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Estrogen receptors in breast cancer stem cells

ABSTRACT: Breast cancer stem cells are considered estrogen receptor negative and estrogen insensitive. However, estrogens potentiate growth of the vast majority of breast tumors. In this study, we characterize the expression of estrogen receptors in breast cancer stem cells. We used microarrays to characterize the global gene expression underlying estrogen receptor activation versus inhibition in breast cancer cells from invasive breast cancers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35031 | GEO | 2012/01/12

SECONDARY ACCESSION(S): PRJNA150863

REPOSITORIES: GEO

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Estrogen receptors in breast cancer stem cells

Project description:Breast cancer stem cells are considered estrogen receptor negative and estrogen insensitive. However, estrogens potentiate growth of the vast majority of breast tumors. In this study, we characterize the expression of estrogen receptors in breast cancer stem cells. We used microarrays to characterize the global gene expression underlying estrogen receptor activation versus inhibition in breast cancer cells from invasive breast cancers. Cancer cells from invasive breast carcinomas are treated with D (DPN), T (4OHT) or untreated (vehicle control).

2012-01-12 | E-GEOD-35031 | biostudies-arrayexpress

A Luminal, Steroid Receptor-Positive Breast Cancer Stem Cell that Generates Intratumoral Heterogeneity is Preserved by Progesterone and Depleted by Estradiol

Project description:Most breast cancers are luminal, depending on estrogens for growth. The remainder lack estrogen receptors, are hormone-resistant and basal-like. It is thought that breast cancers arise from self-renewing normal stem cells that have undergone malignant transformation. However currently reported cancer stem cells are hormone insensitive and generate basal, rather than luminal tumors. We now describe true luminal hormone-responsive breast cancer stem cells that express estrogen and progesterone receptors. Their self-renewal capacity is protected by progesterone. Stem cell levels are depleted by estrogens as tumors transition into differentiated and homogeneous luminal states. But, if added to estrogens, progesterone promotes heterogeneity and “rescues” the stem cells. By keeping luminal cancer stem cells “safe”, progesterone, widely used for contraception and hormone replacement, could be harmful to breast cancer survivors or women with occult disease.

2016-01-31 | GSE65407 | GEO

Catechol-O-methyl transferase suppresses cell invasion and interplays with MET signaling in estrogen dependent breast cancer

Project description:Catechol-O-methyl transferase (COMT) is involved in detoxification of catechol estrogens, playing cancer-protective role in cells producing or utilizing estrogen. Moreover, COMT suppressed migration potential of breast cancer cells. To delineate COMT role in metastasis of estrogen receptor dependent BC, we investigated the effect of COMT overexpression on invasion, transcriptome, proteome and interactome of MCF7 cells, a luminal A breast cancer model, stably transduced with lentiviral vector carrying COMT gene (MCF7-COMT). This PRIDE project includes quantitative analysis results for the total proteome LC-DIA-MS/MS experiment evaluating COMT overexpression in MCF7 breast cancer cell line, and results of pulldown analysis of COMT-interacting proteins in MCF7 cells.

2023-01-31 | PXD033833 | Pride

Estrogen-independent genomic ER binding analysis

Project description:Hormone-independent breast cancer cells (MCF-7/LTED and HCC-1428/LTED) were analyzed by ChIP-seq for estrogen receptor a to identify ER-DNA binding events that occur in the absence of estrogens.

2012-02-10 | GSE27300 | GEO

Estradiol Treated Breast Cancer Cells Expressing Mutant Estrogen Receptors

Project description:MDA-MB-231 Breast Cancer Cells expressing either wild-type estrogen receptor or the mutant estrogen recepor L540Q were treated with estradiol for 1 or 2 hours Keywords: time-course

2004-03-24 | GSE1045 | GEO

Transcription profiling of estradiol-treated human breast cancer cells expressing mutant estrogen receptors

Project description:MDA-MB-231 Breast Cancer Cells expressing either wild-type estrogen receptor or the mutant estrogen recepor L540Q were treated with estradiol for 1 or 2 hours

2007-07-19 | E-GEOD-1045 | biostudies-arrayexpress

Phosphatome profiling of estrogen receptor negative breast cancer

Project description:Purpose: To characterize the expression of phosphatases in estrogen receptor negative breast cancer Little is known about the role of phosphatases in the major estrogen receptor negative breast cancer phenotypes (i.e. those overexpressing ERBB2 and the triple negative). We carried out microarray phosphatome profiling in 41 estrogen receptor negative (ER-) breast cancer patients (as determined by immunohistochemistry (IHC)) containing both ERBB2+ and ERBB2- in order to characterize the differences between these groups by Statistical Analysis of Microarrays (SAM). Our findings point to the importance of the MAPK and PI3K pathways in ER- BCs as some of the most differentially expressed phosphatases (like DUSP4 and DUSP6) share ERK as substrate, or regulate the PI3K pathway (INPP4B, PTEN). These observations are also confirmed by pathway and GSEA analysis. It is shown that both ER- ERBB2+ and triple negative breast cancers have a distinctive pattern of phosphatase RNA expression. Surgical specimens from primary breast cancers that were estrogen receptor negative according to immunohistochemistry

2014-06-30 | E-GEOD-51999 | biostudies-arrayexpress

Mechanotransduction regulates adipose estrogen output and its impact on tumor cell growth

Project description:Adipose stromal cells (ASCs) are the primary source of local estrogens in adipose tissue, aberrant production of which promotes estrogen receptor-positive (ER+) breast cancer. Here we show that extracellular matrix (ECM) rigidity and cell contractility are two opposing determinants for estrogen output of ASCs. Using synthetic ECMs and elastomeric micropost arrays with tunable rigidity, we find that increasing matrix compliance induces transcription of aromatase, a rate-limiting enzyme in estrogen biosynthesis. This mechanical cue is transduced sequentially by Discoidin Domain Receptor 1 (DDR1), c-Jun N-terminal kinase 1 (JNK1), and phosphorylated JunB, which binds to and activates two breast cancer-associated aromatase promoters. In contrast, elevated cell contractility due to actin stress fiber formation dampens aromatase transcription. Mechanically stimulated stromal estrogen production enhances estrogen-dependent transcription in ER+ tumor cells and promotes their growth. This novel mechanotransduction pathway underlies communications between ECM, stromal hormone output, and cancer cell growth within the same microenvironment. Total RNA was isolated from primary adipose stromal cells after 2d culture or 3d Collagen gel for 21 hours. Triplicates for each conditioned were analyzed

2013-03-04 | E-GEOD-44811 | biostudies-arrayexpress

Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor α1 apoprotein

Project description:Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor α1 apoprotein. Basal proliferation persisted in estrogen-sensitive breast cancer cells grown in hormone depleted conditioned media without or with 4-hydroxytamoxifen (OH-Tam). Downregulating ER using siRNA inhibited basal proliferation by promoting cell cycle arrest. The basal expression of RARα1, the only RARα isoform that was expressed in breast cancer cell lines and in most breast tumors, was supported by apo-ER but was unaffected by OH-Tam. The overlapping tamoxifen-insensitive gene regulation by apo-ER and apo-RARα1 comprised activation of mainly genes promoting cell cycle and mitosis and suppression of genes involved in growth inhibition.

2011-05-13 | GSE26298 | GEO

Transcription profiling of human estrogen receptor positive MCF7 cells stably transfected with aromatase gene treated with testosterone, 17 B-estradiol, two aromatase inhibitors (letrozole and anastrozole), and an anti-estrogen (tamoxifen)

Project description:Anti-estrogens and aromatase inhibitors are important drugs in the treatment of estrogen-dependent breast cancer. In order to investigate the effects of these drugs on gene expression in breast cancer cells, we treated estrogen receptor-positive MCF-7 cells, stably transfected with the aromatase gene (known as MCF-7aro cells), with testosterone, 17Î²-estradiol, two aromatase inhibitors (letrozole and anastrozole), and an anti-estrogen (tamoxifen). Microarray analyses using Affymetrix Human Genome U133A GeneChips were carried out using total RNA isolated from the control and treated cells. When comparing the effect of each inhibitor on gene expression we observe that letrozole and anastrozole are more similar in terms of the genes they affect, compared to treatment with tamoxifen. The results of this study provide us with a better understanding of the actions of both aromatase inhibitors and anti-estrogens at the molecular level. We believe that the results of this study serve as the first step in identifying unique expression patterns following drug treatment, and that this will ultimately be useful in customizing patient treatment strategies for estrogen-dependent breast cancer. The data presented here have been processed using the R-Project Bioconductor statistical tools package using the affy library. The following were applied: RMA background correction, pmonly probe-level correction, quantile normalization, avgdiff summary method. Raw data is provided in the form of .CEL files.

2007-10-27 | E-GEOD-2225 | biostudies-arrayexpress

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