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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE6800 | GEO | 2007/09/28

SECONDARY ACCESSION(S): PRJNA99197

REPOSITORIES: GEO

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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

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

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

2008-09-17 | GSE6803 | GEO

Both Tamoxifen and Estradiol accelerate endothelial healing by targeting different sub-functions of ERa and distinct cell types in the arterial wall

Project description:Rationale: Tamoxifen prevents the recurrence of breast cancer and is also beneficial against bone demineralization and arterial diseases, as it acts as an Estrogen Receptor (ER) α antagonist in ER-positive breast cancers, whereas it mimics the protective action of 17β-estradiol (E2) in other tissues such as arteries. However, the mechanisms of these tissue-specific actions remain unclear. Objective: Here we tested whether tamoxifen is able to accelerate endothelial healing and analyzed the underlying mechanisms. Methods and Results: Using three complementary mouse models of carotid artery injury, we demonstrated that both tamoxifen and estradiol accelerated endothelial healing, but only tamoxifen required the presence of the underlying medial smooth muscle cells. Chronic treatment with E2 and tamoxifen elicited differential gene expression profiles in the carotid artery. The use of transgenic models mouse targeting either whole ERα in a cell-specific manner or ERα subfunctions (membrane/extra-nuclear versus genomic/transcriptional) demonstrated that E2-induced acceleration of endothelial healing is mediated by membrane ERα in endothelial cells, while the effect of tamoxifen is mediated by the nuclear actions of ERα in smooth muscle cells. Conclusion: Whereas tamoxifen acts as an anti-estrogen and ERα antagonist in breast cancer, but also on the membrane ERα of endothelial cells, it accelerates endothelial healing through activation of nuclear ERα in smooth muscle cells, inviting to revisit the mechanisms of action of selective modulation of ERα.

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Gene Expression Preferentially Regulated by Tamoxifen in Breast Cancer Cells

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2006-07-28 | GSE4025 | GEO

Transcription profiling of human MCF-7 breast cancer cell line transfected with adenovirus expressing Erbeta treated with estrogen or tamoxifen reveals tamoxifen can selectively regulate a unique set of >60 genes, which are minimally regulated by estradiol (E2) or raloxifene.

Project description:The beneficial effect of the selective estrogen receptor (ER) modulator tamoxifen in the treatment and prevention of breast cancer is assumed to be through its ability to antagonize the stimulatory actions of estrogen, although tamoxifen can also have some estrogen-like agonist effects. Here, we report that, in addition to these mixed agonist/antagonist actions, tamoxifen can also selectively regulate a unique set of >60 genes, which are minimally regulated by estradiol (E2) or raloxifene in ERalpha-positive MCF-7 human breast cancer cells. This gene regulation by tamoxifen is mediated by ERalpha and reversed by E2 or ICI 182,780. Introduction of ERbeta into MCF-7 cells reverses tamoxifen action on approximately 75% of these genes. To examine whether these genes might serve as markers of tamoxifen sensitivity and/or the development of resistance, their expression level was examined in breast cancers of women who had received adjuvant therapy with tamoxifen. High expression of two of the tamoxifen-stimulated genes, YWHAZ/14-3-3z and LOC441453, was found to correlate significantly with disease recurrence following tamoxifen treatment in women with ER-positive cancers and hence seem to be markers of a poor prognosis. Our data indicate a new dimension in tamoxifen action, involving gene expression regulation that is tamoxifen preferential, and identify genes that might serve as markers of tumor responsiveness or resistance to tamoxifen therapy. This may have a potential effect on the choice of tamoxifen versus aromatase inhibitors as adjuvant endocrine therapy.

2007-10-02 | E-GEOD-4025 | biostudies-arrayexpress

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2011-07-13 | E-GEOD-22941 | biostudies-arrayexpress

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Project description:Treatment with the breast cancer drug tamoxifen confers a risk of developing uterine tumors or other endometrial pathologies. Tamoxifen is a selective estrogen receptor modulator, which demonstrates tissue-specific activity although the mechanisms remain poorly understood. Both estradiol and tamoxifen act as estrogen agonists on the human uterus, and therefore have the potential to promote carcinogenicity. Estradiol and tamoxifen elicit cellular responses via the estrogen receptors (ER), which are involved in multiple signalling pathways. The effects at the molecular level are further influenced by the differential recruitment of co-factors and the presence of specific promoter motifs in target genes. In this study, ER positive (+) Ishikawa cells are used as a model to investigate the overall effect of treatment with either 17b-estradiol or 4-hydroxytamoxifen on the gene expression profiles. Keywords: Comparison of estradiol and tamoxifen on Ishikawa human uterine cells after 24h or 48h

2006-02-01 | GSE3762 | GEO

Effect of estradiol and tamoxifen on SPEN-expressing and control T47D cells.

Project description:Split Ends (SPEN) is a transcriptional coregulator that have formerly identified as a tumour suppressor gene in ER-positive breast cancers. However, ER-positive breast cancers are diagnosed at similar frequencies in pre- and post-menopausal women who show significantly different circulating hormone levels. This therefore raises the possibility that SPEN functions under hormone-depleted settings may contrast with its roles in the presence of hormones. We therefore attempted to explore the cellular functions regulated by SPEN under hormone-depleted settings using a previously established model with T47D cells stably transfected with a control vector (non-target) or SPEN-expressing vector. In particular, we attempted to investigate the hormone-independent transcriptional program regulated by SPEN in breast cancer. To achieve this, we have treated previously established T47D cells stably transfected with a control vector (non-target) or SPEN-expressing vector. These cells were allowed to grow in hormone-depleted conditions for 4 days. To minimize external biases introduced by hormone depletion or any transcriptional contribution from the estrogen receptor (ER), we also performed gene expression profiling analyses on the same cells but stimulated with an estrogen receptor (ER) agonist (Estradiol) or antagonist (Tamoxifen).

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