Role of calcium-dependent protein kinases in chronic myeloid leukemia: combined effects of PKC and BCR-ABL signaling on cellular alterations during leukemia development

Calcium-dependent protein kinases (PKCs) function in a myriad of cellular processes, including cell-cycle regulation, proliferation, hematopoietic stem cell differentiation, apoptosis, and malignant transformation. PKC inhibitors, when targeted to these pathways, have demonstrated efficacy against several types of solid tumors as well as leukemia. Chronic myeloid leukemia (CML) represents 20% of all adult leukemia. The aberrant Philadelphia chromosome has been reported as the main cause of CML development in hematopoietic stem cells, due to the formation of the BCR-ABL oncogene. PKCs and BCR-ABL coordinate several signaling pathways that are crucial to cellular malignant transformation. Experimental and clinical evidence suggests that pharmacological approaches using PKC inhibitors may be effective in the treatment of CML. This mini review summarizes articles from the National Center for Biotechnology Information website that have shown evidence of the involvement of PKC in CML.