Protein Inhibitor of Activated STAT3 Regulates Androgen Receptor Signaling in Prostate Carcinoma Cells

Protein inhibitor of activated STAT3 (PIAS3) is a specific inhibitor of signal transducer and activator of transcription 3 (STAT3). PIAS3 binds to STAT3 and inhibits its DNA-binding activity, and thereby STAT3-mediated gene activation. PIAS1, another member of the PIAS family, was recently shown to...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2000-11, Vol.278 (1), p.9-13
Main Authors: Junicho, Akira, Matsuda, Tadashi, Yamamoto, Tetsuya, Kishi, Hiroyuki, Korkmaz, Kemal, Saatcioglu, Fahri, Fuse, Hideki, Muraguchi, Atsushi
Format: Article
Language:English
Subjects:
androgen receptor (AR)
Blotting, Northern
Blotting, Western
Carrier Proteins - biosynthesis
Carrier Proteins - metabolism
Cell Line
cofactor
Dihydrotestosterone - pharmacology
DNA - metabolism
DNA-Binding Proteins - antagonists & inhibitors
DNA-Binding Proteins - metabolism
Gene Expression Regulation - drug effects
Genes, Reporter
Humans
Luciferases - metabolism
Male
PIAS3 protein
Precipitin Tests
prostate carcinoma
Prostatic Neoplasms - metabolism
protein inhibitor of activated STAT3 (PIAS3)
Receptors, Androgen - metabolism
Signal Transduction
STAT3 Transcription Factor
Time Factors
Trans-Activators - antagonists & inhibitors
Trans-Activators - metabolism
Transcription, Genetic - drug effects
Transcriptional Activation
Tumor Cells, Cultured
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Summary:Protein inhibitor of activated STAT3 (PIAS3) is a specific inhibitor of signal transducer and activator of transcription 3 (STAT3). PIAS3 binds to STAT3 and inhibits its DNA-binding activity, and thereby STAT3-mediated gene activation. PIAS1, another member of the PIAS family, was recently shown to interact with the androgen receptor (AR), a nuclear hormone receptor that has an important role in both physiological and pathological processes, and acts as a cofactor for AR. Here we demonstrate that PIAS3 is expressed in prostate cancer cells and its expression is induced in response to dihydrotestosterone (DHT) treatment. Ectopic overexpression of PIAS3 suppressed AR-mediated gene activation induced by DHT-stimulation in LNCaP cells. We provide evidence that these activities were due to direct physical interactions between PIAS3 and AR. These results indicate that PIAS3 acts as a coregulator of AR signaling pathway in prostate cancer cells.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.2000.3753