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

被引：66

作者：

Wang, XJ ^{[1
]}

Yang, J ^{[1
]}

Cang, H ^{[1
]}

Zou, YQ ^{[1
]}

Yi, J ^{[1
]}

机构：

[1] Shanghai Med Univ 2, Dept Cell Biol, Shanghai 200025, Peoples R China

来源：

CELL RESEARCH | 2005年 / 15卷 / 07期

关键词：

microarray; reactive oxygen species; apoptosis; arsenic trioxide; emodin;

D O I：

10.1038/sj.cr.7290321

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 [细胞生物学]; 090102 [作物遗传育种];

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, 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.

引用

页码：511 / 522

页数：12

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