Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA108635 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the oxidant sensitivity of E/ER regulated gene expression, E/ER regulated genes are identified using E deprivation or; ER-alpha siRNA knockdown; and oxidative stress responsive is determined by 8hr exposure to diamide, hydrogen peroxide and menadione Experiment Overall Design: MCF7 cells were treated under various conditions to identifiy oxidative stress responsive E/ER regulated genes. Association of these genes with respect to tumor phenotypes are assessed
2008-11-13 | E-GEOD-10061 | biostudies-arrayexpress
Project description:To investigate the oxidant sensitivity of E/ER regulated gene expression, E/ER regulated genes are identified using E deprivation or ER-alpha siRNA knockdown; and oxidative stress responsive is determined by 8hr exposure to diamide, hydrogen peroxide and menadione Keywords: biomarker identification
2008-11-03 | GSE10061 | GEO
Project description:MCF-7 TET Off cells (MCF-7 wt) were used to produce stable clones expressing ER-beta tagged with TAP-tag respectively at the C-term and at the N-term (C-TAP-ER-beta and N-TAP-ER-beta) or expressing ER-alpha tagged (C-TAP-ER-alpha) as previously described.Cells were cultured in standard growth conditions, then were lysed and RNA was extracted using TRIzol method.Total RNA were fluorescently labelled, amplified and hybridized in triplicate (MCF7-TAP and C-TAP-ER-alpha) and in duplicate (C-TAP-ER-beta_A, C-TAP-ER-beta_B, N-TAP-ER-beta) for 18 hours on Illumina v2 MicroRNA Expression BeadChips and after scanning, analysis was performed with GenomeStudio v.2010.1 software, for quality control and miRNA expression analysis.
2011-10-11 | E-TABM-1053 | biostudies-arrayexpress
Project description:SEPN1 is a type II protein of the endoplasmic reticulum (ER) whose loss of function gives rise to a collection of debilitating autosomal recessive myopathies gathered under the umbrella term of SEPN1-related myopathy (RM). At the moment, SEPN1-RM lacks an effective pharmacological treatment; thus, the medical management of the disease is only supportive. The potentially fatal diaphragmatic weakness leading to respiratory insufficiency in patients still ambulant is the main reason for medical concerns. Thus, studies on SEPN1-RM pathogenesis are necessary to implement a targeted pharmacological therapy aimed at relieving the general muscle weakness and the more worrisome diaphragmatic dysfunction. Here, we show a physical and functional interaction between SEPN1 and the ER stress mediator ERO1 alpha (henceforth, ERO1). Both SEPN1 and ERO1 are involved in the redox regulation of proteins into the ER, although in an opposite way SEPN1 imposes a less oxidant ER poise while ERO1 a more oxidant one, conceivable with a reductase function of SEPN1 and an oxidase one of ERO1. Furthermore, both are mainly localized in a region of the ER in close contact with mitochondria termed mitochondria-associated membranes (MAMs) and their loss impacts oppositely on the short-range MAMs, thereby impinging ER-mitochondria Ca2+ dynamics, OXPHOS, and bioenergetics. We find that ERO1 depletion restores the impaired short-range MAMs due to SEPN1 loss together with mitochondrial ATP. ERO1 knockout in a mouse background of SEPN1 loss blunts ER stress and the consequent Unfolded Protein Response (UPR) while it rescues the diaphragmatic weakness by improving ER/mitochondria contacts, calcium dynamics, and OXPHOS. Importantly, treatments of SEPN1 knock out mice with the chemical chaperone tauroursodeoxycholic acid (TUDCA) mimic the results of ERO1 loss improving calcium dynamics, OXPHOS, ER/mitochondria contacts, thereby rescuing diaphragmatic weakness as well. In addition, TUDCA-treated SEPN1-RM patients-derived myoblasts show a dynamic dose-dependent increase in ATP levels under ER stress conditions suggesting improved mitochondrial function. Thus, our findings point to the ERO1 axis in the pathogenesis of SEPN1-RM thereby impinging on MAMs and mitochondria bioenergetics and recall for the efficacy of a pharmacology therapy with ad hoc ER stress/ERO1 inhibitors for SEPN1-RM.
2024-02-14 | E-MTAB-12460 | biostudies-arrayexpress
Project description:We were interested in determining what genes might be controlled by TFAP2C and/or TFAP2A, either directly or indirectly through regulation of ER-alpha and potentially other signaling pathways. We performed an microarray analysis in MCF7 cells with elimination of either TFAP2C or TFAP2A. The patterns of gene expression with alteration of TFAP2 activity were compared to changes in expression induced by estrogen exposure. Knock-down of TFAP2C in the presence of estrogen altered the pattern of several known ERalpha-regulated genes and a number of genes outside the estrogen-regulated pathways. Keywords: Various siRNA treatments
2007-12-17 | GSE8640 | GEO
Project description:We were interested in determining what genes might be controlled by TFAP2C and/or TFAP2A, either directly or indirectly through regulation of ER-alpha and potentially other signaling pathways. We performed an microarray analysis in MCF7 cells with elimination of either TFAP2C or TFAP2A. The patterns of gene expression with alteration of TFAP2 activity were compared to changes in expression induced by estrogen exposure. Knock-down of TFAP2C in the presence of estrogen altered the pattern of several known ERalpha-regulated genes and a number of genes outside the estrogen-regulated pathways. Experiment Overall Design: 6 samples were analyzed. Experiment Overall Design: 1. MCF7 cells treated with TFAP2C siRNA, without the presence of estrogen. Experiment Overall Design: 2.MCF7 cells treated with TFAP2C siRNA, with the presence of estrogen. Experiment Overall Design: 3.MCF7 cells treated with TFAP2A siRNA, without the presence of estrogen. Experiment Overall Design: 4.MCF7 cells treated with TFAP2A siRNA, with the presence of estrogen. Experiment Overall Design: 5.MCF7 cells with no siRNA treatment, without the presence of estrogen. Experiment Overall Design: 6.MCF7 cells with no siRNA treatment, with the presence of estrogen.
2008-06-16 | E-GEOD-8640 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE22533: Breast cancer cells resistant to hormone deprivation maintain an estrogen receptor alpha-dependent, E2F-directed transcriptional program GSE27300: Estrogen-independent genomic ER binding analysis Refer to individual Series
2012-05-14 | E-GEOD-37955 | biostudies-arrayexpress
Project description:To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). Another group received ED plus the antiestrogen fulvestrant (MCF7 wt only). Tumors with acquired or de novo resistance to these endocrine therapies were profiled for mRNA expression using Affymetrix Genechip arrays. Keywords: multiple group comparison
2008-12-01 | GSE8139 | GEO
Project description:To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). Another group received ED plus the antiestrogen fulvestrant (MCF7 wt only). Tumors with acquired or de novo resistance to these endocrine therapies were profiled for mRNA expression using Affymetrix Genechip arrays. Keywords: multiple group comparison
2008-12-01 | GSE8140 | GEO
Project description:Endocrine therapy is the main therapeutic option for patients with estrogen receptor alpha positive (ER+) breast cancer. Nevertheless, most of them become estrogen-independent and relapse after the treatment. Ret is a tyrosine kinase receptor that shows elevated expression levels in ER+ human breast tumors. In this study, we demonstrate that activation of the Ret receptor promotes proliferation as well as cell migration irrespective of endocrine therapy. Microarray data show that Ret activation involves changes in the expression of inflammatory- and motility-related genes. In vivo treatment with a Ret pathway inhibitor in a ER+/Ret+ mouse mammary cancer model, reduces tumor growth and lung metastasis even after endocrine therapy. Additionally, we show a connection between Ret and inflammatory pathways. The pro-inflamatory cytokine IL6 lies at the core of this regulation, which involves a positive feedback loop with IL6 and the Ret pathway reciprocally stimulating each other to further leading metastasis risk. Our findings provide insight into endocrine resistance mechanism and point at the Ret pathway as a potential target for future therapies. In order to model letrozole-sensitive breast cancer we use aromatase expressing MCF7 cells (MCF7/Aro). Six-day treatment (6 days) of cultures with letrozole (L) or fulvestrant (F) reversed the proliferative effects of the exposure to the estrogen (E2) precursor androstenedione (D4A). The addition of only EtOH (E) to the cells was used as control condition of deprivation. Treatment with the Ret ligand GDNF (G) partially rescues the inhibition of estrogen-dependent proliferation in these cells. To go deeper insight into the pathways involved, we decided to perform a microarray following different treatments (1-8: E, E+G, D, D+G, L, L+G, F, F+G) used in proliferation assays. Three biological replicates (rep 1-3) were used to the array.
2013-09-25 | E-GEOD-41405 | biostudies-arrayexpress