Role of epidermal growth factor in the acquisition of ovarian steroid hormone responsiveness in the normal mouse mammary gland

Ankrapp, David; Bennett, Jessica M.; Haslam, Sandra Z.

doi:10.1002/(sici)1097-4652(199802)174:2<251::aid-jcp12>3.0.co;2-f

Cited by 45 publications

(22 citation statements)

References 30 publications

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“…Epidermal growth factor (EGF), in addition to promoting the proliferation of terminal end-buds, augments estrogen-induced ductal outgrowth and progesterone-induced sidebranching [23]. Indeed, estrogen induces PR isoform expression only in the presence of EGF [24], suggesting the existence of important cross-talk between EGFRs and both SRs. Ligand-activated PRs and ERs are potent breast mitogens, and mammary epithelial cells that express PR also express ERα.…”

Section: Pr and Signaling Cross-talk In Breast Cancersupporting

confidence: 61%

Integration of progesterone receptor action with rapid signaling events in breast cancer models

Lange

2008

The Journal of Steroid Biochemistry and Molecular Biology

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Recent discoveries suggest that several protein kinases are rapidly activated in response to ligand binding to cytoplasmic steroid hormone receptors (SRs), including progesterone receptors (PRs). Thus, PRs act as ligand-activated transcription factor "sensors" for growth factor-initiated signaling pathways in hormonally regulated tissues, such as the breast. Induction of rapid signaling upon progestin-binding to PR-B provides a means to ensure that receptors and co-regulators are appropriately phosphorylated as part of optimal transcription complexes. Alternatively, PR-B activated kinase cascades provide additional avenues for progestin-regulated gene expression independent of PR nuclear action. Herein, an overview of progesterone/PR and signaling cross-talk in breast cancer models is provided. Kinases are emerging as key mediators of PR action. Cross-talk between SR and membrane-initiated signaling events suggests a mechanism for coordinate regulation of gene subsets by mitogenic stimuli in hormonally responsive normal tissues, and is suspected to contribute to cancer biology.

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Section: Pr and Signaling Cross-talk In Breast Cancersupporting

confidence: 61%

Integration of progesterone receptor action with rapid signaling events in breast cancer models

Lange

2008

The Journal of Steroid Biochemistry and Molecular Biology

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“…Several signaling systems have been implicated as potential mediators of the effects of estrogen. These include the epidermal growth factor (EGF) family of ligands and receptors (Ankrapp et al 1998, Sebastian et al 1998, Luetteke et al 1999, Weisen et al 1999, insulin-like growth factor-1 (Kleinberg et al 2000) and hepatocyte growth factor/scatter factor (Yang et al 1995). In addition, transforming growth factor (TGF)-has been shown to be a potent inhibitor of end bud proliferation and ductal growth (Daniel et al 1989, Robinson et al 1991, Pierce et al 1993.…”

Section: Discussionmentioning

confidence: 99%

Temporally regulated overexpression of parathyroid hormone-related protein in the mammary gland reveals distinct fetal and pubertal phenotypes

Dunbar¹,

Dann²,

Brown³

et al. 2001

Journal of Endocrinology

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We have previously demonstrated that overexpression of parathyroid hormone-related protein (PTHrP) in the mammary glands of transgenic mice results in defects in ductal elongation and branching during puberty and in lobuloalveolar development during pregnancy. In addition, we have shown that PTHrP is necessary for the formation of the initial ductal tree during embryonic mammary development. In order to examine the effect of varying the timing of PTHrP overexpression on mammary development, we created tetracycline-regulated, K14-tTA/Tet O -PTHrP double transgenic mice. In this report, we document that this 'tet-off' system directs transgene expression to the mammary gland and that it is fully repressed in the presence of tetracycline. Using these mice, we demonstrate that transient overexpression of PTHrP before birth causes defects in ductal branching during puberty and that overexpression of PTHrP during puberty decreases the rate of ductal elongation. Furthermore, we demonstrate that if PTHrP overexpression is initiated after ductal morphogenesis is completed, lobuloalveolar development is unaffected. Finally, we demonstrate that the impairment in ductal elongation caused by PTHrP is associated with an increase in the basal rate of epithelial cell apoptosis in terminal end buds and a failure to increase end bud cell proliferation and decrease apoptosis in response to estrogen and progesterone.

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“…For example, administration of the anti-estrogen ICI 182780 reduces the response to EGF in the mammary gland (Ankrapp et al 1998). Studies in ERa-knockout mice demonstrated that EGF could not induce DNA synthesis in the uterus even in the presence of wildtype levels of EGF and EGFR (Curtis et al 1996, Ankrapp et al 1998.…”

Section: Role Of the Igf-1r And Egfr In E2 Rapid Actionmentioning

confidence: 99%

Role of receptor complexes in the extranuclear actions of estrogen receptor α in breast cancer

Song¹,

Fan²,

Yue³

et al. 2006

Endocr Relat Cancer

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Our recent studies have examined the role of various receptor complexes in the mediation of rapid, extranuclear effects of estradiol. This review describes 17b-estradiol (E2)-initiated extranuclear signaling pathways, which involve the insulin-like growth factor 1 receptor (IGF-1R) and epidermal growth factor receptor (EGFR) and result in the activation of several kinase cascades. The biologic results of these effects are the enhancement of cell proliferation and diminution of programmed cell death (apoptosis). Until recently, most studies assigned priority to the nuclear transcriptional actions of estrogen receptor a (ERa). Present investigative emphasis focuses on the additional importance of ERa residing in or near the plasma membrane. A small fraction of ERa is associated with the cell membrane and mediates the rapid effects of E2. Unlike classical growth factor receptors, such as IGF-1R and EGFR, ERa has no transmembrane and kinase domains and is known to initiate E2 rapid signals by forming protein/protein complexes with many signaling molecules. Our recent studies demonstrate that the IGF-1R is involved in tethering ERa to the plasma membrane, in activating the EGFR, and in the initiation of mitogen-activated protein kinase and phosphoinositide 3-kinase signaling. The formation of a multi-protein complex containing these receptors as well as adaptor proteins is a critical step in this process. A full understanding of the mechanisms underlying these relationships with the ultimate aim of abrogating specific steps, should lead to more targeted strategies for treatment of hormone-dependent breast cancer.

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Role of epidermal growth factor in the acquisition of ovarian steroid hormone responsiveness in the normal mouse mammary gland

Cited by 45 publications

References 30 publications

Integration of progesterone receptor action with rapid signaling events in breast cancer models

Integration of progesterone receptor action with rapid signaling events in breast cancer models

Temporally regulated overexpression of parathyroid hormone-related protein in the mammary gland reveals distinct fetal and pubertal phenotypes

Role of receptor complexes in the extranuclear actions of estrogen receptor α in breast cancer

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