Glioblastoma (grade IV astrocytoma) is an aggressive and incurable form of brain tumor.
It invariably shows extensive invasion at the time of diagnosis, often involving both hemispheres.
Recent studies have given us a very detailed picture of glioblastoma genetics. These paint a picture
of a disease with extensive heterogeneity, both between patients and within individual patients. This
within patient heterogeneity presents a major challenge in the design of targeted therapies. One
approach is to identify targets that are common downstream elements in signaling pathways that are
aberrantly activated in glioblastoma. Here we review the evidence that the atypical protein kinase C family member PKCι
may fulfill this role. Our current understanding of PKCι activation mechanisms is discussed and related to common
genetic changes in glioblastoma. The data showing an essential role for PKCι in multiple aspects of glioblastoma
pathology are also reviewed. Finally, data on the role of PKCι in normal brain function are reviewed for insights into
potential side effects of PKCι inhibition in the central nervous system.
Keywords: Atypical protein kinase C, glioblastoma, glioma, PKCι, PKCζ, PTEN
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