Nm23-H1 inhibits proliferation of glioma cells via regulation of PKC signaling pathway

Purpose: To explore the influence of nm23-H1 on the proliferation and apoptosis of glioma cells and the mechanism therein. Methods: The changes in the messenger ribonucleic acid (mRNA) expression of nm23-H1 were detected via quantitative real-time-polymerase chain reaction (qRT-PCR), and the relative protein expression level of nm23-H1 was determined using immunohistochemistry. The glioma H4 cells were transfected exogenously with nm23-H1 gene (nm23-H1 group) or empty vector (Vector group), and the biological influences of the expression level of nm23-H1 on H4 cells were then assessed through in vitro functional experiments. Besides, the cells transfected with nm23-H1 were incubated with the protein kinase C (PKC) pathway inhibitor Calphostin C, and functional experiments were performed to observe the changes in the proliferation and apoptosis of cells after incubation. Results: According to the immunohistochemistry and qRTPCR results, the protein and mRNA expression levels of nm23-H1 declined notably in glioma tissues (p<0.01). The cells with up-regulated nm23-H1 expression had substantially weakened proliferation and migration abilities, but exhibited dramatically enhanced apoptosis (p<0.01). The PKC pathway inhibitor considerably potentiated the effects of nm23-H1 protein on the proliferation and apoptosis of H4 cells (p<0.05), and the protein expression level of nm23H1 rose in the cells treated with the PKC inhibitor (p<0.01). Conclusions: Compared with that in normal brain tissues, nm23-H1 is lowly expressed in glioma tissues and affects the expression of PKC to influence the biological behaviors of H4 cells.