» Articles » PMID: 25045273

Role of Calcium-dependent Protein Kinases in Chronic Myeloid Leukemia: Combined Effects of PKC and BCR-ABL Signaling on Cellular Alterations During Leukemia Development

Overview
Publisher Dove Medical Press
Specialty Oncology
Date 2014 Jul 22
PMID 25045273
Citations 8
Authors
Affiliations
Soon will be listed here.
Abstract

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.

Citing Articles

Deregulated calcium signaling in blood cancer: Underlying mechanisms and therapeutic potential.

Immanuel T, Li J, Green T, Bogdanova A, Kalev-Zylinska M Front Oncol. 2022; 12:1010506.

PMID: 36330491 PMC: 9623116. DOI: 10.3389/fonc.2022.1010506.


The Anti-Leukemic Activity of Natural Compounds.

Cotoraci C, Ciceu A, Sasu A, Miutescu E, Hermenean A Molecules. 2021; 26(9).

PMID: 34063044 PMC: 8124534. DOI: 10.3390/molecules26092709.


Homologous recombination defects and how they affect replication fork maintenance.

Son M, Hasty P AIMS Genet. 2019; 5(4):192-211.

PMID: 31435521 PMC: 6690234. DOI: 10.3934/genet.2018.4.192.


Deregulation of calcium homeostasis in Bcr-Abl-dependent chronic myeloid leukemia.

Cabanas H, Harnois T, Magaud C, Cousin L, Constantin B, Bourmeyster N Oncotarget. 2018; 9(41):26309-26327.

PMID: 29899861 PMC: 5995172. DOI: 10.18632/oncotarget.25241.


Synthesis and Cytotoxicity against K562 Cells of 3-O-Angeloyl-20-O-acetyl Ingenol, a Derivative of Ingenol Mebutate.

Liu M, Chen F, Yu R, Zhang W, Han M, Liu F Int J Mol Sci. 2016; 17(8).

PMID: 27548156 PMC: 5000744. DOI: 10.3390/ijms17081348.


References
1.
Obrian C, Vogel V, Singletary S, Ward N . Elevated protein kinase C expression in human breast tumor biopsies relative to normal breast tissue. Cancer Res. 1989; 49(12):3215-7. View

2.
Michor F . Chronic myeloid leukemia blast crisis arises from progenitors. Stem Cells. 2007; 25(5):1114-8. DOI: 10.1634/stemcells.2006-0638. View

3.
Melo J . The diversity of BCR-ABL fusion proteins and their relationship to leukemia phenotype. Blood. 1996; 88(7):2375-84. View

4.
Redig A, Platanias L . The protein kinase C (PKC) family of proteins in cytokine signaling in hematopoiesis. J Interferon Cytokine Res. 2007; 27(8):623-36. DOI: 10.1089/jir.2007.0007. View

5.
Zheng C, Li L, Haak M, Brors B, Frank O, Giehl M . Gene expression profiling of CD34+ cells identifies a molecular signature of chronic myeloid leukemia blast crisis. Leukemia. 2006; 20(6):1028-34. DOI: 10.1038/sj.leu.2404227. View