Journal
NATURE REVIEWS CANCER
Volume 8, Issue 5, Pages 361-375Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrc2374
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Funding
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C197, BBS/E/B/0000C199, BBS/E/B/0000C116, C20001, BBS/E/B/00001116] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C199, BBS/E/B/0000C116, BBS/E/B/00001116, C20001, BBS/E/B/0000C197] Funding Source: Medline
- British Heart Foundation Funding Source: Medline
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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.
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