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

J Biol Chem. 2009 Mar 13;284(11):6832-40. doi: 10.1074/jbc.M808988200. Epub 2009 Jan 5.


Androgen receptor (AR) plays a critical role in development and maintenance of male reproductive functions and the etiology of prostate cancer. As a ligand-regulated transcription factor, identification and characterization of AR coregulators are essential for understanding the molecular mechanisms underlying its diverse biological functions. Here we reported the identification of a novel AR coactivator, deleted in breast cancer 1 (DBC1), through a biochemical approach. DBC1 interacts with AR in a ligand-stimulated manner and facilitates AR transcriptional activation in transfected cells as well as in Xenopus oocytes. In in vitro gel shift experiments, recombinant DBC1 drastically enhanced AR DNA-binding activity. Expression of DBC1 also enhanced the binding of AR to chromatinized template in vivo, whereas knockdown of DBC1 impaired the binding of AR to endogenous prostate-specific antigen (PSA) gene in the prostate cancer cell line LNCaP. Thus, our data identify DBC1 as a novel AR coactivator.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Animals
  • Female
  • HeLa Cells
  • Humans
  • Male
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • Oocytes
  • Prostate-Specific Antigen / biosynthesis*
  • Prostate-Specific Antigen / genetics
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism*
  • Protein Binding
  • Receptors, Androgen / genetics
  • Receptors, Androgen / metabolism*
  • Response Elements*
  • Xenopus


  • AR protein, human
  • Adaptor Proteins, Signal Transducing
  • CCAR2 protein, human
  • Neoplasm Proteins
  • Receptors, Androgen
  • Prostate-Specific Antigen