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Phenethyl isothiocyanate inhibits androgen receptor-regulated transcriptional activity in prostate cancer cells

Chunguang Yu1, Ai-Yu Gong, Dongqing Chen

  • 1Department of Medical Microbiology and Immunology, Creighton University Medical Center, Omaha, NE, USA; Department of Clinical Nursing, School of Nursing, Beijing University of Chinese Medicine, Beijing, P. R. China.

Molecular Nutrition & Food Research
|May 11, 2013
PubMed
Abstract

Insights

Phenethyl isothiocyanate (PEITC) inhibits prostate cancer (PCa) cell growth by downregulating p300/CBP-associated factor (PCAF) expression. This occurs via increased microRNA-17 (miR-17) transcription, suppressing PCAF and AR activity in PCa cells.

Area of Science:

  • Molecular Oncology
  • Cancer Biology
  • Epigenetics

Background:

  • Androgen receptor (AR) signaling drives prostate cancer (PCa) growth and progression.
  • Phenethyl isothiocyanate (PEITC), derived from glucosinolates, shows promise in reducing PCa risk and inhibiting PCa cell growth.
  • p300/CBP-associated factor (PCAF), an AR co-regulator, is upregulated in PCa via mir-17 gene suppression.

Purpose of the Study:

  • To investigate the effects of PEITC on PCAF expression in PCa cells.
  • To determine PEITC's impact on AR-regulated transcriptional activity.
  • To elucidate the role of the miR-17/PCAF axis in PEITC's anti-prostate cancer mechanisms.

Main Methods:

  • Utilized AR-responsive LNCaP cells to assess PEITC's effects.
  • Measured dihydrotestosterone-stimulated AR transcriptional activity and cell growth.
  • Analyzed PCAF expression, miR-17 transcription, and the impact of PCAF overexpression and miR-17 inhibition.

Main Results:

  • PEITC inhibited dihydrotestosterone-stimulated AR transcriptional activity and PCa cell growth.
  • Overexpression of PCAF partially reversed PEITC's inhibitory effects on AR activity.
  • PEITC treatment decreased PCAF expression and increased miR-17 transcription; miR-17 inhibition counteracted PCAF suppression.

Conclusions:

  • PEITC inhibits AR-regulated transcriptional activity and PCa cell growth.
  • The mechanism involves miR-17-mediated suppression of PCAF.
  • This study reveals a novel pathway for PEITC in modulating prostate cancer progression.
Keywords:
Androgen receptorPhenethyl isothiocyanateProstate cancermiR-17p300/CBP-associated factor

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