Roles and regulation of Wnt signaling and β-catenin in prostate cancer
Abstract
The Wnt signaling pathway and its key component beta-catenin play critical roles in embryonic development as well as in human diseases, including various malignancies. Accumulated evidence has demonstrated a significant role for the Wnt pathway in the development and progression of human prostate cancer. The recent discovery of an interaction between beta-catenin and the androgen receptor (AR) suggests a possible mechanism of cross talk between Wnt and androgen signaling pathways. In this review, we summarize the recent progresses in this interesting and growing field. Particularly, we focus on the observation that the activation of the Wnt-mediated signal occurs in a different manner in prostate cancer than in colorectal cancer or other human malignancies. Since mutations in Adenomatous polyposis coli (APC), beta-catenin, and other components of the beta-catenin destruction complex are rare in prostate cancer cells, other regulatory mechanisms appear to play dominant roles in the activation of beta-catenin, such as loss or reduction of E-cadherin, a component of cell adhesion complex, and abnormal expression of Wnt ligands, receptors, inhibitors, and other co-regulators. Understanding the role and regulation of the Wnt signaling pathway in prostate cancer cells may help identify new targets for the prostate cancer therapy.
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When androgen ablation is utilized as a treatment, β-catenin is thought to shift away from the AR signaling pathway to participate in TCF4 signaling.
“When androgen ablation is utilized as a treatment, β-catenin is thought to shift away from the AR signaling pathway to participate in TCF4 signaling, and this could be a reason for relapse [23].”
From The FKBP52 Cochaperone Acts in Synergy with β-Catenin to Potentiate Androgen Receptor Signaling (2015) · cites this paper as [23]
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The FKBP52 Cochaperone Acts in Synergy with β-Catenin to Potentiate Androgen Receptor Signaling
Storer Samaniego, C., Suh, J. H., Chattopadhyay, A., Olivares, K., Guy, N., Sivils, J. C., Dey, P., Yumoto, F., Fletterick, R. J., Strom, A. M., et al. (2015) · PLOS One · doi:10.1371/journal.pone.0134015 · Cited by 13 · see citing works
- Authors
- Verras, M., & Sun, Z.
- Affiliations
- Stanford Medicine (US)
- Corresponding author
- Sun, Zijie
- ORCID
- Sun, Zijie
- Venue
- Cancer Letters
- Publisher
- Elsevier BV
- Published
- 2006-06
- Volume
- 237
- Issue
- 1
- Pages
- 22-32
- ISSN
- 0304-3835 (ISSN-L)
- OpenAlex
- W2139908319
- Cited by
- 180
- References
- 106
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 3 · 2023: 3 · 2022: 5 · 2021: 2 · 2020: 7 · 2019: 7 · 2018: 8 · 2017: 13 · 2016: 10 · 2015: 14 · 2014: 8 · 2013: 12 · 2012: 7
- FWCI
- 0.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (CA87767, CA-70297, R01CA087767, R01CA070297)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK061002, DK 61002, R56DK061002)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Hedgehog Signaling Pathway Studies
- Keywords
- Wnt signaling, β-catenin, prostate cancer, androgen receptor, E-cadherin, β-catenin destruction complex, APC mutation, Wnt ligands, Wnt receptors, Wnt inhibitors, cancer therapy targets
- MeSH terms
- Animals, Cell Transformation, Neoplastic, Humans, Male, Mutation, Prostatic Neoplasms, Receptors, Androgen, Signal Transduction, Cadherins, Cell Line, Tumor, Wnt Proteins, Frizzled Receptors, beta Catenin
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