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Androgen regulates Cdc6 transcription through interactions between androgen receptor and E2F transcription factor in

Ipsita Mallik1, Monica Davila, Tenekua Tapia

  • 1Department of Molecular Biology and Microbiology, Burnett School of Biomedical Sciences, University of Central Florida, USA.

Biochimica Et Biophysica Acta
|June 11, 2008
PubMed

Insights

Androgen receptor (AR) regulates Cdc6 expression in prostate cancer. Androgen stimulation increases Cdc6 transcription via AR interaction with the promoter and E2F transcription factors.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Androgen receptor (AR) is crucial in prostate cancer development and maintenance.
  • Cdc6, a DNA replication regulator, is downregulated in androgen-insensitive prostate cancer cells.

Purpose of the Study:

  • To investigate the role of androgen and AR in regulating Cdc6 expression.
  • To elucidate the molecular mechanisms underlying AR-mediated Cdc6 regulation.

Main Methods:

  • Studied Cdc6 expression in xenograft tumors and prostate cancer cells following androgen treatment.
  • Analyzed AR interaction with the Cdc6 promoter's Androgen Response Element (ARE) and E2F binding sites.
  • Assessed changes in nuclear E2F1, E2F3, and retinoblastoma protein (pRb) levels.
  • Performed DNA-protein interaction assays to evaluate E2F binding to the Cdc6 promoter.

Main Results:

  • Androgen treatment stimulated Cdc6 expression and transcription in prostate cancer models.
  • AR interacted with the Cdc6 promoter's ARE, and intact E2F binding sites were essential for androgen's stimulatory effect.
  • Androgen altered nuclear availability of E2F1 and E2F3 and increased hypophosphorylated pRb.
  • AR interacted with E2F transcription factors in a ligand-independent manner, with ligand-bound AR showing reduced interaction efficiency.

Conclusions:

  • AR regulates Cdc6 transcription through direct interaction with the Cdc6 promoter.
  • AR forms complexes with E2F1 and E2F3 in a differential manner to control Cdc6 expression.
  • These findings reveal a novel regulatory pathway for Cdc6 in prostate cancer.

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