Regulation of fibronectin gene expression by cyclic AMP and phorbol myristate acetate in HT-1080 human fibrosarcoma cells.
- Author:
Byung Heon LEE
1
;
Rang Woon PARK
;
In San KIM
Author Information
1. Department of Biochemistry, School of Medicine, Dongguk University, Kyungju, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
cAMP;
fibronectin;
HT-1080;
phorbol myristate acetate;
protein kinase C
- MeSH:
Blotting, Northern;
Bucladesine/pharmacology*;
Bucladesine/antagonists & inhibitors;
Enzyme-Linked Immunosorbent Assay;
Fibronectins/metabolism;
Fibronectins/genetics*;
Fibrosarcoma/genetics*;
Gene Expression Regulation*;
Human;
Luciferase/metabolism;
Precipitin Tests;
Promoter Regions (Genetics);
RNA, Messenger/metabolism;
Tetradecanoylphorbol Acetate/pharmacology*;
Transfection;
Tumor Cells, Cultured;
beta-Galactosidase/metabolism
- From:Experimental & Molecular Medicine
1998;30(4):240-245
- CountryRepublic of Korea
- Language:English
-
Abstract:
We studied the regulation of fibronectin (FN) gene expression by cAMP and phorbol-12-myristate-13-acetate (PMA) in HT-1080 human fibrosarcoma cells. Dibutyryl cAMP increased FN synthesis and mRNA levels, while PMA inhibited the cAMP-induced FN synthesis. In transient transfection assays, cAMP increased FN promoter activity, while PMA paradoxically enhanced the cAMP-induced promoter activity. Stable transfection experiments, however, showed that neither cAMP or PMA alone nor together affected FN promoter activity. These results suggest that PMA antagonizes the cAMP-induced FN gene expression and that both the action of cAMP and the inhibition of its action by PMA may occur at the posttranscriptional level in HT-1080 cells.
