Deregulated human glioma cell motility : inhibitory effect of somatostatin

Malignant gliomas are highly invasive tumors which are lethal despite aggressive therapy. The motility behavior of two human glioma cell lines i.e. T98G and U87-MG cells was analyzed. The glioma cells showed a high degree of basal motility (esp. U87-MG cells) that may be related to the considerable local invasiveness of such tumors even in the absence of exogenous factors. The two cell lines responded equally well to platelet-derived growth factor (PDGF) as chemoattractant factor. The phosphatidylinositol 3-kinase (PI3-K) signaling, but not the extracellular signal-related kinase (ERK) signaling, was strongly involved in the PDGF-stimulated glioma cell motility. Somatostatin was capable of inhibiting the migration in both glioma cell lines without affecting crucial targets for motility control like PI3-K and Rac activity. These data suggest that somatostatin, by interfering with a target further downstream to Rac, neg. affects glioma cell motility, and may thus offer a pharmacol. approach to controlling the deregulated motility of these aggressive tumoral cells. [on SciFinder (R)]