ArticleThe Prostate2014
Activation of Wnt/β-catenin signaling in a subpopulation of murine prostate luminal epithelial cells induces high grade prostate intraepithelial neoplasia.
Article in The Prostate, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Diverse landscape of genetically engineered mouse models: Genomic and molecular insights into prostate cancer.Cancer letters · 2024Review
- Paracrine Wnt signaling is necessary for prostate epithelial proliferation.The Prostate · 2022Article
- Exploring the Wnt Pathway as a Therapeutic Target for Prostate Cancer.Biomolecules · 2022Review
- miR-425-5p suppresses tumorigenesis and DDP resistance in human-prostate cancer by targeting GSK3β and inactivating the Wnt/β-catenin signaling pathway.Journal of biosciences · 2019Article
- Interplay Between SOX9, Wnt/β-Catenin and Androgen Receptor Signaling in Castration-Resistant Prostate Cancer.International journal of molecular sciences · 2019Review
- Genetically Engineered Mouse Models of Prostate Cancer in the Postgenomic Era.Cold Spring Harbor perspectives in medicine · 2019Review
- Article
- Somatic Mutations in Prostate Cancer: Closer to Personalized Medicine.Molecular diagnosis & therapy · 2017Review
- Dissecting major signaling pathways in prostate cancer development and progression: Mechanisms and novel therapeutic targets.The Journal of steroid biochemistry and molecular biology · 2017Review
- Type II transmembrane serine proteases as potential targets for cancer therapy.Biological chemistry · 2016Review
- Murine Prostate Micro-dissection and Surgical Castration.Journal of visualized experiments : JoVE · 2016Article
- Drug discovery in prostate cancer mouse models.Expert opinion on drug discovery · 2015Review
- Mini-review: Does Notch promote or suppress cancer? New findings and old controversies.American journal of clinical and experimental urology · 2015Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundWnt/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.
methodsTo 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.
resultsLoss 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.
conclusionActivation 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.
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