PTEN Regulates Beta-Catenin in Androgen Signaling: Implication in Prostate Cancer Progression
Abstract
Observations from androgen ablation treatment of prostate cancer have shown that the androgen-signaling pathway is important in the growth and progression of prostate cancer. The growth-promoting effects of androgen are mediated mostly through the androgen receptor (AR). P13K/Akt plays a critical role in prostate cancer cell growth and survival. It has been shown that the effect of P13K/Akt in prostate cells is mediated through androgen signaling. The PI3K inhibitor, LY294002, and a tumor suppressor, PTEN, negatively regulate the PI3K/Akt pathway and repress AR activity. However, the molecular mechanisms whereby P13K/Akt and PTEN regulate the androgen pathway are currently unclear. In this study, we will use several biological relevant experiments to test whether beta-catenin, an AR coactivator, is a major downstream effector of the PI3K/Akt and PTEN pathways in androgen-mediated prostate cell growth and survival. Successful completion of the proposed study should provide fresh insight into the pathogenesis of prostate cancer that may help us to identify new pathways that can be targeted for prostate cancer treatment.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 01, 2004
- Accession Number
- ADA425958
Entities
People
- Zijie Sun
Organizations
- Stanford University