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Calcium Signalling and Disease pp 405–427Cite as

Calcium signalling and cancer cell growth

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Part of the book series: Subcellular Biochemistry ((SCBI,volume 45))

Abstract

Cancer is caused by defects in the mechanisms underlying cell proliferation and cell death. Calcium ions are central to both phenomena, serving as major signalling agents with spatial localization, magnitude and temporal characteristics of calcium signals ultimately determining cell’s fate. There are four primary compartments: extracellular space, cytoplasm, endoplasmic reticulum and mitochondria that participate in the cellular Ca2+ circulation. They are separated by own membranes incorporating divers Ca2+-handling proteins whose concerted action provides for Ca2+ signals with the spatial and temporal characteristics necessary to account for specific cellular response. The transformation of a normal cell into a cancer cell is associated with a major re-arrangement of Ca2+ pumps, Na/Ca exchangers and Ca2+ channels, which leads to the enhanced proliferation and impaired ability to die. In the present chapter we examine what changes in Ca2+ signalling and the mechanisms that support it underlie the passage from normal to pathological cell growth and death control. Understanding this changes and identifying molecular players involved provides new prospects for cancers treatment

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Authors and Affiliations

  1. INSERM U800, Laboratoire de Physiologie Cellulaire, Université des Sciences et Technologies Lille 1, 59655 Villeneuve d’Ascq Cedex, France

    T. CAPIOD, R. SKRYMA & N. PREVARSKAYA

  2. Bogomoletz Institute of Physiology, NASU, Bogomoletz Str, 4, 01024 Kiev-24, Ukraine

    Y. SHUBA

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  1. T. CAPIOD
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  1. University of Padova, Padova, Italy

    Ernesto Carafoli

  2. University of Padova, Padova, Italy

    Marisa Brini

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CAPIOD, T., SHUBA, Y., SKRYMA, R., PREVARSKAYA, N. (2007). Calcium signalling and cancer cell growth. In: Carafoli, E., Brini, M. (eds) Calcium Signalling and Disease. Subcellular Biochemistry, vol 45. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-6191-2_15

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