Membrane estrogen receptor-α levels in MCF-7 breast cancer cells predict cAMP and proliferation responses

Živadinović, Dragoslava; Gametchu, Bahiru; Watson, Cheryl S.

doi:10.1186/bcr958

Cited by 111 publications

(87 citation statements)

References 55 publications

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“…Rather our findings suggest that E 2 's effects on mast cell mediator release are through a membrane-associated (non-genomic) form of ER-α. This type of ER stimulation has been shown to induce rapid cellular responses through G-protein activation, (Bulayeva et al, 2004;Collins and Webb, 1999;Doolan et al, 2000;Improta-Brears et al, 1999;Stefano et al, 1999;Watson et al, 1999) which can include various signaling pathways involving Ca 2+ fluxes, and modulation of mitogen-activated protein kinases and adenyl cyclase (Bulayeva et al, 2004;Collins and Webb, 1999;Doolan and Harvey, 2003;Nadal et al, 2000;Song et al, 2004;Zivadinovic et al, 2005). Indeed, we found that intracellular Ca 2+ was increased within the first 2.5 min after estrogenic stimulation of RBL.…”

Section: Discussionmentioning

confidence: 49%

Estradiol activates mast cells via a non-genomic estrogen receptor-α and calcium influx

Zaitsu

Narita

Lambert

et al. 2007

Molecular Immunology

223

183

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Background-Allergic airway diseases are more common in females than in males during early adulthood. A relationship between female hormones and asthma prevalence and severity has been suggested, but the cellular and molecular mechanisms are not understood.Objective-To elucidate the mechanism(s) by which estrogens enhance the synthesis and release of mediators of acute hypersensitivity.Methods-Two mast cell/basophil cell lines (RBL-2H3 and HMC-1) and primary cultures of bone marrow derived mast cells, all of which naturally express estrogen receptor-α, were examined. Cells were incubated with physiological concentrations of 17-β-estradiol with and without IgE and allergens. Intracellular Ca 2+ concentrations and the release of β-hexosaminidase and leukotriene C 4 were quantified.Results-Estradiol alone induced partial release of the preformed, granular protein β-hexosaminidase from RBL-2H3, BMMC and HMC-1, but not from BMMC derived from estrogen receptor-α knock-out mice. The newly synthesized LTC 4 was also released from RBL-2H3. Estradiol also enhanced IgE-induced degranulation and potentiated LTC 4 production. Intracellular Ca 2+ concentration increased prior to and in parallel with mediator release. Estrogen receptor antagonists or Ca 2+ chelation inhibited these estrogenic effects.Conclusion-Binding of physiological concentrations of estradiol to a membrane estrogen receptor-α initiates a rapid onset and progressive influx of extracellular Ca 2+ , which supports the synthesis and release of allergic mediators. Estradiol also enhances IgE-dependent mast cell activation, resulting in a shift of the allergen dose response.

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Section: Discussionmentioning

confidence: 49%

Estradiol activates mast cells via a non-genomic estrogen receptor-α and calcium influx

Zaitsu

Narita

Lambert

et al. 2007

Molecular Immunology

223

183

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“…In our study, Western blot analyses showed that treatment of the cells with high concentrations of 17h-E induced ERK1/2 activation that was sustained even after 72 h, unlike treatment with lower concentrations of 17h-E, which resulted in an ERK1/2 activation that was not sustained. 17h-E has been shown to activate the mitogen-activated protein kinase pathway in other studies (37) and a constitutive activation of the mitogen-activated protein kinase pathway leads to antiproliferative signals generated to restrict cell proliferation, whereas transient activation may induce proliferation (40,41). Our data suggest that exposure to high levels of 17h-E induces a constitutive activation of ERK1/2, resulting in growth arrest, and that ANXA1 is upstream of ERK1/2 and in turn regulates ERK1/2 activity.…”

Section: Discussionmentioning

confidence: 99%

Annexin-1 Regulates Growth Arrest Induced by High Levels of Estrogen in MCF-7 Breast Cancer Cells

Ang¹,

Nguyen²,

Sim³

et al. 2009

Molecular Cancer Research

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“…Our past studies in both a pituitary tumor cell line selected for robust nongenomic estrogenic responses, and similarly selected MCF-7 breast cancer cells, clearly indicate that a membrane version of ERα is involved. We demonstrated this via antibody (Ab)-elicited responses, increased or decreased receptor expression linked to responses, antisense knockdown of ERα, and the absence of other estrogen receptor types in these cells [31][32][33][34][35][36][37][38].…”

Section: The Debate About the Identity Of Steroid Receptor Proteins Tmentioning

confidence: 99%

Xenoestrogens are potent activators of nongenomic estrogenic responses

et al. 2007

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Studies of the nuclear transcriptional regulatory activities of nonphysiological estrogens have not explained their actions in mediating endocrine disruption in animals and humans at the low concentrations widespread in the environment. However, xenoestrogens have rarely been tested for their ability to participate in the plethora of nongenomic steroid signaling pathways elucidated over the last several years. Here we review what is known about such responses in comparison to our recent evidence that xenoestrogens can rapidly and potently elicit signaling through nongenomic pathways culminating in functional endpoints. Both estradiol (E 2 ) and compounds representing various classes of xenoestrogens (diethylstilbestrol, coumestrol, bisphenol A, DDE, nonylphenol, endosulfan, and dieldrin) act via a membrane version of the estrogen receptor-α on pituitary cells, and can provoke Ca ++ influx via L-type channels, leading to prolactin (PRL) secretion. These hormones and mimetics can also cause the oscillating activation of extracellular regulated kinases (ERKs). However, individual estrogen mimetics differ in their potency and temporal phasing of these activations compared to each other and to E 2 . It is perhaps in these ways that they disrupt some endocrine functions when acting in combination with physiological estrogens. Our quantitative assays allow comparison of these outcomes for each mimetic, and let us build a detailed picture of alternative signaling pathway usage. Such an understanding should allow us to determine the estrogenic or antiestrogenic potential of different types of xenoestrogens, and help us to develop strategies for preventing xenoestrogenic disruption of estrogen action in many tissues.

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Membrane estrogen receptor-α levels in MCF-7 breast cancer cells predict cAMP and proliferation responses

Cited by 111 publications

References 55 publications

Estradiol activates mast cells via a non-genomic estrogen receptor-α and calcium influx

Estradiol activates mast cells via a non-genomic estrogen receptor-α and calcium influx

Annexin-1 Regulates Growth Arrest Induced by High Levels of Estrogen in MCF-7 Breast Cancer Cells

Xenoestrogens are potent activators of nongenomic estrogenic responses

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