Filtered By:
Drug: Estradiol
This page shows you your search results in order of relevance. This is page number 11.
Order by Relevance | Date
Total 353 results found since Jan 2013.
Estrogen and cigarette sidestream smoke particulate matter exhibit ER α-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.
PMID: 28522562 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - May 18, 2017 Category: Cytology Authors: Kuo LC, Cheng LC, Lee CH, Lin CJ, Chen PY, Li LA Tags: Am J Physiol Lung Cell Mol Physiol 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
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
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
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
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
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
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
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
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
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
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
Hyperhomocysteinemia and hyperandrogenemia share PCSK9-LDLR pathway to disrupt lipid homeostasis in PCOS.
Abstract
Women with polycystic ovary syndrome (PCOS) are at increased risk of cardiovascular diseases (CVD); however, the independent role of PCOS in the incident CVD remains unknown. There are reports that hyperhomocysteinemia (HHcy), a potential cause of CVD, is frequently associated with PCOS. The present study investigates the independent attributes of hyperandrogenemia (HA), the integral associate of PCOS, and HHcy in causing atherogenic dyslipidemia. Twenty-five-day old rats were treated with homocysteine (Hcy) at 50 mg/kg/day dose level for 12 weeks. The HepG2 cell lines transfected with siRNA directed to...
Source: Biochemical and Biophysical Research communications - April 13, 2018 Category: Biochemistry Authors: Mondal K, Chakraborty P, Kabir SN Tags: Biochem Biophys Res Commun Source Type: research
Pancreatic Beta-Cell Proliferation Induced by Estradiol-17 β is Foxo1 Dependent
Horm Metab Res DOI: 10.1055/a-0603-3969Estradiol-17β (E2) and the Foxo1 transcription factor have each been implicated in the regulation of β-cell proliferation. Interaction between Foxo1and estrogen receptor alpha (ERα), effecting cell cycle, has been demonstrated in breast cancer cells, but has not been studied thus far in β-cells. Using human islets and the INS1-E β-cell line, this study investigated the contribution of Foxo1 to E2-mediated β-cell replication. Foxo1 expression was knocked down in INS1-E cells using siRNA and Foxo1 activity was inhibited in human islets with a specific Foxo1 inhibitor (AS1842856). ...
Source: Hormone and Metabolic Research - May 4, 2018 Category: Endocrinology Authors: Shaklai, Sigal Grafi-Cohen, Meital Sharon, Orli Sagiv, Nadav Shefer, Gabi Somjen, Dalia Stern, Naftali Tags: Endocrine Research Source Type: research
