Neural stem cell targeting of glioma is dependent on phosphoinositide 3-kinase signaling.

摘要: The utility of neural stem cells (NSCs) has extended beyond regenerative medicine to targeted gene delivery, as NSCs possess an inherent tropism solid tumors, including invasive gliomas. However, for optimal clinical implementation, understanding the molecular events that regulate NSC tumor is needed ensure their safety and maximize therapeutic efficacy. We show human lines responded multiple tumor-derived growth factors hepatocyte factor (HGF) induced strongest chemotactic response. Gliomatropism was critically dependent on c-Met signaling, short hairpin RNA-mediated ablation significantly attenuated Furthermore, inhibition Ras-phosphoinositide 3-kinase (PI3K) signaling impaired migration (hNSCs) toward HGF other factors. Migration a highly regulated process, in which signals converge Ras-PI3K, causing direct modification cytoskeleton. pathways hNSC are similar those promote unregulated glioma invasion, suggesting shared cellular mechanisms responses. Disclosure potential conflicts interest found at end this article.