SMILE upregulated by metformin inhibits the function of androgen receptor in prostate cancer cells

Highlights • Metformin reduces the androgen-dependent growth of prostate cancer cells and the expression of endogenous AR target genes. • Metformin induces SMILE expression in prostate cancer cells, of which knockdown with shRNA abolished the inhibitory effect of metformin on AR function. • SMILE su...

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Veröffentlicht in:	Cancer letters 2014-11, Vol.354 (2), p.390-397
Hauptverfasser:	Lee, Seung-Yon, Song, Chin-Hee, Xie, Yuan-Bin, Jung, Chaeyong, Choi, Hueng-Sik, Lee, Keesook
Format:	Artikel
Sprache:	eng
Schlagworte:	Androgen receptor Androgens Animals Apoptosis Basic-Leucine Zipper Transcription Factors - biosynthesis Basic-Leucine Zipper Transcription Factors - genetics Basic-Leucine Zipper Transcription Factors - metabolism Cell cycle Cell growth Cell Growth Processes - drug effects Cell Growth Processes - physiology Cell Line, Tumor Competition Corepressor Deoxyribonucleic acid Diabetes DNA HEK293 Cells Hematology, Oncology and Palliative Medicine Herpes viruses Humans Kinases Ligands Male Metformin Metformin - pharmacology Mice Neoplasms, Hormone-Dependent - drug therapy Neoplasms, Hormone-Dependent - genetics Neoplasms, Hormone-Dependent - metabolism Plasmids Prostate cancer Prostate cancer cells Prostatic Neoplasms - drug therapy Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Proteins Receptors, Androgen - genetics Receptors, Androgen - metabolism SMILE Studies Transcriptional Activation Tumors Up-Regulation - drug effects
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Beschreibung
Zusammenfassung:	Highlights • Metformin reduces the androgen-dependent growth of prostate cancer cells and the expression of endogenous AR target genes. • Metformin induces SMILE expression in prostate cancer cells, of which knockdown with shRNA abolished the inhibitory effect of metformin on AR function. • SMILE suppresses AR transactivation through physical interaction with AR. • SMILE inhibits the expression of AR target genes and the androgen-dependent growth of prostate cancer cells.
ISSN:	0304-3835 1872-7980
DOI:	10.1016/j.canlet.2014.09.001