Calcium Signaling in Cancer

Dear Colleagues,

It is probably a simple chemical fact that calcium phosphate precipitates make Ca²⁺ such an important intracellular messenger. When the phosphate-containing ATP becomes the prominent energy source during early cell evolution, Ca²⁺ has to be downregulated to prevent precipitation. Hence, there are many transporters and channels which regulate intracellular Ca²⁺ homeostasis and keep its concentration in the nano- to micro- molar range. With Ca²⁺ in the extracellular space, on the other hand, in the millimolar range, there is a large gradient from inside to outside, making Ca²⁺ entry a very efficient way to considerably induce a Ca²⁺ elevation in the intracellular space and precisely modulate its levels in a temporal and spatial manner. In addition, numerous calcium-binding proteins emerged during evolution, the most prominent being those containing the so-called EF-hand structural motif, which is present in many sequences encoding phosphatases and kinases, as well as transcription factors. Well established is the function of Ca²⁺ as a second messenger for electro-mechanical coupling, as well as for electro-secretory coupling in cardiac muscles and neuronal cells, respectively. Here, voltage-gated calcium channels represent the principal calcium regulators. Furthermore, intracellular Ca²⁺ homeostasis can also be regulated by IP₃ dependent mechanisms, ryanodine receptors and non-selective channels of the TRP type, which are involved in many important biological processes, such as cell growth and cell differentiation. Besides endoplasmic reticulum, Ca²⁺ is also taken up by mitochondria during physiological Ca²⁺ signalling, which plays an important functional role in cell physiology and pathophysiology. This Special Issue concentrates on the role of Ca²⁺ signalling in the development of cancer as well as the regulation of calcium in cancer cells. There are numerous examples that demonstrate that defective Ca²⁺ signalling in cancer cells results, in part, from the dysregulation of calcium channels and calcium binding proteins, and is involved in controlling cancer cell motility, cell proliferation and apoptosis. A significant body of new knowledge about the pathological signature of Ca²⁺ signalling in cancer cells has accumulated in recent years, and has a great potential for developing novel therapeutic approaches. This Special Issue will bring together all state of the art knowledge and technologies about Ca²⁺ signalling in cancer.

You are invited to participate in this Special Issue of Cells. We hope that you will find this research field of interest.

Prof. Dr. Jürgen Hescheler
Guest Editor

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• calcium signaling
• cancer
• calcium-binding protein
• cancer cell motility
• cell proliferation
• apoptosis