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http://purl.uniprot.org/citations/25175604http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25175604http://www.w3.org/2000/01/rdf-schema#comment"

Background

Wnt/β-catenin signaling is important for prostate development and cancer in humans. Activation of this pathway in differentiated luminal cells of mice induces high-grade prostate intraepithelial neoplasia (HGPIN). Though the cell of origin of prostate cancer has yet to be conclusively identified, a castration-resistant Nkx3.1-expressing cell (CARN) may act as a cell of origin for prostate cancer.

Methods

To activate Wnt/β-catenin signaling in CARNs, we crossed mice carrying tamoxifen-inducible Nkx3.1-driven Cre to mice containing loxP sites in order to either conditionally knock out adenomatous polyposis coli (Apc) or constitutively activate β-catenin directly. We then castrated and hormonally regenerated these mice to target the CARN population.

Results

Loss of Apc in hormonally normal mice induced HGPIN; however, after one or more rounds of castration and hormonal regeneration, Apc-null CARNs disappeared. Alternatively, when β-catenin was constitutively activated under the same conditions, HGPIN was apparent.

Conclusion

Activation of Wnt/β-catenin signaling via Apc deletion is sufficient to produce HGPIN in hormonally normal mice. Loss of Apc may destabilize the CARN population under regeneration conditions. When β-catenin is constitutively activated, HGPIN occurs in hormonally regenerated mice. A second genetic hit is likely required to cause progression to carcinoma and metastasis."xsd:string
http://purl.uniprot.org/citations/25175604http://purl.org/dc/terms/identifier"doi:10.1002/pros.22868"xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/author"Yu X."xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/author"Williams B.O."xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/author"Matusik R.J."xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/author"De Marzo A.M."xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/author"Spiering T.J."xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/author"Valkenburg K.C."xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/name"Prostate"xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/pages"1506-1520"xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/title"Activation of Wnt/beta-catenin signaling in a subpopulation of murine prostate luminal epithelial cells induces high grade prostate intraepithelial neoplasia."xsd:string
http://purl.uniprot.org/citations/25175604http://purl.uniprot.org/core/volume"74"xsd:string
http://purl.uniprot.org/citations/25175604http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25175604
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