Dexamethasone induces irreversible G 1 arrest and death of a human lymphoid cell line

Growth of a human leukemic T‐cell line (CEM C7) in 10 −6 M dexamethasone results in inhibition of growth and rapid loss of cell viability after a delay of approximately 18 to 24 hours. Analysis of dexamethasonetreated cells by flow‐microfluorometry showed that they were arrested in the G 1 phase of the cell cycle. Loss of cell viability began at the same time as G 1 accumulation was first detectable, and 20% of all cells were found to be blocked in G 1 at this time suggesting that loss of viability and G 1 arrest were coincident events. Half‐maximal and maximal effects on both viability and G 1 arrest after 48 hours in steroid were nearly identical with respect to steroid concentration and corresponded to half‐maximal and full occupancy of glucocorticoid specific receptor by hormone, consistent with a glucocorticoid receptor mediated mechanism for both phenomena. Most non‐viable cells were arrested in G 1 , and accumulation of cells in G 1 was irreversible; removal of steroid in the presence of colcemid did not result in a decreased fraction of G 1 cells. Furthermore, dexamethasone treatment did not protect cells against the effects of 33258 Hoechstamplified killing of bromodeoxyuridine substituted cells exposed to light. These results show that dexamethasone arrests these leukemic cells in G 1 and strongly suggest that dexamethasone‐treated cells are killed upon entry into G 1 .