RNAseq analysis of Human endothelial TeloHAEC in response to Estradiol, 4-hydroxytamoxifen and the cotreatment
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE219159 | GEO | 2024/01/03
REPOSITORIES: GEO
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Project description:RNA-seq: Gene expression profiling in MCF-7 cells treated with vehicle (0), estradiol (E2), the Selective ER Modulator 4-hydroxytamoxifen (OHT), or the pure antiestrogen fulvestrant (ICI). ChIP-seq: Genome-wide DNA binding profile of ERα and SUMO2/3 in MCF-7 cells treated with vehicle, E2 or ICI.
2018-01-09 | GSE108883 | GEO
Project description:MCF-7:PF is a a new in vitro model of antihormone resistant breast cancer that exhibits the characteristics of acquired tamoxifen resistance in vivo. It is well known that estrogen (E2) induces apoptosis in long-term estrogen-deprived breast cancer cells, MCF-7:5C (PubMed References PMID:15862958, PMID:16333030). MCF-7:PF was derived from MCF-7:5C through inhibition of c-Src, which blocks E2-induced apoptosis, coverts E2 responses from apoptosis to proliferation. MCF-7:PF cell growth is stimulated by E2 and SERMS in an ERα-dependent manner. Abstract: A c-Src inhibitor blocks estrogen (E2)-induced stress and converts E2 responses from inducing apoptosis to stimulating growth in E2-deprived breast cancer cells. A resulting cell line, MCF-7:PF, is reprogrammed with features of functional estrogen receptor (ER) and over-expression of insulin-like growth factor-1 receptor beta (IGF-1Rβ). We addressed the question of whether the antiestrogenic selective ER modulator 4-hydroxytamoxifen (4-OHT) could target ER to prevent E2-stimulated growth in MCF-7:PF cells. Unexpectedly, 4-OHT stimulated cell growth in an ER-dependent manner. However, unlike E2, 4-OHT suppressed classic ER-target genes as does the pure antiestrogen ICI 182,780, even during growth stimulation. Chromatin-immunoprecipitation (ChIP) assay indicated that 4-OHT did not recruit ER or nuclear receptor coactivator 3 (SRC3) to the promoter of ER-target gene, pS2. Paradoxically, 4-OHT reduced total IGF-1Rβ but increased phosphorylation of IGF-1Rβ, which was responsible for the activation of the phosphatidylinositol-3 kinases (PI3K)/Akt signaling pathway. Mechanistic studies revealed that 4-OHT rapidly activated the non-genomic pathway through ER, but other membrane-associated proteins such as IGF-1Rβ and c-Src participated. Furthermore, 4-OHT was more potent than E2 to up-regulate membrane remodeling molecules and activated focal adhesion molecules to promote cell growth. Therefore, disruption of membrane-associated signaling completely abolished 4-OHT-stimulated cell growth, but not E2-stimulated cell growth. Despite continued suppression of classic ER-target genes, 4-OHT activated the complex network of cytoskeleton remodeling and extracellular matrix-related signaling which facilitated 4-OHT-stimulated cell growth. This study is the first to recapitulate a cellular model in vitro of acquired tamoxifen (TAM) resistance developed in athymic mice in vivo.
2014-07-14 | GSE54171 | GEO
Project description:Gene expression analyses were carried out to identify genes regulated by 17-beta estradiol (E2) and Hydroxytamoxifen (OHT) through GPR30 in SKBR3 cells, a breast cancer cell-line which expresses GPR30 but lacks Estrogen Receptor alpha or beta. Keywords: Gene expression analysis, Non-genomic signaling in breast cancer cells.
2009-02-19 | GSE11567 | GEO
Project description:Transcriptional profiling of zebrafish (Danio rerio) livers comparing control untreated fish with fish treated with estrogen [17β-estradiol (E2)] for different time points (4, 12, 24, 48 hours).
2013-06-28 | GSE45562 | GEO
Project description:Gene expression analyses were carried out to identify genes regulated by 17-beta estradiol (E2) and Hydroxytamoxifen (OHT) through GPR30 in SKBR3 cells, a breast cancer cell-line which expresses GPR30 but lacks Estrogen Receptor alpha or beta. Keywords: Gene expression analysis, Non-genomic signaling in breast cancer cells. Gene expression analyses were done for control transfected SKBR3 cells: 1) Uninduced, 2) Induced with 10 microM OHT, 3) Induced with 1 microM E2 and 4) GPR30-antisense transfected cells induced with 10 microM OHT. The cells were induced for 1h and all the samples were collected in triplicates.
2009-02-19 | E-GEOD-11567 | biostudies-arrayexpress
Project description:Transcriptional profiling of mussel (Mytilus galloprovincialis) digestive gland tissue comparing control tissue with tissue obtained from animals exposed to sublethal amounts of Chlorpyrifos, animals injected into the posterior adductor muscle with 25 pico-moles 17β-estradiol (E2) and animals pre-exposed for three days to the pesticide and further injected with E2. Background: Many pesticides have been shown to act as endocrine disrupters. Although the potencies of currently used pesticides as hormone agonists/antagonists in vitro are low compared with those of natural ligands, their ability to act via multiple mechanisms might enhance the biological effect. The organophosphate Chlorpyrifos (CHP) has been shown to be weakly estrogenic and cause adverse neurodevelopmental effects in mammals. However, no information is available on the possible endocrine effects of CHP in aquatic organisms. In the digestive gland of the bivalve Mytilus galloprovincialis, a target tissue for the action of both estrogens and pesticides, the possible effects of CHP on the responses to the natural estrogen 17β-estradiol (E2) were investigated. Methodology/Principal findings: Mussels were exposed to CHP (4.5 mg/l, 72 hrs) and subsequently injected with E2 (6.75 ng/g dw). Responses were evaluated in CHP, E2 and CHP/E2 treatment groups at 24 h p.i. by a biomarker/transcriptomic approach. CHP and E2 induced additive, synergistic, and antagonistic effects on lysosomal biomarkers (lysosomal membrane stability, lysosome/cytoplasm volume ratio, lipofuscin and neutral lipid accumulation). Additive and synergistic effects were also observed on the expression of estrogen-responsive genes (GSTπ, catalase and 5-HTR) evaluated by RT-Q-PCR. The use of a 1.7K cDNA Mytilus microarray showed that CHP, E2 and CHP/E2, induced 81, 44, and 65 Differentially Expressed Genes (DEGs), respectively. 24 genes were exclusively shared between CHP and CHP/E2, only 2 genes between E2 and CHP/E2. Moreover, 36 genes were uniquely modulated by CHP/E2. Gene ontology annotation was used to elucidate the putative mechanisms involved in the responses elicited by different treatments. Conclusions: The results show complex interactions between CHP and E2 in mussel digestive gland, indicating that the combination of certain pesticides and hormones may give rise to unexpected effects at the molecular/cellular level. Overall, these data demonstrate that CHP can interfere with the mussel responses to natural estrogens. Four-condition experiment. Dual color competitive hybridizations. Common reference (vehicle treated animals, 0.02% Dimethyl sulfoxide, injected with 50 μl of a solution of Artificial Sea Water containing 0.05 % ethanol); Pools of six animals. Biological replicates: 4 controls, 4 Chlorpyrifos, 4 17β-estradiol, 4 Chlorpyrifos-17β-stradiol. One replicate per array.
2011-12-31 | E-GEOD-26222 | biostudies-arrayexpress
Project description:17β-HSD1 expression modulates T47D transcript profile in in steroid-deprived medium. The enzyme specifically regulates apoptosis and cancer-related genes in T47D cells cultured in steroid-deprived medium. Genes that primarily involved in Cell cycle progression, such as the Cyclin A2 gene, CCNA2, are generally down-regulated whereas most genes involved in apoptosis and cell death, such as the proapoptotic gene XAF1 and FGF12, are on the contrary up-regulated by 17β-HSD1 knockdown, and 21% of the modulated genes belong to this latter functional category. This correborates with its role previously shown in increasing breast cancer cell proliferation (Aka et al, 2010) and indicates that in addition to its direct role as cell proliferation via incresing E2 and decreasing DHT, 17β-HSD1 may also be involved in oncogenesis by favoring its anti-apoptosis pathway in breast cancer cells 17β-HSD1 may also be involved in oncogenesis by favoring anti-apoptosis pathway and/or inhibiting cell survival pathway. We tested the ability of estrogen to induce or repress endogenous genes of T47D by microarray analysis. A total of 131 genes were found to increase or decrease 1.5-fold or higher in response to 17 beta-estradiol (1 nM for 48 h). Besides, the gene regulation occuring in steroid-deprived conditions showed that 17β-HSD1 modulates gene expression in steroid-independent manners. Our study thus demonstrates that 17β-HSD1 modulates the E2-independent transcription of endogenous genes in T47D cells. The E2-dependent transcription as well as the E2-independent transcription are significantly modulated by 17β-HSD1 in breast cancer cells We first report here that breast cancer cell transcript profile is independtly modulated by both 17β-HSD1 and its principale product estradiol.
2016-09-01 | GSE77345 | GEO
Project description:To identify key genes in the early sex development of zebrafish, we generated zebrafish (AB strain) feminized by sex hormone 17β-estradiol (E2, CAS: 50-28-2, 100 ng/L) and masculinized by aromatase inhibitor exemestane (EM, CAS: 107868-30-4, 10 μg/L), and detected their transcriptomes by RNA-seq.
2022-05-11 | GSE126039 | GEO
Project description:Compare the expression pattern of 17b-estradiol responsive genes in parent, OHT-resistant and ICI-resistant breast cancer cells. Keywords: 17b-estradiol responsive genes, OHT resistance, Fulvestrand resistance
2007-09-14 | GSE5840 | GEO
Project description:To uncover genes regulated by mTORC1 and estradiol in uterine Tsc2-null LAM like cells, we performed RNAseq on uteri from 12-week old wild-type (WT) and uterine-specific Tsc2-null (KO) mice that were either untreated (intact), oopherectomized (ovx) or oopherectomized + treated with 17β-estradiol pellets (E2) for 8 weeks. We identified genes that were both estradiol- and TSC2-mediated.
2016-02-26 | GSE78701 | GEO