Arginine deiminase enhances dexamethasone-induced cytotoxicity in human T-lymphoblastic leukemia CCRF-CEM cells

Eun Joo Noh, Sang Wook Kang, Yong Jae Shin, Sang Hyun Choi, Chan Gil Kim, In Sun Park, Denys N. Wheatley, Bon Hong Min

    Research output: Contribution to journalArticlepeer-review

    32 Citations (Scopus)

    Abstract

    Since arginine deiminase (ADI; EC 3.5.3.6) inhibits cell proliferation by arresting cells in the G1 phase, we tested its synergistic effect on cell death induced by dexamethasone (DEX), which also induces apoptosis by G1 cell cycle arrest. ADI inhibited cell proliferation and induced apoptosis in human leukemic CEM cells in a dose-dependent manner. Simultaneous treatment with ADI and DEX showed synergistic effects on DNA fragmentation and LDH release. In addition, ADI exerted its anti-proliferative activity against DEX-resistant CEH cells. ADI suppressed expression of c-myc, a potential key regulator of cell proliferation and apoptosis, and increased expression of p27Kip1 cyclin-dependent kinase inhibitor. These results suggest that ADI efficiently increases the anti-cancer effect of DEX on human leukemic CEM cells through G1 cell cycle arrest involving downregulation of c-myc and upregulation of p27Kip1.

    Original languageEnglish
    Pages (from-to)502-508
    Number of pages7
    JournalInternational Journal of Cancer
    Volume112
    Issue number3
    DOIs
    Publication statusPublished - 2004 Nov 10

    Keywords

    • Arginine
    • Arginine deiminase
    • CEM leukemia cells
    • Dexamethasone
    • Polyamine
    • c-myc

    ASJC Scopus subject areas

    • Oncology
    • Cancer Research

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