Posttranscriptional Mechanisms of Glucocorticoid Antiproliferative Effects: Glucocorticoids Inhibit IL-6-Induced Proliferation of B9 Hybridoma Cells

Abstract

Addition of rIL-6 to IL-6-dependent B9 cells starved for IL-6 for 16 – 20 h stimulated a vigorous proliferative response. Glucocorticoids (GCs), in a concentration-dependent manner, inhibited rIL-6-stimulated proliferation of B9 cells This inhibition was specific for the GCs, evident by the capacity of the GCs, dexamethasone, prednisolone, and hydrocortisone, but not non-GC steroids, to suppress rIL-6-dependent B9 cell proliferation. Furthermore, GC inhibition of IL-6-stimulated B9 cell proliferation was receptor mediated and was abrogated by the GC receptor antagonist, RU486. In addition to their reported effects on inhibition IL-6 expression, the results presented support the notion that GCs also acted distally by suppressing signal transduction through the IL-6 receptor.