Expression of c-Myc in glucocorticoid-treated fibroblastic cells.
Glucocorticoids inhibit proliferation of L929 fibroblastic cells in culture. Inhibition of proliferation is reversible and is not associated with changes in the plating efficiency of the cells. Flow cytometric analysis indicates that glucocorticoid-treated cells exhibit a decrease in the percentage of cells with DNA content > 2 N. Thymidine kinase expression is inhibited as cells with 2 N DNA content accumulate. These observations indicate that glucocorticoids arrest proliferation of L929 cells in the G1 phase of the cell cycle. The abundance of c-Myc mRNA does not decrease in glucocorticoid-treated cells, and c-Myc protein content in dexamethasone-treated cells is approximately the same as that detected in mid-log phase cells. Nuclear run-on transcription of c-Myc is not inhibited by glucocorticoids. These observations indicate that glucocorticoid regulation of fibroblastic cell proliferation does not involve inhibition of c-Myc transcription. Although regulation of c-Myc expression is central to the mechanism whereby glucocorticoids regulate proliferation of lymphoid cells, it is clear that different mechanisms must be involved in glucocorticoid regulation of fibroblastic cell proliferation.
Frost
G H
GH
Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston 77550.
Rhee
K
K
Ma
T
T
Thompson
E A
EA
D000818:Animals; D002453:Cell Cycle / Q000187:drug effects; D003907:Dexamethasone / Q000494:pharmacology*; D005347:Fibroblasts; D005786:Gene Expression Regulation / Q000187:drug effects; D016259:Genes, myc; D007739:L Cells; D051379:Mice; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D013937:Thymidine Kinase / Q000235:genetics
D016271:Proto-Oncogene Proteins c-myc; D012333:RNA, Messenger; D003907:Dexamethasone; D013937:Thymidine Kinase