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

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29 Citations (Scopus)


Since arginine deiminase (ADI; EC inhibits cell proliferation by arresting cells in the G 1 phase, we tested its synergistic effect on cell death induced by dexamethasone (DEX), which also induces apoptosis by G 1 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 p27 Kip1 cyclin-dependent kinase inhibitor. These results suggest that ADI efficiently increases the anti-cancer effect of DEX on human leukemic CEM cells through G 1 cell cycle arrest involving downregulation of c-myc and upregulation of p27 Kip1.

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



  • Arginine
  • Arginine deiminase
  • c-myc
  • CEM leukemia cells
  • Dexamethasone
  • p27
  • Polyamine

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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