Activation of PKCα is required for migration of C6 glioma cells

Most primary central nervous system (CNS) tumors are derived from glial cells and collectively referred to as gliomas. Malignant gliomas exhibit a high rate of cell motility and migration that contributes to the invasiveness of the tumors (Amberger et al. 1998, Griscelli et al. 2000, DeAngelis 2001, Bello et al. 2004). Thus, the understanding of the molecular mechanisms which regulate glioma cell motility is very important. Protein kinase C (PKC) is a member of serine/threonine protein kinase family that are involved in diverse cellular functions, including contraction (Yan et al. 2001), cell motility (Makagiansar et al. 2004), growth (Yokoyama et al. 2005), differentiation (Cannons et al. 2004), proliferation, tumor promotion (Chida et al. 2003), fertilization (Halet 2004), and apoptosis (Baines et al. 2005, Miguel et al. 2008). Accumulating evidence suggests that there is a potential role of PKC in migration of cells (Nakashima 2002, Koivunen et al. 2006). PKCα and PKCβ are two important members of PKC family, and their activation have been often linked to malignant phenotype. However, PKCα and PKCβ have been shown to display variable expression profiles and functions during cancer progression depending on a particular cancer type (Koivunen et al. 2006). The functional role of various isoforms of PKC in gliomas is still poorly understood. Whether PKCα and PKCβ are expressed by glioma cells and plays a role in glioma cell migration remains unknown. In the present study, we provided evidence that PKCα play an important role in migration of C6 cells.