Transcriptional activity of c-Jun is critical for the suppression of AR function

Mol Cell Endocrinol. 2013 Jun 15;372(1-2):12-22. doi: 10.1016/j.mce.2013.03.004. Epub 2013 Mar 21.

Abstract

Androgen receptor (AR) signaling plays a pivotal role in growth and survival of prostate cancer cells. c-Jun is an important member of the activator protein 1 (AP-1) family and was shown to interact with AR. However, the role of c-Jun in AR signaling remains controversial, with being a coactivator or a corepressor reported. Here, utilizing multiple approaches, we show that c-Jun efficiently inhibits AR activity and the growth of prostate cancer cells. Overexpression of c-Jun inhibits not only the activities of various androgen-responsive promoters but also the transcripts of multiple AR target genes. Interestingly, long-term c-Jun overexpression also down-regulates AR expression at both the protein and mRNA levels. Molecular analysis suggests that c-Jun inhibits AR transactivation potential via an unknown target gene. The inhibition of AR by c-Jun occurs in both hormone naïve and castration-resistant prostate cancer cells. Our results unravel a novel mechanism by which c-Jun antagonizes the AR signaling.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • COS Cells
  • Cell Line, Tumor
  • Cell Proliferation
  • Chlorocebus aethiops
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Promoter Regions, Genetic
  • Prostatic Neoplasms
  • Proto-Oncogene Proteins c-jun / physiology*
  • Receptors, Androgen / genetics
  • Receptors, Androgen / metabolism*
  • Signal Transduction
  • Transcription, Genetic*
  • Transcriptional Activation

Substances

  • Proto-Oncogene Proteins c-jun
  • Receptors, Androgen