Involvement of PKC-ι in glioma proliferation


Mildred Acevedo-Duncan, James A. Haley Veterans Hospital, 13000 Bruce B. Downs Blvd. VAR 151, Tampa, FL 33612, USA. Tel.: (813) 972-2000 extension 6967; Fax: (813) 972-7623; E-mail:


Abstract.  Atypical protein kinase C-iota (PKC-ι) protects cells against apoptosis and may play a role in cell proliferation. However, in vivo, the status and function of PKC-ι in human normal brain tissue, gliomas, benign and malignant meningiomas as well as its in vitro status in proliferating and confluent glioma cells, remains unknown. Objectives: The objectives of our research were to determine whether expression of PKC-ι is altered either in gliomas or in benign and malignant meningiomas, compared to normal brain. In addition, we wished to establish the expression of PKC-ι in proliferating plus in cell cycle-arrested glioma cell lines, as well as the relationship between PKC-ι siRNA on PKC-ι protein content and cell proliferation. Materials and Methods: Western blot analyses for PKC-ι were performed on 12 normal brain biopsies, 15 benign meningiomas, three malignant meningiomas and three gliomas. Results: Results demonstrated no (n = 9) or very weak (n = 3) detection of PKC-ι in normal brain tissue. In comparison, PKC-ι was robustly present in the majority of the benign meningiomas. Similarly, PKC-ι was abundant in all malignant meningiomas and gliomas. Western blotting for PKC-ι in confluent or proliferating glioma cell lines depicted substantial quantities of PKC-ι in proliferating T98G and U-138MG glioma cells. In contrast, confluent cells had either 71% (T98G) or 21% (U-138MG) less PKC-ι than proliferating cells. T98 and U-138 MG glioma cells treated with 100 nm PKC-ι siRNA had lower levels of cell proliferation compared to control siRNA-A and complete down-regulation of PKC-ι protein content. Conclusion: These results support the concept that presence of PKC-ι may be required for cell proliferation to take place.