Estrogen Induces Estrogen-related Receptor α Gene Expression and Chromatin Structural Changes in Estrogen Receptor (ER)-positive and ER-negative Breast Cancer Cells

Hu, Peng; Kinyamu, H. Karimi; Wang, Liangli; Martin, J. D.; Archer, Trevor; Teng, Christina T.

doi:10.1074/jbc.m705937200

Cited by 22 publications

(15 citation statements)

References 83 publications

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“…These findings support previous studies which demonstrate direct inhibitory effects of E2 on PEPCK expression via PGC1α (peroxisome proliferator activated receptor gamma co-activator 1 alpha) [35], [36] and studies showing estrogens administration to ob/ob mice reduces G6Pase expression [37]. GSK3β was elevated in the ArKO compared to WT and reduced upon E2 treatment at 3months, but not evident at 6 months of age.…”

Section: Discussionsupporting

confidence: 91%

Hepatic Glucose Intolerance Precedes Hepatic Steatosis in the Male Aromatase Knockout (ArKO) Mouse

et al. 2014

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Estrogens are known to play a role in modulating metabolic processes within the body. The Aromatase knockout (ArKO) mice have been shown to harbor factors of Metabolic syndrome with central adiposity, hyperinsulinemia and male-specific hepatic steatosis. To determine the effects of estrogen ablation and subsequent replacement in males on whole body glucose metabolism, three- and six-month-old male ArKO mice were subjected to whole body glucose, insulin and pyruvate tolerance tests and analyzed for ensuing metabolic changes in liver, adipose tissue, and skeletal muscle. Estrogen-deficient male ArKO mice showed increased gonadal adiposity which was significantly reduced upon 17β-estradiol (E2) treatment. Concurrently, elevated ArKO serum leptin levels were significantly reduced upon E2 treatment and lowered serum adiponectin levels were restored to wild type levels. Three-month-old male ArKO mice were hyperglycemic, and both glucose and pyruvate intolerant. These phenotypes continued through to 6 months of age, highlighting a loss of glycemic control. ArKO livers displayed changes in gluconeogenic enzyme expression, and in insulin signaling pathways upon E2 treatment. Liver triglycerides were increased in the ArKO males only after 6 months of age, which could be reversed by E2 treatment. No differences were observed in insulin-stimulated ex vivo muscle glucose uptake nor changes in ArKO adipose tissue and muscle insulin signaling pathways. Therefore, we conclude that male ArKO mice develop hepatic glucose intolerance by the age of 3 months which precedes the sex-specific development of hepatic steatosis. This can be reversed upon the administration of exogenous E2.

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Section: Discussionsupporting

confidence: 91%

Hepatic Glucose Intolerance Precedes Hepatic Steatosis in the Male Aromatase Knockout (ArKO) Mouse

et al. 2014

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“…Cells derived from human breast tumor tissues were analyzed on HTS affymetrix gene chip resulted with an up-regulation of gene expression when treated by estrogen and even more by ICI-182,780 [58]. Modulation by ICI-182,780 resulted with up regulation of quinine reductase in MCF-7 cells [59], ERRα in SKBR3 cells [60] and spinophilin in hippocampus neurons [61]. The promoter activation by ICI-182,780 is proposed to act via ER binding on AP-1 sites, but not via ERE [62].…”

Section: Discussionmentioning

confidence: 99%

The Regulation of MS-KIF18A Expression and Cross Talk with Estrogen Receptor

Zusev

Benayahu

2009

PLoS ONE

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This study provides a novel view on the interactions between the MS-KIF18A, a kinesin protein, and estrogen receptor alpha (ERα) which were studied in vivo and in vitro. Additionally, the regulation of MS-KIF18A expression by estrogen was investigated at the gene and protein levels. An association between recombinant proteins; ERα and MS-KIF18A was demonstrated in vitro in a pull down assay. Such interactions were proven also for endogenous proteins in MBA-15 cells were detected prominently in the cytoplasm and are up-regulated by estrogen. Additionally, an association between these proteins and the transcription factor NF-κB was identified. MS-KIF18A mRNA expression was measured in vivo in relation to age and estrogen level in mice and rats models. A decrease in MS-KIF18A mRNA level was measured in old and in OVX-estrogen depleted rats as compared to young animals. The low MS-KIF18A mRNA expression in OVX rats was restored by estrogen treatment. We studied the regulation of MS-KIF18A transcription by estrogen using the luciferase reporter gene and chromatin immuno-percipitation (ChIP) assays. The luciferase reporter gene assay demonstrated an increase in MS-KIF18A promoter activity in response to 10−8 M estrogen and 10−7M ICI-182,780. Complimentary, the ChIP assay quantified the binding of ERα and pcJun to the MS-KIF18A promoter that was enhanced in cells treated by estrogen and ICI-182,780. In addition, cells treated by estrogen expressed higher levels of MS-KIF18A mRNA and protein and the protein turnover in MBA-15 cells was accelerated. Presented data demonstrated that ERα is a defined cargo of MS-KIF18A and added novel insight on the role of estrogen in regulation of MS-KIF18A expression both in vivo and in vitro.

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“…In this alternative view, some movements result in the co-localization ("gene kissing") of sets of genes widely separated before stimulation, allowing their spatial co-regulation. One example put forward to support this view described rapid large-scale movements of specific estrogen-inducible genes and of the CTs carrying these genes (Hu et al 2008), but this finding could not be confirmed by carefully executed subsequent studies (Kocanova et al 2010).…”

Section: Stability and Dynamics Of Higher-order Chromatin Arrangementsmentioning

confidence: 94%

The radial nuclear positioning of genes correlates with features of megabase-sized chromatin domains

et al. 2012

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A nonrandom radial nuclear organization of genes has been well documented. This study provides further evidence that radial positioning depends on features of corresponding ∼1 Mbp chromatin domains (CDs), which represent the basic units of higher-order chromatin organization. We performed a quantitative three-dimensional analysis of the radial nuclear organization of three genes located on chromosome 1 in a DG75 Burkitt lymphoma-derived cell line. Quantitative real-time polymerase chain reaction revealed similar transcription levels for the three selected genes, whereas the total expression strength (TES) calculated as the sum of transcription of all genes annotated within a surrounding window of about 1 Mbp DNA differed for each region. Radial nuclear position of the studied CDs correlated with TES, i.e., the domain with the highest TES occupied the most interior position. Positions of CDs with stable TES values were stably maintained even under experimental conditions, resulting in genome-wide changes of the expression levels of many other genes. Our results strongly support the hypothesis that knowledge of the local chromatin environment is essential to predict the radial nuclear position of a gene.

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Estrogen Induces Estrogen-related Receptor α Gene Expression and Chromatin Structural Changes in Estrogen Receptor (ER)-positive and ER-negative Breast Cancer Cells

Cited by 22 publications

References 83 publications

Hepatic Glucose Intolerance Precedes Hepatic Steatosis in the Male Aromatase Knockout (ArKO) Mouse

Hepatic Glucose Intolerance Precedes Hepatic Steatosis in the Male Aromatase Knockout (ArKO) Mouse

The Regulation of MS-KIF18A Expression and Cross Talk with Estrogen Receptor

The radial nuclear positioning of genes correlates with features of megabase-sized chromatin domains

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