Abstract
Canonical Wnt signaling has emerged as an important pathway that underlies the initiation of prostate cancer. Both human cancers and mouse models have confirmed that mutations or altered expression of components of this pathway are associated with prostate tumors. Additionally, several reports suggest that this pathway plays a key role in the establishment of skeletal metastasis. This review discusses our current knowledge of the Wnt signaling pathway in the development of prostate cancer. First, we will overview the Wnt signaling pathway to provide background for the rest of the discussion. We will then review the literature on the role of this pathway and the downstream effector, β-catenin, in the development and progression of prostate cancer and skeletal metastasis. We will also discuss reports that suggest that β-- catenin can directly interact with the androgen receptor to modulate its activity. These recent developments may provide insight into how tumor growth can be achieved under androgen deprivation. Finally, we speculate on how the pathway may be targeted for therapeutic treatment and what agents may be available to achieve this goal.
Current Drug Targets
Title: Wnt Signaling and Prostate Cancer
Volume: 9 Issue: 7
Author(s): Daniel R. Robinson, Cassandra R. Zylstra and Bart O. Williams
Affiliation:
Abstract: Canonical Wnt signaling has emerged as an important pathway that underlies the initiation of prostate cancer. Both human cancers and mouse models have confirmed that mutations or altered expression of components of this pathway are associated with prostate tumors. Additionally, several reports suggest that this pathway plays a key role in the establishment of skeletal metastasis. This review discusses our current knowledge of the Wnt signaling pathway in the development of prostate cancer. First, we will overview the Wnt signaling pathway to provide background for the rest of the discussion. We will then review the literature on the role of this pathway and the downstream effector, β-catenin, in the development and progression of prostate cancer and skeletal metastasis. We will also discuss reports that suggest that β-- catenin can directly interact with the androgen receptor to modulate its activity. These recent developments may provide insight into how tumor growth can be achieved under androgen deprivation. Finally, we speculate on how the pathway may be targeted for therapeutic treatment and what agents may be available to achieve this goal.
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Cite this article as:
Robinson R. Daniel, Zylstra R. Cassandra and Williams O. Bart, Wnt Signaling and Prostate Cancer, Current Drug Targets 2008; 9 (7) . https://dx.doi.org/10.2174/138945008784911831
DOI https://dx.doi.org/10.2174/138945008784911831 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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