Korean J Physiol Pharmacol.  1997 Aug;1(4):457-466.

Association of dexamethasone-induced apoptosis of G|1-arrest of human leukemic CEM cells with polyamine deficit

• Choi SH
• Lee JA
• Chae YS
• Min BH
• Chun YS
• Chun BG

Abstract

The effects of DFMO or/and putrescine on the dexamethasone-induced apoptosis of CEM cells were studied to investigate the role of polyamines in anti-leukemic glucocorticoid action. Dexamethasone-induced apoptosis was preceded by significant decreases of cellular polyamine contents and putrescine uptake activity. But DFMO produced decreases of putrescine and spermidine contents and marked increase of putrescine uptake activity, but did not induce apoptosis. However, dexamethasone and DFMO, respectively, induced G|1-arrest in cell cycle and hypophosphorylation of pRb, resulting in the increase of G|1 to S ratio and decrease of CEM cell count. DFMO enhanced the dexamethasone-induced apoptosis and G|1-arrest. On the other hand, putrescine little affected the apoptotic and G|1-arresting activities of dexamethasone, but almost suppress the effects of DFMO and also the DFMO-dependent enhancement of dexamethasone effects. These results suggested that the dexamethasone-induced apoptosis to be associated with pRb hypophosphorylation and G|1-arrest in CEM cells might be ascribed to the concomitant decreases of cellular polyamine contents and putrescine uptake activity.

Keyword

Leukemic cell; Dexamethasone; DFMO; Polyamine; Putrescine uptake; Apoptosis; pRb

MeSH Terms

Apoptosis*
Cell Count
Cell Cycle
Dexamethasone
Hand
Humans*
Polyamines
Putrescine
Spermidine
Dexamethasone
Polyamines
Putrescine
Spermidine