ARTICLE

Cell Research, 15(7):511-522, July 2005

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

Xiao Jing WANG, Jie YANG, Hui CANG, Yan Qiong ZOU, Jing YI^*

Department of Cell Biology, Shanghai Second Medical University, 280 Chongqing Road, Shanghai 200025, China

Received, Apr 30, 2005 Revised, May 20, 2005 Accepted, May 24, 2005

Correspondence: Jing YI +86-21-63846590 (phone) +86-21-53065329 (Fax) yijing@shsmu.edu.cn

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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.

Keywords: microarray, reactive oxygen species, apoptosis, arsenic trioxide, emodin.