Using a customized DNA microarray for expression profiling of the estrogen-responsive genes to evaluate estrogen activity among natural estrogens and industrial chemicals.

Terasaka, Shunichi; Aita, Yukie; Inoue, Akio; Hayashi, S.; Nishigaki, Michiko; Aoyagi, Kazuhiko; Sasaki, Hiroki; Wada‐Kiyama, Yuko; Sakuma, Yasuo; Akaba, Shuichi; Tanaka, Junko; Sone, Hirohito; Yonemoto, Junzo; Tanji, Masao; Kiyama, Ryoiti

doi:10.1289/ehp.6753

Cited by 98 publications

(88 citation statements)

References 45 publications

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“…The first report used human MCF-7 cells and compared the gene expression profiles of estrogen to a number of other estrogenic endocrine disruptors (Terasaka et al, 2004). Although many of the estrogenic endocrine disruptors examined exhibited global gene expression patterns similar to that of estrogen, we observed little to no correlation to the responses induced by TCDD.…”

Section: Dioxin Induces An Estrogen-like Gene Expression Response 1603mentioning

confidence: 68%

Dioxin Induces an Estrogen-Like, Estrogen Receptor-Dependent Gene Expression Response in the Murine Uterus

et al. 2006

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a ubiquitous environmental contaminant that elicits a broad range of toxicities in a tissue-, sex-, age-, and species-specific manner, including alterations in estrogen signaling. Many, if not all, of these effects involve changes in gene expression mediated via the activation of the aryl hydrocarbon receptor (AhR), a ligand activated transcription factor. Recent data indicate that TCDD may also elicit AhR-mediated estrogenic activity through interactions with the estrogen receptor (ER). In an effort to further characterize the estrogenic activity of TCDD, a comprehensive time-course analysis of uterine gene expression was conducted using ovariectomized C57BL/6 mice. Comparison of the temporal uterine transcriptional response to TCDD with that of ethynyl estradiol (EE) revealed a large proportion of the TCDD-mediated gene expression changes were also responsive to EE. Furthermore, pretreatment of mice with the pure ER antagonist ICI 182 780 (faslodex) inhibited gene expression responses to both EE and TCDD, providing additional evidence that these transcriptional responses involve the ER.

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Section: Dioxin Induces An Estrogen-like Gene Expression Response 1603mentioning

confidence: 68%

Dioxin Induces an Estrogen-Like, Estrogen Receptor-Dependent Gene Expression Response in the Murine Uterus

et al. 2006

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“…As mentioned previously, NIPK is thought to be a negative modulator of Akt (Du et al, 2003;Koo et al, 2004). Recently, NIPK was identified as an estrogen responsive gene by microarray analysis (Ise et al, 2005, Terasaka et al, 2004, suggesting that the presence or absence of estrogen could alter NIPK levels, thus providing a novel transcriptional mechanism through which estrogen could alter Akt activation in IsoPC female brain. Although IsoPC had no effect on NIPK expression 24 h after preconditioning as compared with sham PC mice regardless of gender, we did see overall higher levels of NIPK expression in female cortex as compared with males.…”

Section: Discussionmentioning

confidence: 83%

Gender-Specific Response to Isoflurane Preconditioning in Focal Cerebral Ischemia

Kitano

Young

Cheng

et al. 2007

J Cereb Blood Flow Metab

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Inhalation anesthetics are effective chemical preconditioning agents in experimental cerebral ischemia. However, previous work has been performed exclusively in male animals. We determined if there is a gender difference in ischemic outcome after isoflurane preconditioning (IsoPC), and if this sex-specific response is linked to differences in Akt phosphorylation or expression of neuronal inducible cell-death putative kinase (NIPK), a negative modulator of Akt activation. Young and middle-aged male and female mice were preconditioned for 4 h with air (sham PC) or 1.0% IsoPC and recovered for 24 h. Cortices were subdissected from preconditioned young male and female mice for measurement of Akt phosphorylation (Western blot) and NIPK mRNA (quantitative polymerase chain reaction). Additional cohorts underwent 2 h of reversible middle cerebral artery occlusion. Lastly, male and female Akt1+/+ and Akt1−/– mice were studied to determine if gender differences in ischemic outcome after IsoPC is Akt1-dependent. Infarction volume was determined at 22 h reperfusion (2,3,5-triphenyltetrazolium chloride). As expected, IsoPC decreased ischemic damage as compared with sham PC in young and middle-aged male mice. In contrast, IsoPC markedly increased infarction in young female mice and had no effect in middle-aged female mice. Cortical phospho-Akt was increased by IsoPC versus sham PC only in male mice. No increase was observed in IsoPC female mice. NIPK mRNA was higher in female mice than in male mice regardless of preconditioning status. Male IsoPC neuroprotection was lost in Akt1-deficient male mice. We conclude that IsoPC is beneficial only in ischemic male brain and that sex differences in IsoPC are mediated through Akt activation and basal NIPK expression.

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“…(5) Using this microarray, we have studied several basic issues regarding estrogen signaling, such as the effect of estrogen antagonists and endocrine disruptors on estrogenresponsive gene expression profiles. (6) Studies of the functional analysis of ERβ and identification of novel estrogen responsive genes were also carried out. (7,8) These studies provided information on promising diagnostic or prognostic biomarkers (9) for ER-positive breast cancer, such as histone deacetylase 6, (10,11) insulin-like growth factor binding protein 4, (12) and early growth responsive gene 3.…”

Section: Estrogen Receptor and Hormonal Therapy In Breast Cancermentioning

confidence: 99%

Estrogen signaling pathway and its imaging in human breast cancer

2009

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Recent remarkable progress in hormonal therapy has provided great benefit to breast cancer patients, but it also evokes novel issues: how accurately can the efficacy of each hormonal therapy be predicted and how can hormonal therapy-resistant patients be treated? These clinically important issues must be closely related to the biological events in each cancer, such as the alteration of intracellular multiple estrogen signaling pathways and the estrogen-related cancer microenvironment, which has recently revealed by molecular biological studies on estrogen and its receptors. However, the estrogen signaling status in individual breast cancers has not been clarified yet. Here we present the context of these issues and introduce our study of new tools which enable the visualization of estrogen signals in individual cancers. The assessment of estrogen receptor (ER)-a activity in individual cancers or ER-activating ability of the cancer microenvironment in each breast cancer patient revealed several new findings and interesting observations. We hope that these approaches provide new clues about the estrogen-dependent mechanisms of breast cancer development, and will be useful to advance the diagnosis and treatment of breast cancer patients. (Cancer Sci 2009; 100: 1773-1778) Estrogen receptor and hormonal therapy in breast cancer E strogen controls various physiological functions in many target tissues, and is also involved in diseases such as breast cancer, endometrial cancer, vascular disease, osteoporosis, and others. In particular, breast cancer is well recognized to be a crucial tumor in which estrogen and its receptor (ER) regulate development and progression in most cases, and are therefore the most important and effective targets for the therapy of breast cancer.(1) In this article, ER refers to estrogen receptor α unless specified.The efficacy of hormonal therapies targeting estrogen and ER has been established in numerous clinical trials. Current hormonal therapies are performed by two main strategies: inhibition of ER functions by anti-estrogens and deprivation of estrogen production by luteinizing hormone-releasing hormone agonist (pre-menopause) or aromatase inhibitor (post-menopause). Prediction of the efficiency of these therapies has involved using classical molecular biomarkers such as ERα and progesterone receptor.(2) However, approximately one-third of ER-positive patients do not respond to endocrine therapy, while some ER-negative patients are responsive.(3) These discrepancies could result from different estrogenrelated intracellular signaling pathways in breast cancer cells.One of the approaches to analyze the estrogen signaling status in breast cancer is expression profiling of estrogen-regulated genes in cancer cells. Comprehensive gene expression analysis, such as DNA microarray, may be a useful tool to address this issue. So far, we have analyzed estrogen-responsive gene expression profiles among ER-positive cancer cells using comprehensive DNA microarray (4) and, based on the obtained informa...

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Using a customized DNA microarray for expression profiling of the estrogen-responsive genes to evaluate estrogen activity among natural estrogens and industrial chemicals.

Cited by 98 publications

References 45 publications

Dioxin Induces an Estrogen-Like, Estrogen Receptor-Dependent Gene Expression Response in the Murine Uterus

Dioxin Induces an Estrogen-Like, Estrogen Receptor-Dependent Gene Expression Response in the Murine Uterus

Gender-Specific Response to Isoflurane Preconditioning in Focal Cerebral Ischemia

Estrogen signaling pathway and its imaging in human breast cancer

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