Membrane Oestrogen Receptors on Rat Pituitary Tumour Cells: Immuno‐Identification and Responses to Oestradiol and Xenoestrogens

Watson, Cheryl S.; Campbell, Celeste H; Gametchu, Bahiru

doi:10.1111/j.1469-445x.1999.01903.x

Cited by 84 publications

(37 citation statements)

References 47 publications

(46 reference statements)

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“…Therefore, it is reasonable to suggest that BPA, similarly to E2, binds to ERa and produces changes in these rapid signals. Few data address the ability of BPA to mediate nongenomic estrogenic actions (see [25][26][27][28][29][30][31] and, as far we know, no information focuses on the involvement of these pathways in the proliferative effect of BPA.…”

Section: Introductionmentioning

confidence: 99%

Expression of Concern: Laccase treatment impairs bisphenol A‐induced cancer cell proliferation affecting estrogen receptor α‐dependent rapid signals

et al. 2008

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SummaryA wide variety of environmental contaminants exert estrogenic actions in wildlife, laboratory animals, and in human beings through binding to nuclear estrogen receptors (ERs). Here, the mechanism(s) of bisphenol A (BPA) to induce cell proliferation and the occurrence of its bioremediation by treatment with laccase are reported. BPA, highly present in natural world and considered as a model of environmental estrogen action complexity, promotes human cancer cell proliferation via ERa-dependent signal transduction pathways. Similar to 17b-estradiol, BPA increases the phosphorylation of both extracellular regulated kinase and AKT. Specific inhibitors of these kinase completely block the BPA effect on cancer cell proliferation. Notably, high BPA concentrations (i.e., 0.1 and 1 mM) are cytotoxic even in ERa-devoid cancer cells, indicating that an ERa-independent mechanism participates to BPA-induced cytotoxicity. On the other hand, BPA oxidation by laccase impairs the binding of this environmental estrogen to ERa loosing at all ERa-dependent effect on cancer cell proliferation. Moreover, the laccase-catalyzed oxidation of BPA reduces the BPA cytotoxic effect. Thus, laccase appears to impair BPA action(s), representing an invaluable bioremediation enzyme.2008 IUBMB IUBMB Life, 60(12): 843-852, 2008

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Section: Introductionmentioning

confidence: 99%

Expression of Concern: Laccase treatment impairs bisphenol A‐induced cancer cell proliferation affecting estrogen receptor α‐dependent rapid signals

et al. 2008

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“…However, the dose-response curves for the environmental estrogens were similar to that for E 2 , in that they are biphasic (inverted U-shaped) curves. This type of response is also typical for other steroid-induced responses (Watson et al 1999;Welshons et al 2003). Exposing HMC-1 cells to a combination of suboptimal concentrations of E 2 and an environmental estrogen had an additive effect on degranulation.…”

Section: Dieldrin [Log (M)] β-Hex (% Release)mentioning

confidence: 84%

“…One pathway is via genomic receptors acting as transcription factors on gene expression. However, an alternative pathway acting via plasma membrane receptors is more often involved in the rapid effects of steroids occurring within seconds to minutes (Watson et al 1999;Watson and Gametchu 2003). This nongenomic pathway is involved in secretory responses to both physiologic and nonphysiologic estrogens .…”

Section: Researchmentioning

confidence: 99%

Environmental Estrogens Induce Mast Cell Degranulation and Enhance IgE-mediated Release of Allergic Mediators

Narita

Goldblum

Brooks

et al. 2007

Journal of Allergy and Clinical Immunology

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BACKGROUND: Prevalence and morbidity of allergic diseases have increased over the last decades. Based on the recently recognized differences in asthma prevalence between the sexes, we have examined the effect of endogenous estrogens on a key element of the allergic response. Some lipophilic pollutants have estrogen-like activities and are termed environmental estrogens. These pollutants tend to degrade slowly in the environment and to bioaccumulate and bioconcentrate in the food chain; they also have long biological half-lives. OBJECTIVES: Our goal in this study was to identify possible pathogenic roles for environmental estrogens in the development of allergic diseases. METHODS:We screened a number of environmental estrogens for their ability to modulate the release of allergic mediators from mast cells. We incubated a human mast cell line and primary mast cell cultures derived from bone marrow of wild type and estrogen receptor α (ER-α)-deficient mice with environmental estrogens with and without estradiol or IgE and allergens. We assessed degranulation of mast cells by quantifying the release of β-hexosaminidase.

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“…We considered this likely in light of recent evidence regarding ERα membrane localization. [23][24][25] To test this hypothesis, we immunoprecipitated SHC from nonstimulated and E 2 -stimulated LTED cells and then probed immunoblots with anti-ERα antibodies. Our data showed that the ERα/SHC complex pre-existed before E 2 treatment and E 2 time-dependently increased this association.…”

Section: Phenomenon Of Hypersensitivity: Mechanisms and Pathwaysmentioning

confidence: 99%

Adaptation to Estradiol Deprivation Causes Up-Regulation of Growth Factor Pathways and Hypersensitivity to Estradiol in Breast Cancer Cells

Santen

Song

Masamura

et al. 2008

Advances in Experimental Medicine and Biology

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Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapt and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including upregulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4-10 fold up-regulated as a result of demethylation of its C promoter, is nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. is induces rapid nongenomic effects which are enhanced in LTED cells.The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrane-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membranes. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors.A major question is how ERα locates in the plasma membrane since it does not contain an inherent membrane localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the "glue" which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.In order to abrogate growth factor induced hypersensitivity, we have utilized a drug, farnesylthiosalicylic acid, which blocks the binding of GTP-Ras to its membrane acceptor protein, galectin 1 and reduces the activation of MAP kinase. We have shown that this drug is a potent inhibitor of mTOR and this provides the major means for inhibition of cell proliferation. The concept of "adaptive hypersensitivity" and the mechanisms responsible for this phenomenon have important clinical implications. The efficacy of aromatase inhibitors in patients relapsing on tamoxifen could be explained by this mechanism and inhibitors of growth factor pathways should reverse the hypersensitivity phenomenon and result in prolongation of the efficacy of hormonal therapy for breast cancer.

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Membrane Oestrogen Receptors on Rat Pituitary Tumour Cells: Immuno‐Identification and Responses to Oestradiol and Xenoestrogens

Cited by 84 publications

References 47 publications

Expression of Concern: Laccase treatment impairs bisphenol A‐induced cancer cell proliferation affecting estrogen receptor α‐dependent rapid signals

Expression of Concern: Laccase treatment impairs bisphenol A‐induced cancer cell proliferation affecting estrogen receptor α‐dependent rapid signals

Environmental Estrogens Induce Mast Cell Degranulation and Enhance IgE-mediated Release of Allergic Mediators

Adaptation to Estradiol Deprivation Causes Up-Regulation of Growth Factor Pathways and Hypersensitivity to Estradiol in Breast Cancer Cells

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