WNT5A selectively inhibits mouse ventral prostate development

Allgeier, Sarah H.; Lin, Tien-Min; Vezina, Chad M.; Moore, Robert W.; Fritz, Wayne A.; Chiu, Shing Yan; Zhang, ChuanLi; Peterson, Richard E.

doi:10.1016/j.ydbio.2008.08.018

Cited by 40 publications

(44 citation statements)

References 59 publications

(66 reference statements)

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“…7). This mechanism is consistent with previous reports of paracrine signaling for secreted ligands of the WNT (Allgeier et al, 2008;Huang et al, 2009;Joesting et al, 2008;Keil et al, 2012), FGF (Alarid et al, 1994;Donjacour et al, 2003;Sugimura et al, 1996;Thomson and Cunha, 1999) and TGFβ (Cancilla et al, 2001;Cook Fig. 6.…”

Section: Paracrine Signaling Between the Inductive Urm And Pre Duringsupporting

confidence: 93%

“…Outgrowth of the PrE is dictated by time-specific and cell-specific expression of morphogenetic genes (Prins and Putz, 2008;Thomson and Marker, 2006), including secreted signaling ligands of the hedgehog (Berman et al, 2004;Doles et al, 2006;Freestone et al, 2003;Lamm et al, 2002;Podlasek et al, 1999;Pu et al, 2004;Wang et al, 2003), Wnt (Allgeier et al, 2008;Huang et al, 2009;Joesting et al, 2008;Keil et al, 2012), FGF (Alarid et al, 1994;Donjacour et al, 2003;Sugimura et al, 1996;Thomson and Cunha, 1999) and TGFβ (Cancilla et al, 2001;Cook et al, 2007;Grishina et al, 2005;Itoh et al, 1998;Lamm et al, 2001;Tanji et al, 1994;Tomlinson et al, 2004) gene super-families. These morphogens are thought to communicate autocrine and paracrine signals through their cognate receptors and downstream signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

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RET-mediated glial cell line derived neurotrophic factor signaling inhibits mouse prostate development

Park

Bolton

2017

Development

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In humans and rodents, the prostate gland develops from the embryonic urogenital sinus (UGS). The androgen receptor (AR) is thought to control the expression of morphogenetic genes in inductive UGS mesenchyme, which promotes proliferation and cytodifferentiation of the prostatic epithelium. However, the nature of the AR-regulated morphogenetic genes and the mechanisms whereby AR controls prostate development are not understood. Glial cell line-derived neurotrophic factor (GDNF) binds GDNF family receptor α1 (GFRα1) and signals through activation of RET tyrosine kinase. Gene disruption studies in mice have revealed essential roles for GDNF signaling in development; however, its role in prostate development is unexplored. Here, we establish novel roles of GDNF signaling in mouse prostate development. Using an organ culture system for prostate development and Ret mutant mice, we demonstrate that RET-mediated GDNF signaling in UGS increases proliferation of mesenchyme cells and suppresses androgen-induced proliferation and differentiation of prostate epithelial cells, inhibiting prostate development. We also identify Ar as a GDNF-repressed gene and Gdnf and Gfrα1 as androgen-repressed genes in UGS, thus establishing reciprocal regulatory crosstalk between AR and GDNF signaling in prostate development.

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Section: Paracrine Signaling Between the Inductive Urm And Pre Duringsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

RET-mediated glial cell line derived neurotrophic factor signaling inhibits mouse prostate development

Park

Bolton

2017

Development

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“…Wnt5a mRNA is expressed at the distal tips and along the centro-distal periductal UGM during branching morphogenesis and is focally upregulated as buds emerge from anterior, dorsolateral and ventral UGS regions. Abnormal UGS morphology, bud patterns and decrease in prostatic bud number have been observed in Wnt5a null recombinant fetuses 45 . Prostate buds were decreased in Wnt5a-/-mice but this was secondary to testosterone deficiency as Wnt5a-/-UGS cultured in DHT grew normally.…”

Section: Role Of Wnt Signaling In Prostate Developmentmentioning

confidence: 99%

WNT Signaling in Prostate Development and Carcinogenesis

Kharaishvili¹,

Simkova²,

Makharoblidze³

et al. 2011

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. The Wnt signaling pathway is crucial for cell fate decisions, stem cell renewal, regulation of cell proliferation and differentiation. Deregulated Wnt signaling is also implicated in a number of hereditary and degenerative diseases and cancer.Methods and results. This review highlights the role of the Wnt pathway in the regulation of stem/progenitor cell renewal and prostate gland development and how this signaling is altered in prostate cancer. Recent evidence suggests that Wnt signaling regulates androgen activity in prostate cancer cells, enhances androgen receptor expression and promotes the growth of prostate cancer even after androgen ablation therapy. There is also strong evidence that Wnt signaling is enhanced in androgen-ablation resistant tumors and bone metastases.Conclusions. Further study of the modulators of this pathway will be of therapeutic relevance as inhibition of Wnt signaling may have the potential to reduce the self-renewal and aggressive behaviour of prostate cancer while Wnt signaling activation might enhance stem cell activity when tissue regeneration is required.

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“…Wnt5a-knockout mice have a variety of phenotypes, including skeletal defects (Yamaguchi et al, 1999) and multiple defects associated with internal organs (Allgeier et al, 2008;Andersson et al, 2008;Cervantes et al, 2009;Cha et al, 2004;He et al, 2008;Kim et al, 2005;Li et al, 2002;Qian et al, 2007;Roarty et al, 2009;Tai et al, 2009). Interestingly, the phenotype of Rorknockout mice resembles that of Wnt5a-knockout mice.…”

Section: Introductionmentioning

confidence: 99%

Wnt5a can both activate and repress Wnt/β-catenin signaling during mouse embryonic development

Amerongen

Fuerer

Mizutani

et al. 2012

Developmental Biology

194

142

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Embryonic development is controlled by a small set of signal transduction pathways, with vastly different phenotypic outcomes depending on the time and place of their recruitment. How the same molecular machinery can elicit such specific and distinct responses, remains one of the outstanding questions in developmental biology. Part of the answer may lie in the high inherent genetic complexity of these signaling cascades, as observed for the Wnt-pathway. The mammalian genome encodes multiple Wnt proteins and receptors, each of which show dynamic and tightly controlled expression patterns in the embryo. Yet how these components interact in the context of the whole organism remains unknown. Here we report the generation of a novel, inducible transgenic mouse model that allows spatiotemporal control over the expression of Wnt5a, a protein implicated in many developmental processes and multiple Wnt-signaling responses. We show that ectopic Wnt5a expression from E10.5 onwards results in a variety of developmental defects, including loss of hair follicles and reduced bone formation in the skull. Moreover, we find that Wnt5a can have dual signaling activities during mouse embryonic development. Specifically, Wnt5a is capable of both inducing and repressing β-catenin/TCF signaling in vivo, depending on the time and site of expression and the receptors expressed by receiving cells. These experiments show for the first time that a single mammalian Wnt protein can have multiple signaling activities in vivo, thereby furthering our understanding of how signaling specificity is achieved in a complex developmental context.

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WNT5A selectively inhibits mouse ventral prostate development

Cited by 40 publications

References 59 publications

RET-mediated glial cell line derived neurotrophic factor signaling inhibits mouse prostate development

RET-mediated glial cell line derived neurotrophic factor signaling inhibits mouse prostate development

WNT Signaling in Prostate Development and Carcinogenesis

Wnt5a can both activate and repress Wnt/β-catenin signaling during mouse embryonic development

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