Estrogen Receptor Beta is a Negative Regulator of Mammary Cell Proliferation PDF Download
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Author: Xiaozheng Song
Publisher:
ISBN:
Category :
Languages : en
Pages : 476
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Book Description
The mammary gland cell growth and differentiation are under the control of both systemic honnones and locally produced growth factors. Among all these important honnones and growth factors,· estrogen plays a central role in mammary gland development. The biological function of estrogen is mediated by estrogen receptor Alpha. (ER[Alpha].) and estrogen receptor Beta (ER[Beta]). Both ER[Alpha] and ER[Beta] are expressed in the mammary gland, but with distinct expression patterns. In the mammary gland, ER[Alpha] has been proved to be the estrogen receptor that mediates the mitogenic function of estrogen. However the function of ER[Beta] in mammary cell proliferation is less understood and there remains some controversy. Accumulating evidence indicates that ER[Beta], unlike ER[Alpha], is a negative regulator of mammary epithelial cell proliferation.
Author: Xiaozheng Song
Publisher:
ISBN:
Category :
Languages : en
Pages : 476
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Book Description
The mammary gland cell growth and differentiation are under the control of both systemic honnones and locally produced growth factors. Among all these important honnones and growth factors,· estrogen plays a central role in mammary gland development. The biological function of estrogen is mediated by estrogen receptor Alpha. (ER[Alpha].) and estrogen receptor Beta (ER[Beta]). Both ER[Alpha] and ER[Beta] are expressed in the mammary gland, but with distinct expression patterns. In the mammary gland, ER[Alpha] has been proved to be the estrogen receptor that mediates the mitogenic function of estrogen. However the function of ER[Beta] in mammary cell proliferation is less understood and there remains some controversy. Accumulating evidence indicates that ER[Beta], unlike ER[Alpha], is a negative regulator of mammary epithelial cell proliferation.
Author: Yili Zhong
Publisher:
ISBN:
Category :
Languages : en
Pages : 200
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Book Description
In Mac-T cells overexpressing bovine ER[beta], we found that cell proliferation was significantly inhibited. FACS analysis on cell cycle distribution showed that more cells were in the G2/M phase, suggesting that bovine ER[beta] may induce G2/M arrest in Mac-T cells. Moreover, the inhibitory function of bovine ER[beta] is independent of estrogen binding. In summary, our data support that ER[beta] is a negative regulator of mammary epithelial cell proliferation and the inhibitory effect of ER[beta] is conserved across mammalian species. The inhibitory function of ER[beta] may partly be mediated by causing cell cycle arrest at G2/M phase. Bovine ER[beta] is highly expressed during late lactation and involution stages, stages with extensive apoptosis. The inhibitory role of ER[beta] suggests that ER[beta] may be involved in inducing apoptosis during these stages.
Author: Fritz F. Parl
Publisher: IOS Press
ISBN: 9780967335544
Category : Breast
Languages : en
Pages : 280
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Book Description
Estrogens have been implicated to play a role in the development of breast cancer. The purpose of this book is to provide a comprehensive analysis of experimental, clinical and epidemiological evidence in support of the carcinogenicity of estrogens.
Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 0
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Book Description
Our previous results have shown that the basement membrane (BM) regulated the expression and function of estrogen receptor-alpha (ERa) in mouse mammary epithelial cells. New results shown here indicate that the presence of lactogenic hormones was required for the regulatory effect of BM on ERa levels. We present evidence that cell adhesion to the BM components collagen-IV, through alpha 2 and beta 1 integrin subunits and laminin-l, through alpha 2, alpha 6 and beta 1 subunits are the relevant interactions responsible for transducing the signal of the BM that increases ERa expression. On the other hand, BM- induced changes in cell proliferation and cell morphology were not involved. Thus, the changes observed in ER expression and estrogenic effect when mammary epithelial cells are removed from the gland and placed in culture could be due to the disruption of the tissue organization and, in particular, to the lack of cell-matrix interactions on tissue culture plastic. Our system model could be useful to better understand the mechanisms involved in the regulation of ER expression and function during mammary gland development and breast tumor progression.
Author:
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ISBN:
Category :
Languages : en
Pages :
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Book Description
Transforming growth factor [beta]1 (TGF[beta]1) is a potent inhibitor of mammary epithelial proliferation. In human breast, estrogen receptor [alpha] (ER[alpha]) cells rarely co-localize with markers of proliferation, but their increased frequency correlates with breast cancer risk. To determine whether TGF[beta]1 is necessary for the quiescence of ER[alpha]-positive population, we examined mouse mammary epithelial gland at estrus. Approximately 35% of cells showed TGF[beta]1 activation, which co-localized with nuclear receptor-phosphorylated Smad 2/3, indicating that TGF[beta] signaling is autocrine. Furthermore, nuclear Smad co-localized with nuclear ER[alpha]. To test whether TGF[beta] was functional, we examined genetically engineered mice with different levels of TGF[beta]1. ER[alpha] co-localization with markers of proliferation (i.e. Ki-67 or BrdU) at estrus was significantly increased in the mammary glands of Tgf[beta]1 C57/bl/129SV heterozygote mice. This relationship was maintained following pregnancy, but was absent at puberty. Conversely, mammary epithelial expression of constitutively active TGF[beta]1 via the MMTV promoter suppressed proliferation of ER[alpha] positive cells. Thus, TGF[beta]1 activation functionally restrains ER[alpha] positive cells from proliferating in adult mammary gland. Accordingly, we propose that TGF[beta]1 dysregulation may promote proliferation of ER[alpha] positive cells associated with breast cancer risk in humans.
Author: William L. McGuire
Publisher:
ISBN:
Category : Medical
Languages : en
Pages : 320
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Book Description
Author: Yuxin Feng
Publisher:
ISBN:
Category :
Languages : en
Pages : 161
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Book Description
ERá is a critical regulator in breast cancer and mammary gland development. Deregulation of ER signaling correlates with abnormal mammary gland development and breast cancer. However, the role of epithelial ER remains to be clarified in vivo and the mechanism of ER signaling regulation is far from comprehensive. We hypothesize that 1) mammary epithelial ER plays critical roles in mammary gland development during pregnancy and lactation and that 2) novel, as yet identified factors in ER transcriptional regulation are involved in breast cancer development. The loxP-Cre system was used to generate epithelial ERKO mice. The well characterized MMTV-Cre and WAP-Cre transgenic mice were used to delete ER in mammary epithelial cells at different developmental stages. Early expression of MMTV-Cre arrested mammary gland development at the neonatal stage. Successive pregnancy and lactation activated epithelial ER ablation, which compromised side-branching, alveolar development, and epithelial proliferation. Further analysis revealed a massive loss of luminal epithelial cells presumably caused by apoptosis. The abnormal mammary gland development decreased milk production, thereby, caused growth retardation in the offspring. Similar phenotypes were also observed in MMTV-ERKO females in lactation. Thus, we concluded that epithelial ER is essential for mammary gland development during pregnancy and lactation stages. To further pursue the molecular mechanism of ER signaling regulation, a human mammary gland cDNA library was screened to identify novel factors that interact with ER. One novel ERá binding protein identified in the screen contains two conserved LXXLL motifs (NR-box) and a coiled-coil domain. The protein product, which we named NRCC, consists of 3 isoforms that vary in their N-terminal region. NRCC is conserved in vertebrates and its mRNA was detected in human breast cancer cells and mouse breast tumors. We found that NRCC-A interacts with ERá and enhances ERá transcriptional activity in human cancer cells. Moreover, NRCC-A co-localized with ERá in the cell nucleus and was recruited to ER target gene promoters. SiRNA analysis indicated that NRCC proteins are important for endogenous ERá-mediated transcriptional activity and estrogen dependent cell proliferation. Taken together, these data indicate that NRCC-A is a novel coactivator for ERá.
Author: Ajay K. Singh
Publisher: Academic Press
ISBN: 0080920462
Category : Medical
Languages : en
Pages : 534
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Book Description
The Textbook of Nephro-Endocrinology is the definitive translational reference in the field of nephro-endocrinology, investigating both the endocrine functions of the kidneys and how the kidney acts as a target for hormones from other organ systems. It offers researchers and clinicians expert, gold-standard analyses of nephro-endocrine research and translation into the treatment of diseases such as anemia, chronic kidney disease (CKD), rickets, osteoporosis, and, hypoparathyroidism. Investigates both the endocrine functions of the kidneys and how the kidney acts as a target for hormones from other organ systems Presents a uniquely comprehensive and cross-disciplinary look at all aspects of nephro-endocrine disorders in one reference work Clear translational presentations by the top endocrinologists and nephrologists in each specific hormone or functional/systems field
Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 22
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Book Description
Breast tumorigenesis and breast cancer progression involves the deregulation and hyperactivation of intracellular signalling proteins that lead to uncontrolled cellular proliferation, invasion and eventually, metastasis. During breast cancer development, there is a marked upregulation of estrogen receptor-alpha (ERalpha)(l) expression levels that is accompanied by alterations in estrogen responsiveness. Within normal breast epithelium, the majority of proliferating cells are ERalpha negative(2), while in breast tumors it is the ERalpha positive cells that are associated with an increase in cellular proliferation and metastasis(3), suggesting that estrogen action changes from that of an indirect mitogen to a direct mitogen. Although the mechanism by which ER becomes deregulated during breast tumorigenesis and breast cancer progression is unknown, the fact that alterations in other factors that enhance ER activity also change during breast cancer development(4) may be an underlying factor. In addition to the ER, expression and cellular responses to the transforming growth factor-beta (TGFbeta) signalling pathway also change during breast tumorigenesis and breast cancer progression. For normal mammary epithelial cells, TGFbeta is a potent physiological inhibitor of cell cycle progression(5). In breast cancer, however, cells have lost their natural growth inhibitory response to TGFbeta and may become more aggressive and more likely to metastasize in the presence of this factor(6).
Author: Bert W. O'Malley
Publisher:
ISBN:
Category : Cyclic nucleotides
Languages : en
Pages : 488
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Book Description
Hormone assays; Hormone receptors; Evaluation of biological effects of hormones; Purification and synthesis of hormones.
