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

29 Citations (Scopus)

Abstract

Since arginine deiminase (ADI; EC 3.5.3.6) 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
Volume112
Issue number3
DOIs
Publication statusPublished - 2004 Nov 10

Keywords

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

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'Arginine deiminase enhances dexamethasone-induced cytotoxicity in human T-lymphoblastic leukemia CCRF-CEM cells'. Together they form a unique fingerprint.

Cite this