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Asymmetry along an apical-basal axis or apical-basal polarity within neural stem cells (NSC) is critical for the asymmetric segregation of cell fate and differentiation.NSC-derived differentiating daughters migrate extensively during embryonic development-an event that is also regulated by apical-basal polarity.We have demonstrated that atypical protein kinase C (aPKC) provides an instructive signal for apical-basal polarity in NSC during embryonic development of the chick CNS.aPKC is compartmentalized at the apical membrane of neural progenitors, and disrupting the endogenous localization of this kinase results in loss of apical cell adhesion junctions, increased proliferation of neural progenitors and abnormal migration of these cells within differentiated cell layers.Can aPKC and apical-basal signaling pathway be associated with abnormal cell proliferation and invasiveness of CNS tumors such as Glioblastoma? We have demonstrated that aPKCstaining is significantly enhanced in clinical samples of Glioblastoma multiforme (GBM).The knockdown of aPKC in GBM-derived cell lines decreases cell migration.Our studies suggest that aPKC, a protein kinase and thus a highly attractive target for rational drug design, may be a novel therapeutic target in GBM.