Dataset Information


Transcription profiling by array of human esophageal adenocarcinoma OE33 cells treated with procyanidin

ABSTRACT: Epidemiologic studies have shown a significant inverse correlation between fruit and vegetable consumption and incidence of esophageal adenocarcinoma. Procyanidins are polymeric flavanols found in many fruits and vegetables, and have been shown to possess anti-carcinogenic/chemopreventive properties. We previously showed that an oligomeric procyanidin extracted from apples with an average degree of polymerisation of 3.9 induced cell cycle arrest and apoptosis in the esophageal adenocarcinoma cell line OE33. In order to understand the mechanism of action of this procyanidin we determined genome-wide transcriptomic changes induced by procyanidin treatment of OE33 cells. Pathway analysis of these data implicated the MAP kinase signalling pathways in eliciting these responses. An investigation into the role of these pathways showed that procyanidin specifically induced the activation of the stress-activated protein (SAP) kinases JNK1/2 and p38-? and ? leading to the increased expression of JUN and the phosphatases DUSP1 and -10. Gene-specific knockdown of the expression of JNK1, JNK2, p38-?, p38-? or JUN diminished procyanidin-induced effects on apoptosis demonstrating a clear role for these pathways. JUN is a component of the transcription factor AP-1 and AP-1 binding sites are over-represented in the promoters of procyanidin-induced genes, which together with the demonstration that JUN occupies several such promoters highlight the importance of this transcription factor in mediating the cellular response to procyanidin. These data provide a mechanistic understanding of how procyanidin specifically targets distinct pathways involved in the induction of apoptosis in esophageal adenocarcinoma cells and will inform future studies investigating its use as a chemopreventive/therapeutic agent.

ORGANISM(S): Homo sapiens  

DISEASE(S): Adenocarcinoma

SUBMITTER: Michiel Adriaens  

PROVIDER: E-MEXP-2993 | ArrayExpress | 2011-06-16


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