J Cancer 2017; 8(5):716-729. doi:10.7150/jca.17779
The controversial role of phospholipase C epsilon (PLCε) in cancer development and progression
1. OncoRay - National Center for Radiation Research in Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden and Helmholtz-Zentrum Dresden-Rossendorf, Fetscherstrasse 74, 01307 Dresden, Germany.
2. The Institute of Molecular Biology and Genetics of NASU, Kyiv, Ukraine.
3. German Cancer Consortium (DKTK), Dresden, Germany.
4. Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, Germany.
The phospholipase C (PLC) enzymes are important regulators of membrane phospholipid metabolism. PLC proteins can be activated by the receptor tyrosine kinases (RTK) or G-protein coupled receptors (GPCR) in response to the different extracellular stimuli including hormones and growth factors. Activated PLC enzymes hydrolyze phosphoinositides to increase the intracellular level of Ca2+ and produce diacylglycerol, which are important mediators of the intracellular signaling transduction. PLC family includes 13 isozymes belonging to 6 subfamilies according to their domain structures and functions. Although importance of PLC enzymes for key cellular functions is well established, the PLC proteins belonging to the ε, ζ and η subfamilies were identified and characterized only during the last decade. As a largest known PLC protein, PLCε is involved in a variety of signaling pathways and controls different cellular properties. Nevertheless, its role in carcinogenesis remains elusive.
The aim of this review is to provide a comprehensive and up-to-date overview of the experimental and clinical data about the role of PLCε in the development and progression of the different types of human and experimental tumors.
Keywords: Phospholipase Cε, cancer development, intracellular signaling, oncogene, tumor suppressor
Tyutyunnykova A, Telegeev G, Dubrovska A. The controversial role of phospholipase C epsilon (PLCε) in cancer development and progression. J Cancer 2017; 8(5):716-729. doi:10.7150/jca.17779. Available from http://www.jcancer.org/v08p0716.htm