Peroxisome proliferator-activated receptor α expression is regulated by estrogen receptor α and modulates the response of MCF-7 cells to sodium butyrate

Faddy, Helen M.; Robinson, J. A.; Lee, Won Jae; Holman, N. A.; Monteith, Gregory R.; Roberts‐Thomson, Sarah J.

doi:10.1016/j.biocel.2005.09.002

Cited by 21 publications

(15 citation statements)

References 42 publications

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“…These results suggest that ER overexpression enhanced the effect of PPARα on the promotion of breast cancer cell growth. The ability of ER-modulated PPARα expression was also previously reported [42]. In addition, crosstalk between MAP kinase and ER was reported to enhance estrogen-mediated signaling and tumor growth in ER-positive breast tumors [43].…”

Section: Discussionmentioning

confidence: 79%

High levels of arachidonic acid and peroxisome proliferator-activated receptor-alpha in breast cancer tissues are associated with promoting cancer cell proliferation

Chang

Chen

et al. 2013

The Journal of Nutritional Biochemistry

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Section: Discussionmentioning

confidence: 79%

High levels of arachidonic acid and peroxisome proliferator-activated receptor-alpha in breast cancer tissues are associated with promoting cancer cell proliferation

Chang

Chen

et al. 2013

The Journal of Nutritional Biochemistry

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“…Indeed, NR1C1-activation in mammary-tumor cells suppresses Hypoxia-Inducible-Factor-1-α signaling , reduces Vascular-Endothelial-Growth-Factor secretion and tube formation by endothelial cells, suggesting anti-angiogenic effects [10]. NR1C1 anti-tumor activity may be of particular relevance in ER + /breast-cancer, since anti-estrogens induce NR1C1-mRNA in ER + / MCF-7 cells and ERα over-expression into ER − / MDA-MB-231 cells decreases NR1C1-mRNA [11]. …”

Section: Lipid-sensorsmentioning

confidence: 99%

Lipid-sensors, enigmatic-orphan and orphan nuclear receptors as therapeutic targets in breast-cancer

et al. 2016

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Breast-cancer is heterogeneous and consists of various groups with different biological characteristics. Innovative pharmacological approaches accounting for this heterogeneity are needed. The forty eight human Nuclear-Hormone-Receptors are ligand-dependent transcription-factors and are classified into Endocrine-Receptors, Adopted-Orphan-Receptors (Lipid-sensors and Enigmatic-Orphans) and Orphan-receptors. Nuclear-Receptors represent ideal targets for the design/synthesis of pharmacological ligands. We provide an overview of the literature available on the expression and potential role played by Lipid-sensors, Enigmatic-Orphans and Orphan-Receptors in breast-cancer. The data are complemented by an analysis of the expression levels of each selected Nuclear-Receptor in the PAM50 breast-cancer groups, following re-elaboration of the data publicly available. The major aim is to support the idea that some of the Nuclear-Receptors represent largely unexploited therapeutic-targets in breast-cancer treatment/chemo-prevention. On the basis of our analysis, we conclude that the Lipid-Sensors, NR1C3, NR1H2 and NR1H3 are likely to be onco-suppressors in breast-cancer. The Enigmatic-Orphans, NR1F1 NR2A1 and NR3B3 as well as the Orphan-Receptors, NR0B1, NR0B2, NR1D1, NR2F1, NR2F2 and NR4A3 exert a similar action. These Nuclear-Receptors represent candidates for the development of therapeutic strategies aimed at increasing their expression or activating them in tumor cells. The group of Nuclear-Receptors endowed with potential oncogenic properties consists of the Lipid-Sensors, NR1C2 and NR1I2, the Enigmatic-Orphans, NR1F3, NR3B1 and NR5A2, as well as the Orphan-Receptors, NR2E1, NR2E3 and NR6A1. These oncogenic Nuclear-Receptors should be targeted with selective antagonists, reverse-agonists or agents/strategies capable of reducing their expression in breast-cancer cells.

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“…Recently, it has been reported that the anti-inflammatory effects of EETs on endothelial cells may be mediated by a/g peroxisome proliferator-activated receptor (PPAR; Liu et al 2005, Wray & Bishop-Bailey 2007. Sex hormones might operate via such a pathway since it has been demonstrated that estrogen regulates PPAR expression (Campbell et al 2003, Faddy et al 2006. Although, more recent evidence in isolated arteries suggest that while PPARg might enhance endothelial vasodilator release in conduit vessels, in resistance arteries activation of this receptor is inhibitory for EDHF release (O'Sullivan et al 2006).…”

Section: Sex Differences In Leukocyte Recruitmentmentioning

confidence: 99%

Sex differences in vascular function: implication of endothelium-derived hyperpolarizing factor

Villar¹,

Hobbs²,

Ahluwalia

2008

Journal of Endocrinology

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The vascular endothelium plays a crucial role in the regulation of vascular homeostasis by controlling vascular tone, coagulation, and inflammatory responses. These actions are exerted by endothelial factors including nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF). The greater incidence of cardiovascular disease (CVD) in men and postmenopausal women compared with premenopausal women implies a vasoprotective phenotype of females, which may be influenced by sex hormones. These hormones, particularly estrogen, have modulatory effects on the endothelium and circulating cells that have been implicated in vascular inflammation and in the development of CVD. EDHF seems to be the predominant endothelial factor in the resistance vasculature of females and this mediator could afford the beneficial cardiovascular risk profile observed in premenopausal woman. In this review, we discuss sex differences in EDHF biology and how sex hormones can modulate EDHF responses. We also review the implication of sex hormone-dependent regulation of EDHF in inflammatory processes, platelet function, and repair after vascular damage, each of which have a critical role in several aspects of the pathogenesis of CVD.

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Peroxisome proliferator-activated receptor α expression is regulated by estrogen receptor α and modulates the response of MCF-7 cells to sodium butyrate

Cited by 21 publications

References 42 publications

High levels of arachidonic acid and peroxisome proliferator-activated receptor-alpha in breast cancer tissues are associated with promoting cancer cell proliferation

High levels of arachidonic acid and peroxisome proliferator-activated receptor-alpha in breast cancer tissues are associated with promoting cancer cell proliferation

Lipid-sensors, enigmatic-orphan and orphan nuclear receptors as therapeutic targets in breast-cancer

Sex differences in vascular function: implication of endothelium-derived hyperpolarizing factor

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