Arsenic trioxide induces apoptosis of p53 null osteosarcoma MG63 cells through the inhibition of catalase

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• 作者：Yang Wang (1)
  Yudan Wei (2)
  Haiying Zhang (1)
  Yanfen Shi (1)
  Yulin Li (1)
  Ronggui Li (1)
  
• 关键词：Arsenic trioxide ; Catalase ; Osteosarcoma ; Apoptosis ; ROS
• 刊名：Medical Oncology
• 出版年：2012
• 出版时间：June 2012
• 年：2012
• 卷：29
• 期：2
• 页码：1328-1334
• 全文大小：433KB
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• 作者单位：Yang Wang (1)
  Yudan Wei (2)
  Haiying Zhang (1)
  Yanfen Shi (1)
  Yulin Li (1)
  Ronggui Li (1)
  
  1. The Key Laboratory of Pathobiology, Ministry of Education, Jilin University, 130021, Changchun, People’s Republic of China
  2. Department of Community Medicine, Mercer University School of Medicine, Macon, GA, USA
  

文摘

This study is aimed at investigating the effect of arsenic trioxide (ATO) on p53 null human osteosarcoma MG63 cells and the mechanisms underlying the effect. Apoptotic cells were detected by flow cytometry with Annexin-V-FITC/PI dual staining. Intracellular ROS was measured by flow cytometry using a cell-based ROS assay kit. Catalase activity and mRNAs were analyzed by ELISA and real-time qRT–PCR, respectively. Apoptosis and intracellular ROS of MG63 cells increased in a dose-dependent manner following arsenic treatments. Both were prevented by the presence of the anti-oxidative reagent N-acetyl-l-cysteine (NAC) or catalase (CAT). Furthermore, the activity and mRNA of catalase were decreased strikingly following arsenic exposure. The present study indicates that p53 null osteosarcoma MG63 cells are susceptible to the ATO; the inhibition of catalase and the resulted intracellular ROS accumulation are an important molecular mechanism under which ATO induces apoptosis of p53-deficient osteosarcoma cells.