¹Department of Cell Biology, Shanghai Second Medical University, 280 Chongqing Road, Shanghai 200025, China

Correspondence: Jing YI, Tel: +86-21-63846590(ext 776565); Fax: +86-21-53065329; E-mail: yijing@shsmu.edu.cn

Received 30 April 2005; Revised 20 May 2005; Accepted 24 May 2005.

Abstract

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.