Association of Dexamethasone-induced Apoptosis and G1-Arrest of Human Leukemic CEM Cells with Polyamine Deficit

• 영문명: Association of Dexamethasone-induced Apoptosis and G₁-Arrest of Human Leukemic CEM Cells with Polyamine Deficit
• 발행기관: 대한생리학회-대한약리학회
• 저자명: Sang-Hyun Choi Jung-Ae Lee Yang-Seok Chae Bon-Hong Min Yeon-Sook Chun Boe-Gwun Chun
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제1권 제4호, 457~466쪽, 전체 10쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 1997.01.01

영문 초록

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 G₁-arrest in cell cycle and hypophosphorylation of pRb, resulting in the increase of G₁ to S ratio and decrease of CEM cell count. DFMO enhanced the dexamethasone-induced apoptosis and G₁-arrest. On the other hand, putrescine little affected the apoptotic and G₁-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 G₁-arrest in CEM cells might be ascribed to the concomitant decreases of cellular polyamine contents and putrescine uptake activity.

키워드

Leukemic cell Dexamethasone DFMO Polyamine Putrescine uptake Apoptosis pRb