signaling in ECs. Here, we sought to assess whether in TNFα-induced inflammation Notch is involved in E2-mediated protection...
Source: Journal of Biological Chemistry - November 3, 2017 Category: Chemistry Authors: Francesca Fortini, Francesco Vieceli Dalla Sega, Cristiana Caliceti, Giorgio Aquila, Micaela Pannella, Antonio Pannuti, Lucio Miele, Roberto Ferrari, Paola Rizzo Tags: Cell Biology Source Type: research

Activation of insulin-like growth factor 1 receptor participates downstream of GPR30 in estradiol-17 β-D-glucuronide-induced cholestasis in rats.
In conclusion, the activation of IGF-1R is a key factor in the alteration of canalicular transporter function and localization induced by E17G, and its activation follows that of GPR30 and precedes that of PI3K/Akt. PMID: 29090346 [PubMed - as supplied by publisher]
Source: Archives of Toxicology - October 31, 2017 Category: Toxicology Authors: Barosso IR, Miszczuk GS, Ciriaci N, Andermatten RB, Maidagan PM, Razori V, Taborda DR, Roma MG, Crocenzi FA, Sánchez Pozzi EJ Tags: Arch Toxicol Source Type: research

Non ‐steroidal Estrogen Receptor Isoform Selective Biphenyls
This article is protected by copyright. All rights reserved. Novel substituted biphenyl‐2,6‐diethanones are designed and synthesized targeting ERα isoform. MD simulations along with MM‐GBSA accounted for the binding selectivity of 3b towards ERα over ERβ. Co‐treatment and E‐screen studies indicated the ERα selective nature of 3b and anti‐estrogenicity. ERα siRNA silencing experiments further confirmed the isoform selectivity.
Source: Chemical Biology and Drug Design - October 20, 2017 Category: Biology Authors: Seema Bhatnagar, Anjali Soni, Swati Kaushik, Megha Rikhi, T R Santhosh Kumar, B. Jayaram Tags: Research Article Source Type: research

Estradiol-ER β2 signaling axis confers growth and migration of CRPC cells through TMPRSS2-ETV5 gene fusion.
We report that non-canonical activation of estradiol (E2)-ERβ2 signaling axis primes growth, colony-forming ability and migration of the androgen receptor (AR)-null castration-resistant PC (CRPC) cells under androgen-deprived conditions (ADC). The non-classical E2-ERβ2 mediates phosphorylation and activation of Src-IGF-1R complex, which in turn triggers p65-dependent transcriptional upregulation of the androgen-regulated serine protease TMPRSS2:ETV5a/TMPRSS2:ETV5b gene fusions under ADC. siRNA silencing of TMPRSS2 and/or ETV5 suggests that TMPRSS2:ETV5 fusions facilitates the E2-ERβ induced growth and migration effects ...
Source: Oncotarget - October 6, 2017 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

The activation of the G protein-coupled estrogen receptor (GPER) inhibits the proliferation of mouse melanoma K1735-M2 cells
Publication date: Available online 22 September 2017 Source:Chemico-Biological Interactions Author(s): Mariana P.C. Ribeiro, Armanda E. Santos, José B.A. Custódio The activation of the G protein-coupled estrogen receptor (GPER) by its specific agonist G-1 inhibits prostate cancer and 17β-estradiol-stimulated breast cancer cell proliferation. Tamoxifen (TAM), which also activates the GPER, decreases melanoma cell proliferation, but its action mechanism remains controversial. Here we investigated the expression and the effects of GPER activation by G-1, TAM and its key metabolite endoxifen (EDX) on melanoma cells. Mouse ...
Source: Chemico Biological Interactions - September 22, 2017 Category: Biochemistry Source Type: research

The activation of the G protein-coupled estrogen receptor (GPER) inhibits the proliferation of mouse melanoma K1735-M2 cells.
Abstract The activation of the G protein-coupled estrogen receptor (GPER) by its specific agonist G-1 inhibits prostate cancer and 17β-estradiol-stimulated breast cancer cell proliferation. Tamoxifen (TAM), which also activates the GPER, decreases melanoma cell proliferation, but its action mechanism remains controversial. Here we investigated the expression and the effects of GPER activation by G-1, TAM and its key metabolite endoxifen (EDX) on melanoma cells. Mouse melanoma K1735-M2 cells expressed GPER and G-1 reduced cell biomass, and the number of viable cells, without increasing cell death. Rather, G-1 decr...
Source: Chemico-Biological Interactions - September 22, 2017 Category: Molecular Biology Authors: Ribeiro MPC, Santos AE, Custódio JBA Tags: Chem Biol Interact Source Type: research

The effects of 17 alpha-estradiol to inhibit inflammation in vitro
ConclusionsIn conclusion, we demonstrate for the first time that 17 α-E2, as well as 17 β-E2, suppresses inflammation through their effects on ERα and NFκB-p65.
Source: Biology of Sex Differences - September 6, 2017 Category: Biology Source Type: research

Estrogen and cigarette sidestream smoke particulate matter exhibit ER{alpha}-dependent tumor-promoting effects in lung adenocarcinoma cells
This study demonstrates that estrogen has ERα-dependent tumor-promoting activity. CSSP acts like estrogen and shows a potential to enhance estrogen-induced ERα action.
Source: AJP: Lung Cellular and Molecular Physiology - September 1, 2017 Category: Respiratory Medicine Authors: Kuo, L.-C., Cheng, L.-C., Lee, C.-H., Lin, C.-J., Chen, P.-Y., Li, L.-A. Tags: RESEARCH ARTICLE Source Type: research

Williams syndrome transcription factor (WSTF) acts as an activator of estrogen receptor signaling in breast cancer cells and the effect can be abrogated by 1 α,25-dihydroxyvitamin D3
This study reports a novel transcription factor critical to 1α,25-dihydroxyvitamin D3-mediated regulation of estrogenic signaling in MCF-7 breast cancer cells. We have investigated the molecular mechanisms for the 1α,25-dihydroxyvitamin D3-mediated down-regulation of CYP19A1 and ERα gene expression in human MCF-7 breast cancer cells and found that Williams syndrome transcription factor (WSTF) plays a key role by binding to the promoters of CYP19A1 and ERα. Although sometimes reported as an inhibitor of gene expression, we found that WSTF acts as an activator of the promoter activity of both CYP19A1 and ERα. Silencing ...
Source: The Journal of Steroid Biochemistry and Molecular Biology - June 11, 2017 Category: Biochemistry Source Type: research