Microarray analysis of vanillin-regulated gene expression profile in human hepatocarcinoma cells

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Title:	Microarray analysis of vanillin-regulated gene expression profile in human hepatocarcinoma cells
Authors:	鄭文裕(Wen-Yu Cheng);項千芸(Chien-Yun Hsiang);包大靝(Da-Tian Bau);陳兆群(Jaw-Chyun Chen);沈偉舜(Wei-Shuen Shen);李佳橙(Chia-Cheng Li);羅欣宜(Hsin-Yi Lo);吳世祿(Shih-Lu Wu);江素瑛(Su-yin Chiang);侯庭鏞(Tin-Yun Ho)*
Contributors:	中醫學院中國醫學研究所
Keywords:	Vanillin;Gene expression profile;Microarray;Activator protein 1;Extracellular signal-regulated protein kinase;Apoptosis;Cell cycle
Date:	2007-12
Issue Date:	2009-08-24 14:47:23 (UTC+8)
Abstract:	Vanillin is one of the most widely used flavor compounds in food and personal products. It has been reported that vanillin is able to inhibit mutagenesis induced by chemical and physical mutagens, and to suppress the invasion and migration of cancer cells. Herein we used the oligonucleotide microarray approach to study gene expression profile of vanillin-treated human hepatocarcinoma cells. Microarray data followed by gene ontology (GO) investigation displayed that vanillin-affected clusters of genes involved in cell cycle and apoptosis. Genes down-regulated by vanillin were grouped into three GO categories, regulation of cellular process, cell cycle, and death. Furthermore, most of the down-regulated genes were associated with cancer progression. Knowledge-based analysis further indicated that Fos may play a central role in the regulation of gene expression network. Analysis of Fos-related transcription factor, activator protein 1 (AP-1), showed that vanillin inhibited AP-1 activity in a dose-dependent manner. Furthermore, the phosphorylation of extracellular signal-regulated protein kinase (ERK) was diminished with increasing concentrations of vanillin, indicating that vanillin-regulated AP-1 activity via ERK pathway. In conclusion, our data suggested that vanillin exhibited the anticancer potential by the regulations of cell cycle and apoptosis. Moreover, its regulation may involve the suppression of a central molecule, AP-1.
Relation:	PHARMACOLOGICAL RESEARCH 56(6)474 ~482
Appears in Collections:	[Graduate Institute of Chinese Medical Science] Journal articles

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