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

Abstract

ABSTRACTEmodin (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… (More)
DOI: 10.1038/sj.cr.7290321

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