Targeting Ca²⁺ transport in cancer: close reality or long perspective?

Cancer is caused by defects in the mechanisms underlying cell proliferation, death and migration. Calcium ions are central to all of these phenomena, serving as major signalling agents with the spatial localisation, magnitude and temporal characteristics of calcium signals ultimately determining cell's fate. The transformation of a normal cell into a malignant derivative is associated with a major rearrangement of Ca(2+) pumps, Na/Ca exchangers and Ca(2+) channels, which leads to enhanced proliferation and invasion under compromised/impaired ability to die.

This paper examines the changes in Ca(2+) signalling and the mechanisms that underlie the passage from normal to pathological cell growth and death control. Understanding these changes and identifying the molecular players involved provide new perspectives for cancer treatment.

Despite compelling evidence that the disruption of Ca(2+) homeostasis in cancer cells leads to the promotion of certain malignant phenotypes as well as the identification of key Ca(2+)-transporting molecules whose altered expression and/or function underlies pathological changes, the therapeutic utilisation of these findings for cancer treatment is still at its infancy. However, the rapid development of the field warrants the development of improved molecular Ca(2+) transport-targeting tools for cancer diagnosis and treatment.