Abstract

Increases in cytosolic free Ca²⁺ ([Ca²⁺]_i) represent a ubiquitous signalling mechanism that controls a variety of cellular processes, including proliferation, metabolism and gene transcription, yet under certain conditions increases in intracellular Ca²⁺ are cytotoxic. Thus, in using Ca²⁺ as a messenger, cells walk a tightrope in which [Ca²⁺]_i is strictly maintained within defined boundaries. To adhere to these boundaries and to sustain their modified phenotype, many cancer cells remodel the expression or activity of their Ca²⁺ signalling apparatus. Here, we review the role of Ca²⁺ in promoting cell proliferation and cell death, how these processes are remodelled in cancer and the opportunities this might provide for therapeutic intervention.

Author affiliations

1. Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1PD, UK.
2. Laboratory of Molecular Signalling, Babraham Institute, Babraham Research Campus, Babraham, Cambridge CB22 3AT, UK.

Correspondence to: H. Llewelyn Roderick^1,2 Email: llewelyn.roderick@bbsrc.ac.uk

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