Polyamine-depletion induces p27(Kip1) and enhances dexamethasone-induced G1 arrest and apoptosis in human T lymphoblastic leukemia cells

Sang Hyun Choi, Seong Woo Kim, Dong Hee Choi, Bon Hong Min, Boe Gwun Chun

    Research output: Contribution to journalArticlepeer-review

    26 Citations (Scopus)


    Glucocorticoid-induced apoptosis is preceded by G1 arrest and supposed to be up-regulated by polyamine-depletion, which also induces G1 arrest. In CEM leukemia cells, dexamethasone showed an antileukemic effect by inducing G1 arrest and apoptosis. DFMO, which depleted cellular polyamines by inhibiting ornithine decarboxylase, induced G1 arrest but without apoptosis, though it enhanced dexamethasone-induced G1 arrest and apoptosis. The G1 arrest was associated with hypophosphorylation of pRb. Dexamethasone inhibited the increase of mutated p53 expression but had little effect on p21(Waf1/Cip1) expression. The p27(Kip1) level was increased by dexamethasone or/and DFMO in line with the kinetics of G1 arrest. Therefore, the up-regulation of dexamethasone-induced apoptosis by polyamine-depletion may be associated with additive down-regulation of G1 progression via the p27(Kip1)-pRb pathway.

    Original languageEnglish
    Pages (from-to)119-127
    Number of pages9
    JournalLeukemia Research
    Issue number2
    Publication statusPublished - 2000 Feb


    • Apoptosis
    • CEM leukemia cells
    • DL-α-Difluoromethylornithine
    • Dexamethasone
    • G arrest
    • p27(Kip1)
    • pRb

    ASJC Scopus subject areas

    • Hematology
    • Oncology
    • Cancer Research


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