Dexamethasone-induced killing of neoplastic cells of lymphoid derivation: lack of early calcium involvement.
The role of calcium influx in dexamethasone-induced fragmentation of DNA was studied in the glucocorticoid-sensitive human lymphoid line of T cell derivation (CEM-C7). Reduction of calcium content in the medium or the use of EGTA increased DNA fragmentation and appeared to slightly enhance the effect of dexamethasone. Incubation of isolated nuclei in the presence of high concentrations of calcium did not bring about significant DNA fragmentation. Calmidazolium, an antagonist of calmodulin dependent reactions did not reduce the sensitivity of CEM-C7 cells to dexamethasone nor did it modify the response to dexamethasone of the resistant CEM-C1 line. It appears that in contrast to rodent thymocytes, massive calcium influx is not per se responsible for the initiation of directed cell killing (apoptosis).
Bansal
N
N
Department of Microbiology, University of Kansas Medical Center, Kansas City 66103.
Houle
A G
AG
Melnykovych
G
G
D001692:Biological Transport; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002147:Calmodulin / Q000037:antagonists & inhibitors; D002455:Cell Division / Q000187:drug effects; D002467:Cell Nucleus / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects*; D004249:DNA Damage; D003907:Dexamethasone / Q000494:pharmacology*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D066298:In Vitro Techniques; D008214:Lymphocytes / Q000187:drug effects* / Q000502:physiology; D014407:Tumor Cells, Cultured
D002147:Calmodulin; D007093:Imidazoles; D000001:Calcimycin; C031938:calmidazolium; D003907:Dexamethasone; D002118:Calcium