Procyanidin-induced apoptosis of esophageal adenocarcinoma cells is mediated via stress-activated protein kinase activation of JUN-dependent transcription.

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

ORGANISM(S): Homo sapiens

SUBMITTER: Michiel Adriaens 

PROVIDER: E-MEXP-2993 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress