Filtered By:
Drug: Estradiol

This page shows you your search results in order of relevance. This is page number 9.

Order by Relevance | Date

Total 353 results found since Jan 2013.

17-beta estradiol inhibits oxidative stress-induced accumulation of AIF into nucleolus and PARP1-dependent cell death via estrogen receptor alpha.
Abstract Oxidative stress-induced DNA damage results in over-activation of poly(ADP-ribose) polymerase 1 (PARP1), leading to parthanatos, a newly discovered cell elimination pathway. Inhibition of PARP1-dependent cell death has shown to improve the outcome of diseases, including stroke, heart ischemia, and neurodegenerative diseases. In the present study we aimed to detect whether estrogen plays a protective role in inhibiting parthanatos. We utilized human mammary adenocarcinoma cells (MCF7) that abundantly express the estrogen receptor alpha and beta (ERα and ERβ). Parthanatos was induced by challenging the ce...
Source: Toxicology Letters - September 30, 2014 Category: Toxicology Authors: Batnasan E, Wang R, Wen J, Ke Y, Li X, Bohio AA, Zeng X, Huo H, Han L, Boldogh I, Ba X Tags: Toxicol Lett Source Type: research

Estrogen mediated epithelial proliferation in the uterus is directed by stromal Fgf10 and Bmp8a
Publication date: Available online 7 November 2014 Source:Molecular and Cellular Endocrinology Author(s): Daesuk Chung , Fei Gao , Anil G. Jegga , Sanjoy K. Das To define endometrial stromal-derived paracrine mediators that participate in estradiol-17β (E2)-induced epithelial proliferation, microarray analysis of gene expression was carried out in mouse uterine epithelial-stromal co-culture systems under the condition of E2 or vehicle (control). Our results demonstrated gene alteration by E2: in epithelial cells, we found up-regulation of 119 genes and down-regulation of 28 genes, while in stroma cells we found up-regul...
Source: Molecular and Cellular Endocrinology - November 7, 2014 Category: Endocrinology Source Type: research

Nrf2, the master redox switch: The Achilles' heel of ovarian cancer?
Publication date: December 2014 Source:Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Volume 1846, Issue 2 Author(s): Monique G.P. van der Wijst , Robert Brown , Marianne G. Rots Ovarian cancer is the most lethal gynecological tumor type in the world due to late stage detection, and resistance to chemotherapy. Therefore, alternative additional therapies are required. The etiology of ovarian cancer remains largely unknown, but risk factors point toward an important role for oxidative stress. Both healthy and tumor cells can cope with oxidative stress by activating the transcription factor Nrf2 (also known as Nfe...
Source: Biochimica et Biophysica Acta (BBA) Reviews on Cancer - October 12, 2014 Category: Cancer & Oncology Source Type: research

Phytoestrogen-Induced Apoptosis
Phytoestrogens have been investigated as natural alternatives to hormone replacement therapy and their potential as chemopreventive agents. We investigated the effects of equol, genistein, and coumestrol on cell growth in fully estrogenized MCF7 cells, simulating the perimenopausal state, and long-term estrogen-deprived MCF7:5C cells, which simulate the postmenopausal state of a woman after years of estrogen deprivation, and compared the effects with that of steroidal estrogens: 17β estradiol (E2) and equilin present in conjugated equine estrogen. Steroidal and phytoestrogens induce proliferation of MCF7 cells at phys...
Source: Cancer Prevention Research - September 1, 2014 Category: Cancer & Oncology Authors: Obiorah, I. E., Fan, P., Jordan, V. C. Tags: Preclinical Intervention, Preclinical Intervention: In Vivo (Animals): Drugs, Nutritional Interventions, Mechanisms Research Articles Source Type: research

NF-κB increased expression of 17β-hydroxysteroid dehydrogenase 4 promotes HepG2 proliferation via inactivating estradiol
In this study, HepG2 cells were used to investigate the role of HSD17B4 in the proliferation of liver cancer cells treated with the NF-κB activator, tumor necrosis factor-alpha (TNF-α), with the inhibitor of NF-κB activation, pyrrolidinedithiocarbamate (PDTC), or with a related specific siRNA. We demonstrated that the human HSD17B4 gene is a target for NF-κB activation in inflammation-stimulated HepG2 cells. HSD17B4 is up-regulated via the binding of activated NF-κB to the distal NF-κB-responsive element via TNF-α stimulation, which then promotes cell proliferation by decreasing the levels of E2 and enhancing the ex...
Source: Molecular and Cellular Endocrinology - December 12, 2014 Category: Endocrinology Source Type: research

Wild‐type and Specific Mutant Androgen Receptor Mediates Transcription via 17β‐Estradiol in Sex Hormone‐sensitive Cancer Cells
This article is protected by copyright. All rights reserved
Source: Journal of Cellular Physiology - December 23, 2014 Category: Cytology Authors: Takao Susa, Reina Ikaga, Takashi Kajitani, Masayoshi Iizuka, Hiroko Okinaga, Mimi Tamamori‐Adachi, Tomoki Okazaki Tags: Original Research Article Source Type: research

A precisely substituted benzopyran targets androgen refractory prostate cancer cells through selective modulation of estrogen receptors.
Abstract Dietary consumption of phytoestrogens like genistein has been linked with lower incidence of prostate cancer. The estradiol-like benzopyran core of genistein confers estrogen receptor-β (ER-β) selectivity that imparts weak anti-proliferative activity against prostate cancer cells. DL-2-[4-(2-piperidinoethoxy)phenyl]-3-phenyl-2H-1-benzopyran (BP), a SERM designed with benzopyran core, targeted androgen independent prostate cancer (PC-3) cells 14-times more potently than genistein, ~25% more efficiently than tamoxifen and 6.5-times more actively than ICI-182780, without forfeiting significant specificity ...
Source: Toxicology and Applied Pharmacology - February 2, 2015 Category: Toxicology Authors: Kumar R, Verma V, Sharma V, Jain A, Singh V, Sarswat A, Maikhuri JP, Sharma VL, Gupta G Tags: Toxicol Appl Pharmacol Source Type: research

EGFR participates downstream of ERα in estradiol-17β-D-glucuronide-induced impairment of Abcc2 function in isolated rat hepatocyte couplets.
In conclusion, activation of EGFR is a key factor in the alteration of canalicular transporter function and localization induced by E17G and it occurs before that of Src and after that of ERα. PMID: 25813982 [PubMed - as supplied by publisher]
Source: Archives of Toxicology - March 27, 2015 Category: Toxicology Authors: Barosso IR, Zucchetti AE, Miszczuk GS, Boaglio AC, Taborda DR, Roma MG, Crocenzi FA, Sánchez Pozzi EJ Tags: Arch Toxicol Source Type: research

Abstract PD6-1: The long noncoding RNA M41 promotes aggressiveness and tamoxifen resistance in ER-positive breast cancers
In this study, we identify M41 as the top outlier lncRNA in ER-positive vs ER-negative breast cancer and investigate its role in preclinical cancer phenotypes and clinical outcomes. Methods and Materials: RNA sequencing was performed on 89 breast cancer samples and cell lines, including 42 ER+ cases, and a modified cancer outlier analysis was used to identify lncRNAs enriched in ER-positive disease. To assess ER regulation of the top enriched lncRNA (M41), ChIP-Seq and ChIP-PCR was used to detect binding of ER to M41 promoter and qPCR was used to determine changes in M41 expression following 10 nM estradiol treatment in MC...
Source: Cancer Research - April 30, 2015 Category: Cancer & Oncology Authors: Feng, F. Y., Ma, T., Speers, C., Iyer, M. K., Zhao, S., Prensner, J. R., Rae, J. M., Pierce, L. J., Chinnaiyan, A. M. Tags: Poster Discussion Abstracts Source Type: research

C-jun NH2-terminal kinase and p38 inhibition suppresses Prostaglandin E2- stimulated aromatase and estrogen receptor levels in human endometriosis.
CONCLUSIONS: PGE2 activates p38 and JNK signaling pathways, further stimulating c-Jun and ATF2 binding to aromatase and ERB promoter regions with elevated estradiol production. Inhibition of JNK and P38 may be a potential way in the treatment of human endometriosis. PMID: 26394174 [PubMed - as supplied by publisher]
Source: The Journal of Clinical Endocrinology and Metabolism - September 22, 2015 Category: Endocrinology Authors: Zeng C, Xu JN, Zhou Y, Yang HX, Zhou YF, Xue Q Tags: J Clin Endocrinol Metab Source Type: research

Sphingosine-1-phosphate receptor 1 transmits estrogens’ effects in endothelial cells
In this study we report that treatment of endothelial cells (ECs) with 17β-estradiol (E2) resulted in a rapid, transient, and dose-dependent increase in SphK activity and increased S1P production. The effect was not reproduced by the inactive E2 analogue 17α-E2. Expression of the dominant-negative mutant SphK1G82D or transfection of SphK1-targeted siRNA in ECs caused not only a defect in SphK activation by E2, but also a significant inhibition of E2-induced activation of Akt/eNOS. Furthermore, E2 treatment induced internalization of plasma membrane S1P1 receptor, accompanied with an increase in the amount of cytosolic S1...
Source: Steroids - October 22, 2015 Category: Drugs & Pharmacology Source Type: research

Abstract P098: G-protein Coupled Estrogen Receptor Stimulates Capillary Formation by Human Umbilical Vein Endothelial Cells via ALK1-SMAD 1/5/8 Pathway Activation Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception
Estradiol (E2) induces vascular repair by promoting endothelial growth and capillary formation. Based on our previous findings that the capillary stimulating effects of E2 are mimicked by its non-permeable analog, BSA-tagged E2, we hypothesize that the stimulatory effects are potentially mediated via the newly discovered membrane bound G-protein coupled estrogen receptor (GPER). To investigate this, we assessed capillary formation by endothelial cells in response to E2, and GPER agonist (G1)and antagonist (G15) in a 2-D matrigel based assay. Capillary formation was assessed microscopically by quantifying junction/sprout fo...
Source: Hypertension - November 3, 2015 Category: Cardiology Authors: Unterleutner, E., Rigassi, L., Barchiesi, F., Imthurn, B., Dubey, R. K. Tags: Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception Source Type: research

Licorice Root Components in Dietary Supplements are Selective Estrogen Receptor Modulators with a Spectrum of Estrogenic and Anti-Estrogenic Activities
Publication date: Available online 26 November 2015 Source:Steroids Author(s): Nittaya Boonmuen, Ping Gong, Zulfiqar Ali, Amar G. Chittiboyina, Ikhlas Khan, Daniel R. Doerge, William G. Helferich, Kathryn E. Carlson, Teresa Martin, Pawinee Piyachaturawat, John A. Katzenellenbogen, Benita S. Katzenellenbogen Licorice root extracts are often consumed as botanical dietary supplements by menopausal women as a natural alternative to pharmaceutical hormone replacement therapy. In addition to their components liquiritigenin (Liq) and isoliquiritigenin (Iso-Liq), known to have estrogenic activity, licorice root extra...
Source: Steroids - November 27, 2015 Category: Drugs & Pharmacology Source Type: research

Tanshinone IIA Prevents Leu27IGF-II-induced Cardiomyocyte Hypertrophy Mediated by Estrogen Receptor and Subsequent Akt Activation.
This study investigates the role of ER signaling in mediating the protective effects of tanshinone IIA on IGF-IIR-induced myocardial hypertrophy. Leu27IGF-II (IGF-II analog) was shown in this study to specifically activate IGF-IIR expression and ICI 182,780 (ICI), an ER antagonist used to investigate tanshinone IIA estrogenic activity. We demonstrated that tanshinone IIA significantly enhanced Akt phosphorylation through ER activation to inhibit Leu27IGF-II-induced calcineurin expression and subsequent NFATc3 nuclear translocation to suppress myocardial hypertrophy. Tanshinone IIA reduced the cell size and suppressed ANP a...
Source: The American Journal of Chinese Medicine - November 30, 2015 Category: Complementary Medicine Authors: Weng YS, Wang HF, Pai PY, Jong GP, Lai CH, Chung LC, Hsieh DJ, HsuanDay C, Kuo WW, Huang CY Tags: Am J Chin Med Source Type: research

Abstract A84: Regulation of 6-phosphofructo-2-kinase (PFKFB3) by estradiol and implications for the treatment of ER+ metastatic breast cancer
Estradiol (E2) administered to estrogen receptor positive (ER+) breast cancer patients stimulates glucose uptake by tumors. This E2-induced metabolic flare is predictive of the clinical effectiveness of anti-estrogens and downstream metabolic regulators of E2 are expected to have utility as targets for the development of anti-breast cancer agents. While the stimulation of glucose metabolism by E2 has been demonstrated, relatively little is known about the precise downstream effectors required for E2 to stimulate glucose metabolism in breast cancer. The family of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFB1...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Clem, B., Tapolsky, G., Chesney, J. Tags: Therapeutic Targets From Cancer: Poster Presentations - Proffered Abstracts Source Type: research