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

Chunguang Yu, Ai Yu Gong, Dongqing Chen, Daniel Solelo Leon, Charles Yf Young, Xian-Ming Chen

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Scope: Androgen receptor (AR) signaling is critical for all aspects of prostate growth and tumorigenesis. The glucosinolate-derived phenethyl isothiocyanate (PEITC) has recently been demonstrated to reduce the risk of prostate cancer (PCa) and inhibit PCa cell growth. We previously reported that p300/CBP-associated factor (PCAF), a co-regulator for AR, is upregulated in PCa cells through suppression of the mir-17 gene. Here, we assessed the effects of PEITC on PCAF expression and AR-regulated transcriptional activity in PCa cells. Methods and results: Using AR-responsive LNCaP cells, we observed the inhibitory effects of PEITC on the dihydrotestosterone-stimulated AR transcriptional activity and cell growth of PCa cells. Interestingly, overexpression of PCAF attenuated the inhibitory effects of PEITC on dihydrotestosterone-stimulated AR transcriptional activity. Expression of PCAF was upregulated in PCa cells through suppression of miR-17. PEITC treatment significantly decreased PCAF expression and promoted transcription of miR-17 in LNCaP cells. Functional inhibition of miR-17 attenuated the suppression of PCAF in cells treated by PEITC. Conclusion: Our results indicate that PEITC inhibits AR-regulated transcriptional activity and cell growth of PCa cells through miR-17-mediated suppression of PCAF, suggesting a new mechanism by which PEITC modulates PCa cell growth.

Original languageEnglish
Pages (from-to)1825-1833
Number of pages9
JournalMolecular Nutrition and Food Research
Volume57
Issue number10
DOIs
StatePublished - Oct 2013

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isothiocyanates
Androgen Receptors
prostatic neoplasms
Prostatic Neoplasms
cell growth
Growth
Dihydrotestosterone
neoplasm cells
androgen receptors
p300-CBP-associated factor
phenethyl isothiocyanate
cells
glucosinolates
carcinogenesis
Glucosinolates
transcription (genetics)
Prostate
Carcinogenesis

All Science Journal Classification (ASJC) codes

  • Food Science
  • Biotechnology

Cite this

Phenethyl isothiocyanate inhibits androgen receptor-regulated transcriptional activity in prostate cancer cells through suppressing PCAF. / Yu, Chunguang; Gong, Ai Yu; Chen, Dongqing; Solelo Leon, Daniel; Young, Charles Yf; Chen, Xian-Ming.

In: Molecular Nutrition and Food Research, Vol. 57, No. 10, 10.2013, p. 1825-1833.

Research output: Contribution to journalArticle

Yu, Chunguang ; Gong, Ai Yu ; Chen, Dongqing ; Solelo Leon, Daniel ; Young, Charles Yf ; Chen, Xian-Ming. / Phenethyl isothiocyanate inhibits androgen receptor-regulated transcriptional activity in prostate cancer cells through suppressing PCAF. In: Molecular Nutrition and Food Research. 2013 ; Vol. 57, No. 10. pp. 1825-1833.
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abstract = "Scope: Androgen receptor (AR) signaling is critical for all aspects of prostate growth and tumorigenesis. The glucosinolate-derived phenethyl isothiocyanate (PEITC) has recently been demonstrated to reduce the risk of prostate cancer (PCa) and inhibit PCa cell growth. We previously reported that p300/CBP-associated factor (PCAF), a co-regulator for AR, is upregulated in PCa cells through suppression of the mir-17 gene. Here, we assessed the effects of PEITC on PCAF expression and AR-regulated transcriptional activity in PCa cells. Methods and results: Using AR-responsive LNCaP cells, we observed the inhibitory effects of PEITC on the dihydrotestosterone-stimulated AR transcriptional activity and cell growth of PCa cells. Interestingly, overexpression of PCAF attenuated the inhibitory effects of PEITC on dihydrotestosterone-stimulated AR transcriptional activity. Expression of PCAF was upregulated in PCa cells through suppression of miR-17. PEITC treatment significantly decreased PCAF expression and promoted transcription of miR-17 in LNCaP cells. Functional inhibition of miR-17 attenuated the suppression of PCAF in cells treated by PEITC. Conclusion: Our results indicate that PEITC inhibits AR-regulated transcriptional activity and cell growth of PCa cells through miR-17-mediated suppression of PCAF, suggesting a new mechanism by which PEITC modulates PCa cell growth.",
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