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Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch Galveston, Texas 77550
Department of Pharmacology, University of South Carolina Medical School Columbia, South Carolina 29208
Address requests for reprints to: Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, TX 77550.
Abstract
Glucocorticoids regulate proliferation of lymphosarcoma P1798 in culture. Treatment with dexamethasone caused a redistribution of cells with respect to the cell cycle. A decrease in cells in S and G2 + M phases was observed. This was accompanied by a corresponding increase in G1 cells. Growth arrest was preceded by a rapid and precipitous decrease in the expression of the cellular c-myc gene. Restriction analysis of the c-myc gene indicated that this locus was neither amplified nor grossly rearranged in P1798 cells. Glucocorticoids caused a decrease in the abundance of c-myc mRNA. After 24 h in 0.1µM dexamethasone, c-myc mRNA levels declined to less than 5% of control. Fifty percent inhibition occurred within 90 min. The effects of dexamethasone were completely reversible. The amount of c-myc mRNA returned to control levels within 4 h after withdrawal of the hormone. Nuclear run-on transcription analysis indicated that glucocorticoids regulate transcription of the c-myc gene in P1798 cells. Transcription of exons I and II was inhibited to the same extent, suggesting that glucocorticoids inhibit initiation of transcription. Inhibition of transcription may account for decreased expression of c-myc which may, in turn, account for the antiproliferative effects of the hormone.
FOOTNOTES
This work was supported in part by NIH Grant CA-24347 (to E.A.T.).
* Recipient of American Cancer Society Faculty Research Award FRA299.
Received for publication August 31, 1987. Accepted for publication October 6, 1987.
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