Estrogen Receptor in Mammary Gland Physiology

2000 ◽  
pp. 1-16
Author(s):  
Elizabeth Anderson ◽  
Robert B. Clarke ◽  
Anthony Howell
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland

scholarly journals Cross-Talk in the Female Rat Mammary Gland: Influence of Aryl Hydrocarbon Receptor on Estrogen Receptor Signaling

2016 ◽  
Vol 124 (5) ◽  
pp. 601-610 ◽  
Author(s):  
Janina Helle ◽  
Manuela I. Bader ◽  
Annekathrin M. Keiler ◽  
Oliver Zierau ◽  
Günter Vollmer ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland ◽  
Aryl Hydrocarbon Receptor ◽  
Cross Talk ◽  
Female Rat ◽  
Receptor Signaling ◽  
Aryl Hydrocarbon ◽  
Estrogen Receptor Signaling ◽  
Rat Mammary Gland

scholarly journals Future perspectives of selective estrogen receptor modulators used alone and in combination with DHEA

2006 ◽  
Vol 13 (2) ◽  
pp. 335-355 ◽  
Author(s):  
F Labrie
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Mammary Gland ◽  
Cancer Prevention ◽  
Women’S Health ◽  
Women's Health ◽  
Aromatase Inhibitors ◽  
Estrogenic Activity ◽  
Antagonistic Activity ◽  
Breast Cancer Prevention

Breast cancer is the most frequently diagnosed and the second cause of cancer death in women, thus making breast cancer a most feared disease. Since breast cancer metastasizes early and it is unlikely that improvements in the treatment of metastatic disease could permit a cure in most cases in the foreseeable future, it is clear that prevention is essential in order practically to eliminate deaths from breast cancer. Tamoxifen is the only selective estrogen receptor modulator (SERM) currently registered for use in breast cancer prevention; the tamoxifen versus raloxifene study should indicate the efficacy of this compound compared with raloxifene. The recent benefits of aromatase inhibitors over tamoxifen indicate the advantages of a blockade of estrogens more complete than the one achieved with tamoxifen, a SERM having some estrogenic activity in the mammary gland and an even higher estrogenic action in the uterus. However, it is unlikely that the general estrogen ablation achieved with aromatase inhibitors will be acceptable for the long-term use required for prevention. It is thus important to develop SERMs with highly potent and pure antagonistic activity in the mammary gland and uterus while possessing estrogen-like activity in tissues of particular importance for women’s health, namely the bones and the cardiovascular system. However, it is expected that a SERM alone will not meet all the requirements of women’s health at the postmenopause when ovarian estrogen secretion has ceased and peripheral formation of androgens and estrogens from DHEA by intracrine mechanisms is decreased by 60% or more. One possibility is to combine a SERM with DHEA, a precursor of sex steroids that permits, somewhat like SERMs, tissue-specific formation of androgens and/or estrogens according to the level of expression of the steroidogenic and steroid-inactivating enzymes. DHEA could thus compensate for the important loss of androgens that accompanies aging and could also permit sex steroid formation and action in the brain while breast cancer prevention would be achieved by the SERM.

Downregulation of Estrogen Receptor Gene Expression by Exogenous 17β-Estradiol in the Mammary Glands of Lactating Mice

2006 ◽  
Vol 231 (3) ◽  
pp. 311-316 ◽  
Author(s):  
Toshinobu Hatsumi ◽  
Yutaka Yamamuro
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Mammary Gland ◽  
Single Injection ◽  
Receptor Gene ◽  
Self Regulation ◽  
Estrogen Receptor Gene ◽  
17Β Estradiol ◽  
Nuclear Estrogen Receptor ◽  
Receptor Gene Expression

The biological actions of estrogen are mostly conveyed through interaction with the nuclear estrogen receptor (ER). Previous evidence indicated that estrogen participates in self-regulation through the modulation of the expression of its own receptors. However, the self-regulation of estrogen against ER in the mammary gland during established lactation has not yet been investigated. The present study evaluated ER gene expression in the lactating gland activated by large doses of 17β-estradiol (E2). Repeated E2 treatments dose-dependently decreased the gene, expression of ER, especially its subtype ER-α mRNA, Which was decreased to 10% of the vehicle-injected control by 1 μg E2 injection, whereas it was decreased by 73% for another subtype, ER-β. A single injection of 5 μg of E2 drastically downregulated both ER genes within 12 hrs of injection, and they did not recover to pretreatment level within 48 hrs. Western blot analysis verified that E2 treatment inhibited the phosphorylation of Stat5, which is a potent transcriptional regulator for ER mRNA. The present findings demonstrate that E2 treatment decreases the gene expression of its own receptor in the mammary gland during galactopoesis and induces an apparent transition of the ER profile in the mammary gland during lactation into postlactation.

scholarly journals Estrogen receptor signaling is reprogrammed during breast tumorigenesis

2019 ◽  
Vol 116 (23) ◽  
pp. 11437-11443 ◽  
Author(s):  
David Chi ◽  
Hari Singhal ◽  
Lewyn Li ◽  
Tengfei Xiao ◽  
Weihan Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
Breast Tumors ◽  
Normal Mammary Gland ◽  
Breast Tumorigenesis ◽  
Effective Prevention ◽  
Significant Difference ◽  
Estrogen Stimulation

Limited knowledge of the changes in estrogen receptor (ER) signaling during the transformation of the normal mammary gland to breast cancer hinders the development of effective prevention and treatment strategies. Differences in estrogen signaling between normal human primary breast epithelial cells and primary breast tumors obtained immediately following surgical excision were explored. Transcriptional profiling of normal ER+ mature luminal mammary epithelial cells and ER+ breast tumors revealed significant difference in the response to estrogen stimulation. Consistent with these differences in gene expression, the normal and tumor ER cistromes were distinct and sufficient to segregate normal breast tissues from breast tumors. The selective enrichment of the DNA binding motif GRHL2 in the breast cancer-specific ER cistrome suggests that it may play a role in the differential function of ER in breast cancer. Depletion of GRHL2 resulted in altered ER binding and differential transcriptional responses to estrogen stimulation. Furthermore, GRHL2 was demonstrated to be essential for estrogen-stimulated proliferation of ER+ breast cancer cells. DLC1 was also identified as an estrogen-induced tumor suppressor in the normal mammary gland with decreased expression in breast cancer. In clinical cohorts, loss of DLC1 and gain of GRHL2 expression are associated with ER+ breast cancer and are independently predictive for worse survival. This study suggests that normal ER signaling is lost and tumor-specific ER signaling is gained during breast tumorigenesis. Unraveling these changes in ER signaling during breast cancer progression should aid the development of more effective prevention strategies and targeted therapeutics.

scholarly journals The genomic landscape of estrogen receptor α binding sites in mouse mammary gland

PLoS ONE ◽  
2019 ◽  
Vol 14 (8) ◽  
pp. e0220311 ◽  
Author(s):  
Murugesan Palaniappan ◽  
Loc Nguyen ◽  
Sandra L. Grimm ◽  
Yuanxin Xi ◽  
Zheng Xia ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland ◽  
Binding Sites ◽  
Estrogen Receptor Α ◽  
Mouse Mammary Gland ◽  
Genomic Landscape

Activity of three selective estrogen receptor modulators on hormone-dependent responses in the mouse uterus and mammary gland

2008 ◽  
Vol 287 (1-2) ◽  
pp. 40-46 ◽  
Author(s):  
Judy S. Crabtree ◽  
Bryan J. Peano ◽  
Xiaochun Zhang ◽  
Barry S. Komm ◽  
Richard C. Winneker ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland ◽  
Selective Estrogen Receptor Modulators ◽  
Mouse Uterus ◽  
Estrogen Receptor Modulators ◽  
Receptor Modulators

scholarly journals Early exposure of the rat mammary gland to estrogen and progesterone blocks co-localization of estrogen receptor expression and proliferation

2001 ◽  
Vol 171 (1) ◽  
pp. 75-83 ◽  
Author(s):  
L Sivaraman ◽  
SG Hilsenbeck ◽  
L Zhong ◽  
J Gay ◽  
OM Conneely ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland ◽  
Protective Effect ◽  
Tumor Development ◽  
Positive Association ◽  
Receptor Expression ◽  
Target Cells ◽  
Proliferating Cells ◽  
Estrogen Receptor Positive ◽  
Er Positive

An early single full-term pregnancy induces a long-lasting protective effect against mammary tumor development in humans and rodents. This protective effect can be mimicked in rats by short-term administration of estrogen and progesterone hormones prior to carcinogen administration. The hormones of pregnancy are able to induce a proliferative block upon carcinogen challenge that is not observed in the age-matched virgin. We wished to determine whether carcinogen is needed to induce a paracrine-to-autocrine shift of proliferation in steroid receptor positive cells or if such a cell population already exists in the age-matched virgin mammary gland. Here we show that estrogen receptor positive (ER+) proliferating cells are rare in the developing mammary gland of the virgin rat but represent the majority of the proliferating cells in the mature (96-day-old) mammary gland of the virgin rat. As the majority of the proliferating cells before carcinogen challenge were ER positive, the ER+ proliferating cells in the mature mammary gland may represent the target cells for carcinogen-induced transformation. Importantly, prior exposure of the mammary gland to pregnancy levels of estrogen/progesterone blocked this positive association. This ability to block the proliferation of the ER+ cells may be one factor by which pregnancy induces protection against breast cancer.

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