Abstract
Abstract CD109 is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein whose expression is predominantly detected in squamous cell carcinomas of esophagus, lung, uterus and oral cavity. In the previous study, we found CD109 expression in cell lines derived from human glioblastomas by Northern blot analysis, however, the role of CD109 expression in glioblastoma cells is unclear. Here, we describe our study on significance of CD109 expression in biology of human glioblastoma cells. CD109-overexpressing glioblastoma cells exhibit upregulation of cell growth, motility and invasion ability compared with control cells. Evaluation of intracellular signaling status revealed that the CD109-overexpressing cells showed enhanced phosphorylation of ERK, AKT, and p38MAPK. After epidermal growth factor (EGF) stimulation, strong and sustained phosphorylation of these molecules and EGF receptor (EGFR) was observed in the CD109-overexpressing cells. In addition, we found an interaction between CD109 and EGFR and colocalization of these molecules without EGF stimulation. However, the interaction and colocalization were abolished after EGF stimulation, and EGFR internalization was not affected by CD109 overexpression. These findings suggest that CD109 facilitates EGF signaling via binding to EGFR and its expression is associated with the malignant behavior of glioblastoma cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1050.
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