Glucocorticoid inhibition of c-myc, c-myb, and c-Ki-ras expression in a mouse lymphoma cell line.

Abstract

Glucocorticoid hormone treatment of certain T-cell-derived lymphomas and leukemias and of immature thymocytes results in cell death. Furthermore, glucocorticoid-mediated killing of S49 mouse lymphoma cells appears to involve the control of the cell cycle; i.e., S49 cells treated with glucocorticoids are arrested in G1 of the cell cycle when events controlling cell proliferation occur. The protooncogenes, c-myc, c-myb, and c-Ki-ras may be involved in cell cycle regulation and proliferation state in both normal and neoplastic cells. We report here that the steady state mRNA levels of c-myc, c-myb, and c-Ki-ras in S49 cells are dramatically and rapidly decreased after glucocorticoid treatment. Minimal expression is observed after 9 h, remaining at a constant low level at 11 h. Flow cytometry reveals no significant alteration in the cell cycle distribution of S49 cells up to 12 h after treatment. These findings suggest that glucocorticoids suppress the expression of these protooncogenes and that this may be the mechanism whereby glucocorticoids inhibit cell cycle progression in T-lymphoid cell lines.