Roderick H Llewelyn, Cook Simon J
Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1PD, UK.
Nat Rev Cancer. 2008 May;8(5):361-75. doi: 10.1038/nrc2374.
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.
胞质游离钙离子浓度([Ca2+]i)的升高代表一种普遍存在的信号传导机制,它控制着包括增殖、代谢和基因转录在内的多种细胞过程,但在某些情况下,细胞内钙离子浓度升高具有细胞毒性。因此,在将钙离子用作信使时,细胞如履薄冰,[Ca2+]i被严格维持在特定范围内。为了维持这些范围并维持其改变的表型,许多癌细胞重塑其钙离子信号传导装置的表达或活性。在这里,我们综述钙离子在促进细胞增殖和细胞死亡中的作用,这些过程在癌症中是如何重塑的,以及这可能为治疗干预提供的机会。