Chloramphenicol Arrests Transition of Cell Cycle and Induces Apoptotic Cell Death in Myelogenous Leukemia Cells

  • KANG KI YOUNG (Department of Anatomy, Seonam University College of Medicine) ;
  • CHOI CHUL HEE (Department of Microbiology and Institute of Infectious Diseases, Kyungpook National University School of Medicine) ;
  • OH JAE YOUNG (Department of Microbiology and Institute of Infectious Diseases, Kyungpook National University School of Medicine) ;
  • KIM HYUN (Department of Anatomy, Kosin University College of Medicine) ;
  • KWEON GI RYANG (Department of Biochemistry, Seonam University College of Medicine) ;
  • LEE JE CHUL (Department of Microbiology and Institute of Infectious Diseases, Kyungpook National University School of Medicine)
  • 발행 : 2005.10.01

초록

Chloramphenicol is a broad-spectrum antimicrobial agent against Gram (+) and Gram (-) bacteria. Its clinical application has recently been limited, due to severe side effects such as bone marrow suppression and aplastic anemia. In the present study, the cytotoxic effects of chloramphenicol were investigated in vitro using chronic myelogenous leukemia K562 cells. Chloramphenicol inhibited the growth of K562 cells in a dose-dependent manner, but their growth was restored after the cessation of chloramphenicol, indicating reversible cytotoxic effects. The expression of cell cycle regulatory molecules, including E2F-1 and cyclin D1, was decreased at the translational and/or transcriptional level after being treated with a therapeutic blood level ($20{\mu}g/ml$) of chloramphenicol. Chloramphenicol also induced apoptotic cell death through a caspase-dependent pathway, which was verified by Western blot analysis and the enzymatic activity of caspase-3. These results demonstrated that chloramphenicol inhibited the cell growth through arresting the transition of the cell cycle, and induced apoptotic cell death through a caspase-dependent pathway at therapeutic concentrations.

키워드

참고문헌

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