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Mol. Cells 2009; 28(3): 189-194

Published online August 20, 2009

https://doi.org/10.1007/s10059-009-0118-8

© The Korean Society for Molecular and Cellular Biology

Insulin-Like Growth Factor-I Induces Androgen
Receptor Activation in Differentiating C2C12
Skeletal Muscle Cells

Hye Jin Kim, and Won Jun Lee

Received: July 2, 2009; Revised: July 15, 2009; Accepted: July 16, 2009

Abstract

The modulating effect of IGF-I on the regulation of AR gene expression and activation in skeletal muscle cells remains poorly understood. In this study, the effects of IGF-I treatment on AR induction and activation in the absence of AR ligands were examined. Differentiating C2C12 cells were treated with different concentrations (0-250 ng/ml) of IGF-I or for various periods of time (0-60 min) of 250 ng/ml IGF-I. Treatment of C2C12 cells with IGF-I resulted in a dose- and time-dependent increase in total AR and phosphorylated AR (Ser 213). IGF-I treatment also led to significantly increased AR mRNA expression when compared with the control. The levels of skeletal α-actin and myogenin mRNA, known target genes of AR, were also significantly upregulated after 5 or 10 min of treatment with IGF-I. Confocal images revealed that IGF-I stimulated nuclear localization of AR in the absence of ligands. In addition, an electrophoretic mobility shift assay indicated that IGF-I stimulated the AR DNA binding activity in a time-dependent manner. The present results suggest that IGF-I stimulates the expression and activation of AR by ligand-independent mechanism in differentiating C2C12 mouse skeletal muscle cells.

Keywords androgen receptor, insulin-like growth factor-I, ligand-independent mechanism, skeletal muscle, steroid receptors

Article

Research Article

Mol. Cells 2009; 28(3): 189-194

Published online September 30, 2009 https://doi.org/10.1007/s10059-009-0118-8

Copyright © The Korean Society for Molecular and Cellular Biology.

Insulin-Like Growth Factor-I Induces Androgen
Receptor Activation in Differentiating C2C12
Skeletal Muscle Cells

Hye Jin Kim, and Won Jun Lee

Received: July 2, 2009; Revised: July 15, 2009; Accepted: July 16, 2009

Abstract

The modulating effect of IGF-I on the regulation of AR gene expression and activation in skeletal muscle cells remains poorly understood. In this study, the effects of IGF-I treatment on AR induction and activation in the absence of AR ligands were examined. Differentiating C2C12 cells were treated with different concentrations (0-250 ng/ml) of IGF-I or for various periods of time (0-60 min) of 250 ng/ml IGF-I. Treatment of C2C12 cells with IGF-I resulted in a dose- and time-dependent increase in total AR and phosphorylated AR (Ser 213). IGF-I treatment also led to significantly increased AR mRNA expression when compared with the control. The levels of skeletal α-actin and myogenin mRNA, known target genes of AR, were also significantly upregulated after 5 or 10 min of treatment with IGF-I. Confocal images revealed that IGF-I stimulated nuclear localization of AR in the absence of ligands. In addition, an electrophoretic mobility shift assay indicated that IGF-I stimulated the AR DNA binding activity in a time-dependent manner. The present results suggest that IGF-I stimulates the expression and activation of AR by ligand-independent mechanism in differentiating C2C12 mouse skeletal muscle cells.

Keywords: androgen receptor, insulin-like growth factor-I, ligand-independent mechanism, skeletal muscle, steroid receptors

Mol. Cells
Mar 31, 2023 Vol.46 No.3, pp. 131~189
COVER PICTURE
The physiologically important cytoprotective signaling in normal cells (background area in turquoise) mediated by NRF2 (blue chain) is often hijacked by cancer cells (red ball) in the tumor microenvironment (yellow area). However, the differential roles of NRF2 throughout the multistage carcinogenesis remains largely unresolved (white-colored overlapping misty areas).

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