Volume 15, No 7, Jul 2005

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 15 Issue 7, July 2005: 511-522

ORIGINAL ARTICLES

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 Correspondence: Jing YI(yijing@shsmu.edu.cn)

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.

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