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Effects of Leuzea carthamoides (maral root) in MCF-7 cells

ABSTRACT: Products derived from roots of Leuzea carthamoides DC. (maral root) are being promoted as anti-aging and adaptogenic. The phytoecdysteroids are considered as active principles with numerous beneficial effects, but little is known about the pharmacological properties of Leuzea extracts. We, therefore, investigated the effects of a lipophilic Leuzea root extract on ER+ breast cancer MCF-7 cells at transcriptional level in comparison to 17beta-estradiol and the ER antagonist tamoxifen. With the extract 241 genes were regulated more than 1.5 fold. We observed gene regulation in an anti-proliferative and pro-apoptotic manner. Additionally, expression of several enzymes with oxidoreductase activity was induced including a very strong increase of the phase I enzyme CYP1A1, a possible link to the AhR pathway, which might explain other expression results, e.g. the correlated regulation of about 20 genes by Leuzea compared to 17beta-estradiol. Keywords: treatment with Leuzea carthamoides

ORGANISM(S): Homo sapiens

PROVIDER: GSE6803 | GEO | 2008/09/17

SECONDARY ACCESSION(S): PRJNA99203

REPOSITORIES: GEO

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Transcription profiling of human MCF-7 cell line treated with Leuzea carthamoides (maral root)

Project description:Products derived from roots of Leuzea carthamoides DC. (maral root) are being promoted as anti-aging and adaptogenic. The phytoecdysteroids are considered as active principles with numerous beneficial effects, but little is known about the pharmacological properties of Leuzea extracts. We, therefore, investigated the effects of a lipophilic Leuzea root extract on ER+ breast cancer MCF-7 cells at transcriptional level in comparison to 17beta-estradiol and the ER antagonist tamoxifen. With the extract 241 genes were regulated more than 1.5 fold. We observed gene regulation in an anti-proliferative and pro-apoptotic manner. Additionally, expression of several enzymes with oxidoreductase activity was induced including a very strong increase of the phase I enzyme CYP1A1, a possible link to the AhR pathway, which might explain other expression results, e.g. the correlated regulation of about 20 genes by Leuzea compared to 17beta-estradiol. Experiment Overall Design: MCF-7 cells were treated for 24 h with a lipophilic (dichloromethane) Leuzea root extract, 17beta-estradiol, tamoxifen and the solvent control (0,1% DMSO) in duplicate

2008-10-25 | E-GEOD-6803 | biostudies-arrayexpress

Transcription profiling of human MCF7 cell response toCimicfuga racemosa (black cohosh)

Project description:Extracts from the rhizome of Cimicifuga racemosa (black cohosh) are increasingly popular as herbal alternative to hormone replacement therapy (HRT) for the alleviation of postmenopausal disorders. However, the molecular mode of action and the active principles are presently not clear. Previously published data have been largely contradictory. We, therefore, investigated the effects of a lipophilic Cimicifuga rhizome extract on the ER+ breast cancer MCF-7 cells at transcriptional level in comparision to 17beta-estradiol and the ER antagonist tamoxifen. With the extract 431 genes were regulated more than 1.5 fold. The overall expression pattern differed from those of 17Î²-estradiol or the estrogen receptor antagonist tamoxifen. We observed an enrichment of genes in an anti-proliferative and apoptosis-sensitizing manner, together with an increase of mRNAs coding for gene products involved in several stress response pathways. Regulated genes of these functional groups were highly overrepresented among all regulated genes. Various transcripts coding for oxidoreductases were induced, as for example the cytochrome P450 family members 1A1 and 1B1. In addition, some transcripts associated with antitumor but also tumor-promoting activity were regulated. Experiment Overall Design: MCF-7 cells were treated for 24 h with a lipophilic (dichloromethane) Cimicifuga rhizome extract, 17beta-estradiol, tamoxifen and the solvent control (DMSO 0,1%) in duplicate

2008-06-15 | E-GEOD-6800 | biostudies-arrayexpress

Effects of Cimicfuga racemosa (black cohosh) in MCF-7 cells

Project description:Extracts from the rhizome of Cimicifuga racemosa (black cohosh) are increasingly popular as herbal alternative to hormone replacement therapy (HRT) for the alleviation of postmenopausal disorders. However, the molecular mode of action and the active principles are presently not clear. Previously published data have been largely contradictory. We, therefore, investigated the effects of a lipophilic Cimicifuga rhizome extract on the ER+ breast cancer MCF-7 cells at transcriptional level in comparision to 17beta-estradiol and the ER antagonist tamoxifen. With the extract 431 genes were regulated more than 1.5 fold. The overall expression pattern differed from those of 17β-estradiol or the estrogen receptor antagonist tamoxifen. We observed an enrichment of genes in an anti-proliferative and apoptosis-sensitizing manner, together with an increase of mRNAs coding for gene products involved in several stress response pathways. Regulated genes of these functional groups were highly overrepresented among all regulated genes. Various transcripts coding for oxidoreductases were induced, as for example the cytochrome P450 family members 1A1 and 1B1. In addition, some transcripts associated with antitumor but also tumor-promoting activity were regulated. Keywords: treatment with black cohosh

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Tamoxifen treatment of MCF-7 breast cancer cells

Project description:Tamoxifen is an anti-estrogen drug used in the treatment of Estrogen Receptor (ER) positive breast cancer. Effects and side effects of tamoxifen is the sum of tamoxifen and all its metabolites. Using concentrations that mimic the clinical situation we examined effects of 4OHtam, 4OHNDtam and NDtam on global gene expression in 17beta-estradiol (E2) treated MCF-7 cells.

2014-10-24 | E-MTAB-2729 | biostudies-arrayexpress

Expression Profiling of Inflammatory Breast Cancer Cells Treated with the Novel Histone Deacetylase Inhibitor, CG-1521

Project description:Studies of gene expression profiles using the whole genome wide microarray analysis in SUM149PT cells (ER-, p53mut) and SUM190PT cells (ER-, p53mut) when treated with 5 or 7.5 uM CG-1521 alone and in combination with 10 nM 17beta-estradiol. Comparisons between each treatment group provides evidence for the dysregulation of genes associated with the spindle assembly checkpoint. Three independent experiments were carried out in SUM149PT and SUM190PT cells, which were treated with vehicle (ethanol/DMSO), 10nM 17beta-estradiol, 5 or 7.5 uM CG-1521, and the combination of 17 beta-estradiol and CG-1521. Total RNA was extracted from cell lysates using QIAGEN RNeasy mini kit after 48h of treatment.

2011-04-12 | E-GEOD-28542 | biostudies-arrayexpress

Genome-wide analysis of ERalpha binding sites in U2OS-ERalpha cells

Project description:ChIP followed by deep sequencing was performed with antibodies to ERalpha in U2OS-ERalpha cells treated with 17beta-estradiol.

2011-05-03 | GSE28918 | GEO

Genome-wide copy number profiling of MCF-7 and fulvestrant-resistant MCF-7/FR cells by SNP microarray.

Project description:Estrogens have been shown to elicit anti-cancer effects against estrogen receptor alpha (ER)-positive breast cancer. We sought to determine the underlying mechanism of therapeutic response. Response to 17b-estradiol was assessed in ER+ breast cancer models with resistance to estrogen deprivation: WHIM16 patient-derived xenografts, C7-2-HI and C4-HI murine mammary adenocarcinomas, and long-term estrogen-deprived MCF-7 cells. As another means to reactivate ER, the anti-estrogen fulvestrant was withdrawn from fulvestrant-resistant MCF-7 cells. Transcriptional, growth, apoptosis, and molecular alterations in response to ER reactivation were measured. 17b-estradiol treatment and fulvestrant withdrawal induced transcriptional activation of ER, and cells adapted to estrogen deprivation or fulvestrant were hypersensitive to 17b-estradiol. ER transcriptional response was followed by an unfolded protein response and apoptosis. Such apoptosis was dependent upon the unfolded protein response, p53, and JNK signaling. Anti-cancer effects were most evident in models exhibiting genomic amplification of the gene encoding ER (ESR1), suggesting that engagement of ER at high levels is cytotoxic. These data indicate that long-term adaptation to estrogen deprivation or ER inhibition alters sensitivity to ER reactivation. In such adapted cells, 17b-estradiol treatment and anti-estrogen withdrawal hyperactivate ER, which drives an unfolded protein response activation and subsequent growth inhibition and apoptosis. 17b-estradiol treatment should be considered as an alternative therapy for anti-estrogen-resistant disease, particularly in patients with tumors harboring ESR1 amplification or overexpression. Furthermore, therapeutic strategies that enhance an unfolded protein response may enhance the therapeutic effects of ER reactivation.

2019-08-19 | GSE121631 | GEO

Fulvestrant withdrawal from fulvestrant-resistant MCF-7/FR cells

2019-08-19 | GSE121379 | GEO

Cell-type specific analysis of physiological action of estrogen in mouse oviducts

Project description:The goal of this study is to determine the oviduct responds to 17beta-estradiol (E2) in an in vivo environment using mouse models

2021-01-06 | GSE164291 | GEO

Estrogen's and progesterone's impact on gene expression in the mouse lacrimal and meibomoan gland.

Project description:PURPOSE: The hypothesis tested in the study was that the effect of estrogen and progesterone on the lacrimal gland is mediated through specific receptors and that hormonal effects involve the regulation of gene expression and protein synthesis. METHODS: Lacrimal glands were collected from young adult, ovariectomized mice, that were treated with 17beta-estradiol, progesterone, 17beta-estradiol plus progesterone or vehicle for 2 weeks. Glands were pooled according to treatment, processed for the isolation of RNA, and evaluated for differentially expressed mRNAs by using gene microarrays. Bioarray data were analyzed with sophisticated bioinformatics and statistical programs. The expression of selected genes was verified by using gene chips and quantitative real-time PCR methods. RESULTS: The results demonstrate that 17beta-estradiol, progesterone, or both hormones together significantly influences the expression of hundreds of genes in the mouse lacrimal gland. Sex steroid treatment led to numerous alterations in gene activities related to transcriptional control, cell growth and/or maintenance, cell communication, signal transduction, enzyme catalysis, immune expression, and the binding and metabolism of nucleic acids and proteins. A number of the 17beta-estradiol, progesterone or 17beta-estradiol plus progesterone effects on gene expression were similar, but most were unique to each treatment. Of particular interest was the finding that these hormones seem to contribute little to the known sex-related differences in gene expression of the lacrimal gland. CONCLUSIONS: These results support the hypothesis that estrogen's and progesterone's action on the lacrimal gland involves the regulation of numerous genes. However, these hormone effects do not appear to represent a major factor underlying the sexual dimorphism of gene expression in lacrimal tissue. Keywords: Placeco vs Hormone Treatment

2008-01-01 | GSE5783 | GEO

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