IGF Ligand and Receptor Regulation of Mammary Development

Rowzee, Anne; Lazzarino, Deborah A.; Rota, Lauren; Sun, Zhaoyu; Wood, Teresa L.

doi:10.1007/s10911-008-9102-8

Cited by 35 publications

(22 citation statements)

References 86 publications

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“…On one hand, the estrogen-ER signaling stimulates the local synthesis of Igf-1 [50], [55]; while on the other hand, ER transcriptional activity can be induced by the Igf-1 signaling in an estrogen-independent manner [52], [54]. Igf-1 is essential for TEB formation and ductal morphogenesis in pubertal mammary gland [34], [56]. The Myc protein is a well established stimulator of cell proliferation, differentiation and apoptosis [57].…”

Section: Discussionmentioning

confidence: 99%

Atbf1 Regulates Pubertal Mammary Gland Development Likely by Inhibiting the Pro-Proliferative Function of Estrogen-ER Signaling

et al. 2012

PLoS ONE

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ATBF1 is a candidate tumor suppressor that interacts with estrogen receptor (ER) to inhibit the function of estrogen-ER signaling in gene regulation and cell proliferation control in human breast cancer cells. We therefore tested whether Atbf1 and its interaction with ER modulate the development of pubertal mammary gland, where estrogen is the predominant steroid hormone. In an in vitro model of cell differentiation, i.e., MCF10A cells cultured in Matrigel, ATBF1 expression was significantly increased, and knockdown of ATBF1 inhibited acinus formation. During mouse mammary gland development, Atbf1 was expressed at varying levels at different stages, with higher levels during puberty, lower during pregnancy, and the highest during lactation. Knockout of Atbf1 at the onset of puberty enhanced ductal elongation and bifurcation and promoted cell proliferation in both ducts and terminal end buds of pubertal mammary glands. Enhanced cell proliferation primarily occurred in ER-positive cells and was accompanied by increased expression of ER target genes. Furthermore, inactivation of Atbf1 reduced the expression of basal cell markers (CK5, CK14 and CD44) but not luminal cell markers. These findings indicate that Atbf1 plays a role in the development of pubertal mammary gland likely by modulating the function of estrogen-ER signaling in luminal cells and by modulating gene expression in basal cells.

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Section: Discussionmentioning

confidence: 99%

Atbf1 Regulates Pubertal Mammary Gland Development Likely by Inhibiting the Pro-Proliferative Function of Estrogen-ER Signaling

et al. 2012

PLoS ONE

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“…It should be noted that these two models are not mutually exclusive, as a regulatory feedback loop would be possible if both hypotheses are correct. Furthermore, IGF receptor plays important roles in both mammary development (53, 54) and tumorigenesis (55), and cross regulation between ER and IGFR signaling pathways has been demonstrated (30, 56). …”

Section: Discussionmentioning

confidence: 99%

AKT regulates BRCA1 stability in response to hormone signaling

Nelson

Lyons

Young

et al. 2010

Molecular and Cellular Endocrinology

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BRCA1, with its binding partner BARD1, regulates the cellular response to DNA damage in multiple tissues, yet inherited mutations within BRCA1 result specifically in breast and ovarian cancers. This observation, along with several other lines of evidence, suggests a functional relationship may exist between hormone signaling and BRCA1 function. Our data demonstrates that AKT activation promotes the expression of BRCA1 in response to estrogen and IGF-1 receptor signaling. Further, we have identified a novel AKT phosphorylation site in BRCA1 at S694 which is responsive to activation of these signaling pathways. This rapid increase in BRCA1 protein levels appears to occur independently of new protein synthesis and treatment with the clinically utilized proteasome inhibitor bortezomib similarly leads to a rapid increase in BRCA1 protein levels. Together, these data suggest that AKT phosphorylation of BRCA1 increases total protein expression by preventing proteasomal degradation. AKT activation also appears to support nuclear localization of BRCA1, and co-expression of activated AKT with BRCA1 decreases radiation sensitivity, suggesting this interaction has functional consequences for BRCA1's role in DNA repair. We conclude that AKT regulates BRCA1 protein stability and function through direct phosphorylation of BRCA1. Further, the responsiveness of the AKT-BRCA1 regulatory pathway to hormone signaling may, in part, underlie the tissue specificity of BRCA1 mutant This is an un

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“…Indeed, in the absence of pituitary hormones little or no mammogenic activity could be recorded (Lamote et al, 2004). Growth factors have been shown to modulate mammary cell survival (epidermal growth factor, amphiregulin, insulin like growth factor, erythropoietin (EPO), tumor necrosis factor-a) (Hynes and Watson, 2010, Pelekanou et al, 2010, Rowzee et al, 2008, Varela and Ip, 1996 or apoptosis (tumor necrosis factor-a, transforming growth factor b) (Rosfjord andDickson, 1999, Varela andIp, 1996). However, the molecular mechanism underlying the influence of sex steroid hormones and/or growth factors remains largely undetermined.…”

Section: Cross-talk Mechanisms Between Er and Signal Transduction Undmentioning

confidence: 99%

Recent insights into the effect of natural and environmental estrogens on mammary development and carcinogenesis

Pelekanou¹,

Leclercq²

2011

Int. J. Dev. Biol.

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The present �or� revie�s recent � ndings related to the action of steroidal �physiolo�The present �or� revie�s recent �ndings related to the action of steroidal �physiolo� gical) estrogens on normal mammary gland development and carcinogenesis, as �ell as effects of related environmental mediators �phyto� and xeno�estrogens), the role of �hich remains controver� sial. Orchestration by estrogen receptors �i.e. ERa and ERb) and coregulators of gro�th, apoptosis and differentiation of epithelial cells, directed our analysis. The bidirectional coordination bet�een epithelium and stroma in parallel �ith maintenance of stemness are also investigated. The rele� vance of nuclear and extranuclear localization of ERs and other eventual estrogen binding sites, mediating differential actions in regard to these various topics, is critically addressed to delineate the importance of direct and indirect activation procedures and delicate feedbac� loops �ligand� induced or/and cross�tal� activation, respectively). The inclusion of the outlined regulatory concepts in drug design programs for the prevention and treatment of breast cancer may have potent effects.

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IGF Ligand and Receptor Regulation of Mammary Development

Cited by 35 publications

References 86 publications

Atbf1 Regulates Pubertal Mammary Gland Development Likely by Inhibiting the Pro-Proliferative Function of Estrogen-ER Signaling

Atbf1 Regulates Pubertal Mammary Gland Development Likely by Inhibiting the Pro-Proliferative Function of Estrogen-ER Signaling

AKT regulates BRCA1 stability in response to hormone signaling

Recent insights into the effect of natural and environmental estrogens on mammary development and carcinogenesis

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