title: 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.
authors.affiliation: Department of Laboratory Medicine, St. Georges-Orthodox Hospital, Beirut, Lebanon.
authors.forename: W Y
authors.initials: WY
authors.lastname: Almawi
authors.forename: H
authors.initials: H
authors.lastname: Tamim
mesh_terms: D000818:Animals; D002455:Cell Division / Q000187:drug effects*; D002460:Cell Line; D003907:Dexamethasone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D006825:Hybridomas / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D006854:Hydrocortisone / Q000494:pharmacology; D015850:Interleukin-6 / Q000494:pharmacology*; D007700:Kinetics; D051379:Mice; D011239:Prednisolone / Q000494:pharmacology; D011994:Recombinant Proteins / Q000037:antagonists & inhibitors / Q000494:pharmacology; D000093242:Interleukin-6 Inhibitors
chemical_list: D003907:Dexamethasone; D005938:Glucocorticoids; D006854:Hydrocortisone; D015850:Interleukin-6; D011239:Prednisolone; D011994:Recombinant Proteins; D000093242:Interleukin-6 Inhibitors