Effects of Ca ++ mobilization on expression of androgen-regulated genes

Interference with androgen receptor-mediated transactivation by AP-I proteins

Patricia E. Murtha, Wen Zhu, Jianye Zhang, Shaobo Zhang, Charles Y.F. Young

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

BACKGROUND. The adult prostate is maintained through an equilibrium between cell growth and death rates. Androgen deprivation induces an increase in intracellular Ca ++ , AP-1 gene expression of androgen-inducible genes. METHODS. Northern blot analysis, band-shift assays, and transient cotransfection essays were used to study the effects of Ca ++ mobilizer A23187 on gene expression in human prostate cancer cells. RESULTS. A23187 repressed androgen-upregulated mRNAs for prostate-specific antigen (PSA) and hKLK2, and rapidly induced mRNA levels for c-fos and c-jun. AP-1 protein-DNA binding activities were elevated after A23187 treatments. Androgen receptor (AR)-mediated induction of chloramphenicol acetyltransferase (CAT) reporter was repressed by AP-1 proteins. CONCLUSIONS. The repression of AR-mediated induction of PSA and hKLK2 genes by Ca ++ mobilizers is due to the interference of AR transactivation activity by AP-1 proteins.

Original languageEnglish (US)
Pages (from-to)264-270
Number of pages7
JournalProstate
Volume33
Issue number4
DOIs
StatePublished - Dec 1 1997
Externally publishedYes

Fingerprint

Transcription Factor AP-1
Androgen Receptors
Transcriptional Activation
Androgens
Calcimycin
Prostate-Specific Antigen
Genes
Proteins
Gene Expression
Messenger RNA
Chloramphenicol O-Acetyltransferase
DNA-Binding Proteins
Northern Blotting
Prostate
Prostatic Neoplasms
Cell Death
Mortality
Growth

Keywords

  • C-jun
  • C-los
  • HKLK2
  • Prostate
  • PSA

ASJC Scopus subject areas

  • Oncology
  • Urology

Cite this

Effects of Ca ++ mobilization on expression of androgen-regulated genes : Interference with androgen receptor-mediated transactivation by AP-I proteins. / Murtha, Patricia E.; Zhu, Wen; Zhang, Jianye; Zhang, Shaobo; Young, Charles Y.F.

In: Prostate, Vol. 33, No. 4, 01.12.1997, p. 264-270.

Research output: Contribution to journalArticle

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AU - Zhu, Wen

AU - Zhang, Jianye

AU - Zhang, Shaobo

AU - Young, Charles Y.F.

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N2 - BACKGROUND. The adult prostate is maintained through an equilibrium between cell growth and death rates. Androgen deprivation induces an increase in intracellular Ca ++ , AP-1 gene expression of androgen-inducible genes. METHODS. Northern blot analysis, band-shift assays, and transient cotransfection essays were used to study the effects of Ca ++ mobilizer A23187 on gene expression in human prostate cancer cells. RESULTS. A23187 repressed androgen-upregulated mRNAs for prostate-specific antigen (PSA) and hKLK2, and rapidly induced mRNA levels for c-fos and c-jun. AP-1 protein-DNA binding activities were elevated after A23187 treatments. Androgen receptor (AR)-mediated induction of chloramphenicol acetyltransferase (CAT) reporter was repressed by AP-1 proteins. CONCLUSIONS. The repression of AR-mediated induction of PSA and hKLK2 genes by Ca ++ mobilizers is due to the interference of AR transactivation activity by AP-1 proteins.

AB - BACKGROUND. The adult prostate is maintained through an equilibrium between cell growth and death rates. Androgen deprivation induces an increase in intracellular Ca ++ , AP-1 gene expression of androgen-inducible genes. METHODS. Northern blot analysis, band-shift assays, and transient cotransfection essays were used to study the effects of Ca ++ mobilizer A23187 on gene expression in human prostate cancer cells. RESULTS. A23187 repressed androgen-upregulated mRNAs for prostate-specific antigen (PSA) and hKLK2, and rapidly induced mRNA levels for c-fos and c-jun. AP-1 protein-DNA binding activities were elevated after A23187 treatments. Androgen receptor (AR)-mediated induction of chloramphenicol acetyltransferase (CAT) reporter was repressed by AP-1 proteins. CONCLUSIONS. The repression of AR-mediated induction of PSA and hKLK2 genes by Ca ++ mobilizers is due to the interference of AR transactivation activity by AP-1 proteins.

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