摘要
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, wecarried 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 substantiallyaltered at two time points. These genes are involved in different aspects of cell function. In addition to redox regulationand 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 resourcethrough which the As2O3–induced apoptosis is facilitated.
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.
基金
This study was supported by grants from National Natural Science Foundation of China(No.30170475)
Shanghai Municipal Education Commission(No.zdxk2001).
