Open AccessInvolvement of PKC‐ι in glioma proliferation
Author(s) -
Patel R.,
Win H.,
Desai S.,
Patel K.,
Matthews J. A.,
AcevedoDuncan M.
Publication year - 2008
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.2007.00506.x
Subject(s) - protein kinase c , glioma , cell growth , apoptosis , western blot , proliferating cell nuclear antigen , cancer research , blot , cell culture , cell , biology , cell cycle , pathology , microbiology and biotechnology , kinase , medicine , biochemistry , genetics , gene
. 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 n m 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.