PTEN Regulates Beta-Catenin in Androgen Signaling: Implication in Prostate Cancer Progression

摘要

The androgen-signaling pathway is essential in male sexual development and in normal and malignant prostate cell growth and survival. PI3K/Akt plays a critical role in prostate cancer cell growth and survival. Recent studies demonstrate that the effect of PI3K/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 the androgen receptor (AR) activity. However, the molecular mechanisms whereby PI3K/Akt and PTEN regulate the androgen pathway are currently unclear. During this funding year, we continue examining whether Beta-catenin is a major downstream effector or the PI3K/Akt and PTEN pathways in androgen-induced cell growth. Several sets or in vivo and in vitro experiments have been performed in this regard. The results suggest that the interactions between PI3K, Wnt, and androgen pathways are the key events in the tumorigenesis or prostate cancer.