Abstract
Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a multifunctional serine/threonine kinases best known for its critical role in learning and memory. Recent studies suggested that high levels of CaMKII also expressed in variety of malignant diseases. In this review, we focus on the structure and biology properties of CaMKII, including the role of CaMKII in the regulation of cancer progression and therapy response. We also describe the role of CaMKII in the diagnosis of different kinds of cancer and recent progress in the development of CaMKII inhibitors. These data establishes CaMKII as a novel target whose modulation presents new opportunities for cancer diagnosis and treatment.
Highlights
Calcium ion (Ca2+) is a ubiquitous intracellular signal responsible for a broad range of cellular events, such as cell growth, cytoskeletal organization, regulation of synaptic transmission, and Ca2+ homeostasis[1,2,3]
Expression of CaMKIV inhibited autophosphorylation and activation of calmodulin-dependent protein kinase II (CaMKII), and elicited G0/G1 cell cycle arrest, impairing cell proliferation. These data reveal a novel cross-talk between CaMKII and CaMKIV and suggest that CaMKII suppresses the expression of CaMKIV to promote leukemia cell proliferation
Umemura et al.[38] found another mechanism of CaMKII involving cancer cell invasion. They showed that store-operated Ca2+ entry (SOCE) promoted melanoma progression by enhancing cell invasion and metastasis through activation of Erk signaling via the CaMKII/Raf-1/Erk pathway, irrespective of the status of Braf
Summary
Keywords: Ca2+/calmodulin-dependent protein kinase II (CaMKII), cancer, cell cycle, therapeutic target, CaMKII inhibitor This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
