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Mol. Cells 2009; 28(6): 589-593

Published online November 19, 2009

https://doi.org/10.1007/s10059-009-0167-z

© The Korean Society for Molecular and Cellular Biology

Ligand-Independent Activation of the Androgen
Receptor by Insulin-Like Growth Factor-I and the
Role of the MAPK Pathway in Skeletal Muscle Cells

Hye Jin Kim, and Won Jun Lee

Received: September 29, 2009; Accepted: October 19, 2009

Abstract

In this study, the roles of the p38 MAPK, ERK1/2 and JNK signaling pathway in IGF-I-induced AR induction and activation were examined. C2C12 cells were treated with IGF-I in the absence or presence of various inhibitors of p38 MAPK (SB203580), ERK1/2 (PD98059), and JNK (SP600125). Inhibition of the MAPK pathway with SB203580, PD98059, or SP600125 significantly decreased IGF-I-induced AR pho-sphorylation and total AR protein expression. IGF-I-induced nuclear fraction of total AR and phosphorylated AR were significantly inhibited by SB203580, PD98059, or SP600125. Furthermore, IGF-I-induced AR mRNA and skeletal α-actin mRNA were blocked by those inhibitors in dose-dependent manner. Confocal images showed that IGF-I-induced AR nuclear translocation from cytosol was significantly blocked by SB203580, PD98059, or SP600125, suggesting that the MAPK pathway regulates IGF-I-induced AR nuclear localization in skeletal muscle cells. The present results suggest that the MAPK pathways are required for the ligand-independent activation of AR by IGF-I in C2C12 skeletal muscle cells.

Keywords androgen receptor, insulin-like growth factor-I, ligand-independent mechanism, mitogen-activated protein kinase, steroid receptor

Article

Communication

Mol. Cells 2009; 28(6): 589-593

Published online December 31, 2009 https://doi.org/10.1007/s10059-009-0167-z

Copyright © The Korean Society for Molecular and Cellular Biology.

Ligand-Independent Activation of the Androgen
Receptor by Insulin-Like Growth Factor-I and the
Role of the MAPK Pathway in Skeletal Muscle Cells

Hye Jin Kim, and Won Jun Lee

Received: September 29, 2009; Accepted: October 19, 2009

Abstract

In this study, the roles of the p38 MAPK, ERK1/2 and JNK signaling pathway in IGF-I-induced AR induction and activation were examined. C2C12 cells were treated with IGF-I in the absence or presence of various inhibitors of p38 MAPK (SB203580), ERK1/2 (PD98059), and JNK (SP600125). Inhibition of the MAPK pathway with SB203580, PD98059, or SP600125 significantly decreased IGF-I-induced AR pho-sphorylation and total AR protein expression. IGF-I-induced nuclear fraction of total AR and phosphorylated AR were significantly inhibited by SB203580, PD98059, or SP600125. Furthermore, IGF-I-induced AR mRNA and skeletal α-actin mRNA were blocked by those inhibitors in dose-dependent manner. Confocal images showed that IGF-I-induced AR nuclear translocation from cytosol was significantly blocked by SB203580, PD98059, or SP600125, suggesting that the MAPK pathway regulates IGF-I-induced AR nuclear localization in skeletal muscle cells. The present results suggest that the MAPK pathways are required for the ligand-independent activation of AR by IGF-I in C2C12 skeletal muscle cells.

Keywords: androgen receptor, insulin-like growth factor-I, ligand-independent mechanism, mitogen-activated protein kinase, steroid receptor

Mol. Cells
Jan 31, 2023 Vol.46 No.1, pp. 1~67
COVER PICTURE
RNAs form diverse shapes and play multiple functions as central molecules of gene expression. In this special issue on RNA, seven minireviews illustrate how basic concepts and recent RNA biology findings are transformed into new and exciting RNA therapeutics.

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