Gene expression alteration during redox-dependent enhancement of arsenic cytotoxicity by emodin in HeLa cells

Cell Res. 2005 Jul;15(7):511-22. doi: 10.1038/


Emodin (1,3,8-trihydroxy-6-methylanthraquinone) could enhance the sensitivity of tumor cells to arsenic trioxide (As2O3)-induced apoptosis via generation of ROS, but the molecular mechanism has not been elucidated. Here, we carried out cDNA microarray-based global transcription profiling of HeLa cells in response to As2O3/emodin cotreatment, comparing with As2O3-only treatment. The results showed that the expression of a number of genes was substantially altered at two time points. These genes are involved in different aspects of cell function. In addition to redox regulation and apoptosis, ROS affect genes encoding proteins associated with cell signaling, organelle functions, cell cycle, cytoskeleton, etc. These data suggest that based on the cytotoxicity of As2O3, emodin mobilize every genomic resource through which the As2O3-induced apoptosis is facilitated.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Arsenic Trioxide
  • Arsenicals
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • Dose-Response Relationship, Drug
  • Emodin / pharmacology*
  • Gene Expression Profiling*
  • Gene Expression Regulation, Neoplastic / drug effects*
  • HeLa Cells
  • Humans
  • Microarray Analysis / methods
  • Oxidation-Reduction
  • Oxides / toxicity*
  • RNA, Messenger* / drug effects
  • RNA, Messenger* / genetics
  • Reactive Oxygen Species / metabolism
  • Sensitivity and Specificity
  • Time Factors


  • Arsenicals
  • Oxides
  • RNA, Messenger
  • Reactive Oxygen Species
  • Emodin
  • Arsenic Trioxide