The Role of Siah1-Induced Degradation of Beta-Catenin in Androgen Receptor Signaling

Abstract

The androgen receptor (AR) signaling-pathway plays crucial roles in the growth and progression of prostate cancer cells. Recent studies indicate that beta-Catenin physically binds to AR and enhances its transcriptional activity in a ligand dependent manner. p53 has also been implicated in AR signaling because of its ability to induce expression of Siah1, which hinds and activates E3 ligase complexes which degrade beta-Catenin. In this study, we demonstrated the biological significance and molecular mechanisms by which AR is regulated by the p53-induced Siah1 protein. Moreover, we identified the relevant proteins that are targeted for degradation by Siah1 besides beta-Catenin. Thus, enhanced Siah function may suppress the ability of androgen to promote tumor cell growth. Understanding more about the functions of Siah-family proteins may therefore suggest novel strategies for chemoprevention and for improved treatment of prostate cancer.

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Document Details

Document Type
Technical Report
Publication Date
Nov 01, 2006
Accession Number
ADA463208

Entities

People

  • Shu-ichi Matsuzawa

Organizations

  • Sanford Burnham Prebys Medical Discovery Institute

Tags

DTIC Thesaurus Topics

  • Androgen Receptors
  • Androgens
  • Biomedical Research
  • Cell Physiological Processes
  • Cells
  • Databases
  • Genetic Structures
  • Genetics
  • Genomic Instability
  • Lymphatic System
  • Lymphocytes
  • Neoplasms
  • Polymerase Chain Reaction
  • Prostate
  • Prostate Cancer
  • Proteins
  • Tissues

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics
  • Oncology

Technology Areas

  • Biotechnology