Insulin-like growth factor I stimulates transcription of the c-jun proto-oncogene in Balb c 3T3 cells

Shean Tai Chiou; Wen Chang Chang

doi:10.1016/0006-291X(92)90513-K

Insulin-like growth factor I stimulates transcription of the c-jun proto-oncogene in Balb c 3T3 cells

Shean Tai Chiou, Wen Chang Chang

Research output: Contribution to journal › Article

17 Citations (Scopus)

Abstract

Treatment of quiescent Balb c 3T3 cells with insulin-like growth factor I (IGF I) resulted in the stimulation of proto-oncogene c-jun transcription. Cells exposed to cycloheximide and IGF I together showed super-induction of c-jun transcripts. Nuclear run-off assay revealed that IGF I up-regulated c-jun only while cycloheximide was present. The stability of c-jun mRNA was markedly increased in the cells treated with IGF I. These results suggest that IGF I controls the expression of c-jun by increasing the transcriptional activity and stabilizing the existing transcripts.

Original language	English
Pages (from-to)	524-531
Number of pages	8
Journal	Biochemical and Biophysical Research Communications
Volume	183
Issue number	2
DOIs	https://doi.org/10.1016/0006-291X(92)90513-K
Publication status	Published - Mar 16 1992
Externally published	Yes

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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Chiou, S. T., & Chang, W. C. (1992). Insulin-like growth factor I stimulates transcription of the c-jun proto-oncogene in Balb c 3T3 cells. Biochemical and Biophysical Research Communications, 183(2), 524-531. https://doi.org/10.1016/0006-291X(92)90513-K

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AB - Treatment of quiescent Balb c 3T3 cells with insulin-like growth factor I (IGF I) resulted in the stimulation of proto-oncogene c-jun transcription. Cells exposed to cycloheximide and IGF I together showed super-induction of c-jun transcripts. Nuclear run-off assay revealed that IGF I up-regulated c-jun only while cycloheximide was present. The stability of c-jun mRNA was markedly increased in the cells treated with IGF I. These results suggest that IGF I controls the expression of c-jun by increasing the transcriptional activity and stabilizing the existing transcripts.

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