Glucocorticoid inhibition of c-myc, c-myb, and c-Ki-ras expression in a mouse lymphoma cell line.
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.
D000199:Actins / Q000235:genetics; D000818:Animals; D002453:Cell Cycle / Q000187:drug effects; D002460:Cell Line; D004247:DNA / Q000096:biosynthesis; D005786:Gene Expression Regulation / Q000187:drug effects; D006133:Growth Substances / Q000235:genetics; D007700:Kinetics; D008223:Lymphoma; D008324:Mammary Tumor Virus, Mouse / Q000235:genetics; D051379:Mice; D011519:Proto-Oncogenes; D012333:RNA, Messenger / Q000235:genetics; D014221:Triamcinolone / Q000494:pharmacology*; D014404:Tubulin / Q000235:genetics
D000199:Actins; D006133:Growth Substances; D012333:RNA, Messenger; D014404:Tubulin; D014221:Triamcinolone; D004247:DNA