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Gene expression profiles elicited by estradiol and endoxifen in MCF7 parental and ER-beta expressing breast cancer cells

ABSTRACT: We have previously demonstrated that endoxifen is the most important tamoxifen metabolite responsible for eliciting the anti-estrogenic effects of this drug in breast cancer cells expressing estrogen receptor-alpha. However, the relevance of estrogen receptor-beta in mediating endoxifen action has yet to be explored. Therefore, the goals of this study were to determine the differences in the global gene expression profiles elicited by estradiol treatment and endoxifen between parental MCF7 breast cancer cells (expressing estrogen receptor alpha only) and MCF7 cells stably expressing estrogen receptor beta.

ORGANISM(S): Homo sapiens

PROVIDER: GSE27375 | GEO | 2011/02/18

SECONDARY ACCESSION(S): PRJNA137281

REPOSITORIES: GEO

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Gene expression profiles elicited by estradiol and endoxifen in MCF7 parental and ER-beta expressing breast cancer cells

Project description:We have previously demonstrated that endoxifen is the most important tamoxifen metabolite responsible for eliciting the anti-estrogenic effects of this drug in breast cancer cells expressing estrogen receptor-alpha. However, the relevance of estrogen receptor-beta in mediating endoxifen action has yet to be explored. Therefore, the goals of this study were to determine the differences in the global gene expression profiles elicited by estradiol treatment and endoxifen between parental MCF7 breast cancer cells (expressing estrogen receptor alpha only) and MCF7 cells stably expressing estrogen receptor beta. Total RNA was isolated from parental or estrogen-receptor beta expressing MCF7 cells following 24 hour treatments with either ethanol vehicle, 1nM 17-beta-estradiol or 1nM estradiol plus 40nM endoxifen. All studies were conducted in biological replicates of 2.

2011-02-18 | E-GEOD-27375 | biostudies-arrayexpress

Gene expression profiles of MCF7 breast cancer cells following estrogen and anti-estrogen treatment.

Project description:We have previously demonstrated that endoxifen is the most important tamoxifen metabolite responsible for eliciting the anti-estrogenic effects of this drug in breast cancer cells expressing estrogen receptor-alpha. The goals of this study were to compare the gene expression profiles elicited by endoxifen to that of other anti-estrogens in MCF7 cells. We also examined the gene expression profiles elicited by various endoxifen concentrations in the presence of tamoxifen and its other primary metabolites in order to better understand the molecular contributions of endoxifen to the effects of tamoxifen. Total RNA was isolated from parental MCF7 cells following 24 hour treatments with various individual or combined ligands. All studies were conducted in replicates of 3.

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Gene expression profiles of MCF7 breast cancer cells following estrogen and anti-estrogen treatment.

Project description:We have previously demonstrated that endoxifen is the most important tamoxifen metabolite responsible for eliciting the anti-estrogenic effects of this drug in breast cancer cells expressing estrogen receptor-alpha. The goals of this study were to compare the gene expression profiles elicited by endoxifen to that of other anti-estrogens in MCF7 cells. We also examined the gene expression profiles elicited by various endoxifen concentrations in the presence of tamoxifen and its other primary metabolites in order to better understand the molecular contributions of endoxifen to the effects of tamoxifen.

2013-03-01 | GSE43702 | GEO

Endoxifen Downregulates AKT Phosphorylation Through Protein Kinase C Beta 1 in ER+/HER2- Breast Cancer

Project description:In phase I/II clinical trials, Z-endoxifen demonstrated substantial oral bioavailability and promising antitumor activity in endocrine-refractory estrogen-receptor positive breast cancer (ER+ BC) and other solid tumors, with plasma concentrations reportedly as high as 5 ï�M. Therefore, we explored the potential mechanisms of Z-endoxifen antitumor activity that extends beyond ERÎ± inhibition. In estrogen unstimulated aromatase-expressing ER+/human epidermal growth factor 2 receptor negative (HER2-) MCF7AC1 BC cells, Z-endoxifen at 5 ï�M, but not ERï�¡-targeting 0.01 and 0.1 ï�M concentrations inhibited growth and induced apoptosis, suggesting an ERÎ±-independent effect. Utilizing an unbiased mass spectrometry approach, we explored Z-endoxifen effects on other signaling pathways. Z-endoxifen at 5 ÂµM profoundly altered the phosphoproteome with minimal impact on total proteome. Computational analysis revealed Protein kinase C beta (PKCï�¢) and AKT1 as the prevalent upstream kinases for Z-endoxifen-downregulated protein phosphorylations. Notably, in ER+/HER2- BC models, Z-endoxifen at 5 ï�M attenuated AKTSer473 and AKT substrates in vitro in the presence of insulin and PKC agonist PMA and in vivo. Further, Z-endoxifen inhibited PKCï�¢1 kinase activity compared to other PKC isoforms in vitro and bound to PKCÎ²1. While PMA stimulated PKCï�¢1Ser661 phosphorylation correlated with AKTSer473 and AKT substrate phosphorylation, Z-endoxifen at 5 ï�M uniquely blocked these effects and induced PKCÎ²1 protein degradation. siRNA-mediated PKCï�¢1 knockdown attenuated AKTSer473 phosphorylation, suggesting PKCÎ²1-mediated suppression of AKT signaling by Z-endoxifen. Further, Z-endoxifen at 5 ï�M replicates the pan-AKT inhibitor MK-2206 effects on apoptosis. These findings implicate PKCÎ²1 as a novel Z-endoxifen substrate responsible for suppressing AKT signaling and inducing apoptosis in breast cancer.

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Gene expression profile in MCF7 breast cancer cells after siRNA knock down of estrogen receptor alpha (ESR1)

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Transcriptional profile of human breast cancer MCF7 cells and clones thereof expressing human ERβ1 or ERβ2 upon treatment with antiestrogens and retinoids.

Project description:The aim of the experiment was to gain insight into the role of estrogen receptor beta (ERβ) isoforms in the response of breast cancer MCF7 cells to antiestrogens and retinoids. To this end, clones of MCF7 cells constitutively expressing human ERβ1 (MCF7-ERβ1) or ERβ2 (MCF7-ERβ2) were established and used for the determination of the global transcriptional changes induced upon treatment with hydroxytamoxifen (OHT) and all-trans retinoic acid (ATRA). Gene signatures associated with each clone will shed light to the mechanism underlying the ERβ1- and ERβ2-mediated response of MCF7 cells to antiestrogens and retinoids.

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Nuclear Estrogen Receptor alpha (ERα) interactome following estrogen and antiestrogen treatment.

Project description:The Estrogen Receptor alpha (ERα) controls key cellular functions in hormone responsive breast cancer by assembling in large functional multiprotein complexes. ERα ligands are classified as agonists and antagonist, according to the response they elicit, thus the molecular characterization of the of ERα nuclear iteractome composition following estrogen and antiestrogen stimulation whose is needed to understand their effects on estrogen target tissues, in particular breast cancer. To this aim interaction proteomics coupled to mass spectrometry (MS) was applied to map the ERα nuclear interacting partners in MCF7 breast cancer cell nuclei following estrogen and antiestrogen stimuli.

2020-09-02 | PXD018709 | Pride

ER/PR RIME Experiments in MCF7 and T47D cell lines

Project description:Immuno-precipitation followed by MS was performed using the RIME protocol in this study. Estrogen Receptor (ER) and Progestorone Receptor (PR) were targetted using antibodies. The experiments were performed in a quantitative manner using SILAC labelling. Cells grown in complete serum (estrogenic) conditions were compared against an cells in similar complete media, however supplemented with Progesterone (PG) or R5020 for 4 hours. Experiments were performed in MCF7 and T47D cell lines

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