Repression of glucocorticoid receptor gene transcription by c-Jun

Molecular and Cellular Endocrinology
A L CabralV R Martins

Abstract

The regulation of glucocorticoid receptor gene expression by members of the AP-1 family was examined in glucocorticoid-free NIH3T3 cells transfected with the human glucocorticoid receptor gene promoter driving expression of a CAT reporter gene. c-Jun inhibited the promoter activity by 80% and JunB by 30%, whereas c-Fos and JunD had no inhibitory effect. Electrophoretic mobility shift assays showed that c-Jun is unable to efficiently interact with the AP-1-like site present in the human glucocorticoid receptor promoter. Moreover, c-Jun was still able to repress promoter mutants in which the region containing the AP-1-like site was deleted. NIH3T3 cell clones overexpressing c-Jun exhibited lower glucocorticoid receptor mRNA levels, which suggests that the murine glucocorticoid receptor gene can also be regulated by AP-1. These results provide a new mechanism for cross-talk between the glucocorticoid receptor and the AP-1 family of transcription factors in the absence of glucocorticoid ligands.

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Citations

Jul 30, 2002·Brain Research·Deanna L McCullersJames P Herman
Oct 16, 2002·The International Journal of Biochemistry & Cell Biology·Sumudra Periyasamy, Edwin R Sánchez
Nov 17, 2004·The Journal of Steroid Biochemistry and Molecular Biology·Patricia B RozenchanM Mitzi Brentani

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