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Deleted in breast cancer 1, a novel androgen receptor (AR) coactivator that promotes AR DNA-binding activity

Junjiang Fu1, Jun Jiang, Jiwen Li

  • 1The Institute of Biomedical Sciences, College of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai 200241, China.

The Journal of Biological Chemistry
|January 8, 2009
PubMed

Insights

Researchers discovered deleted in breast cancer 1 (DBC1) as a novel coactivator for the androgen receptor (AR). DBC1 enhances AR

Area of Science:

  • Molecular Biology
  • Endocrinology
  • Cancer Research

Background:

  • The androgen receptor (AR) is crucial for male reproductive functions and prostate cancer development.
  • Understanding AR molecular mechanisms requires identifying its coregulators.
  • AR functions as a ligand-regulated transcription factor.

Purpose of the Study:

  • To identify and characterize novel coregulators of the androgen receptor.
  • To investigate the role of deleted in breast cancer 1 (DBC1) as an AR coactivator.

Main Methods:

  • Biochemical approaches were used for identification.
  • Interaction studies in transfected cells and Xenopus oocytes.
  • In vitro gel shift assays and in vivo chromatin binding experiments.
  • Knockdown studies in LNCaP prostate cancer cells.

Main Results:

  • Deleted in breast cancer 1 (DBC1) was identified as a novel AR coactivator.
  • DBC1 interacts with AR in a ligand-dependent manner.
  • DBC1 enhances AR transcriptional activity and DNA-binding.
  • DBC1 facilitates AR binding to the prostate-specific antigen (PSA) gene promoter.

Conclusions:

  • DBC1 is a novel coactivator that modulates androgen receptor activity.
  • DBC1 plays a significant role in AR-mediated gene regulation, including the PSA gene.
  • DBC1 represents a potential therapeutic target in prostate cancer.

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