O128 TGF-BETA1 AND TGF-BETA2 MEDIATED EPITHELIAL-MESENCHYMAL TRANSITION IN ESOPHAGEAL ADENOCARCINOMA CELLS

Abstract

Abstract Aim he esophageal adenocarcinoma (EAC) is characterized by an early lymphogenic dissemination and a poor prognosis. The tumor biology and the impact of autocrine, paracrine and endocrine mediators are involved in these mechanisms. For dissemination, the tumor cells need to escape the solid tumor and invade into new target structures. This mechanism is described as epitheliale-mesenchymal transition (EMT), which could be initiated by TGF-beta Methods Two proliferation and motility of the esophageal adenocarcinoma cell lines (OE33, OE19) were analyzed after TGF-beta1 and TGF-beta2 treatment. EMT marker gene expressions (e.g. vimentin) were assessed by qRT-PCR. Results TGF-beta2 led to a deceased proliferation rate compared to untreated and TGF-beta1 treated cells in OE33 cells. In OE19 cells both, TGF-beta1 and TGF-beta2 treatment resulted in an increased proliferation compared to untreated cells. In OE33 cells the motility was affected by TGF-beta1 only, while in OE19 cells the motility was increased by TGF-beta1 and TGF-beta2 compared to untreated cells. The vimentin mRNA-expression in OE33 cells was increased by TGF-beta1 and TGF-beta2 (14.7-fold and 25.9-fold). However TGF-beta1 and TGF-beta2 only led to a moderate increase in the vimentin mRNA-expression (4.0-fold and 1.8-fold) in OE19 cells. Conclusion TGF-beta1 and TGF-beta2 induce EMT and cellular motility in a cell line specific pattern. The responsible intracellular signaling cascades addressed by TGF-beta1 and TGF-beta2 and their contribution for dissemination in EAC patients need to be investigated with full details.